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1.  The impact of diurnal fasting during Ramadan on the lipid profile, hs-CRP, and serum leptin in stable cardiac patients 
To study the effect of strict prolonged fasting on lipid profile, serum leptin, and high- sensitivity C-reactive protein (hs-CRP) in patients with different stable cardiac illnesses and look for associated new cardiac events and any correlation between entire variables.
A total of 56 patients of different stable cardiac illnesses were followed in our cardiology outpatient for 3 months. Data concerning their ability to fast were collected: New York Heart Association class of congestive cardiac failure, angina class, previous myocardial infarction, previous coronary artery bypass graft, percutaneous coronary intervention, severity of valvular lesion, metallic prosthetic valve, and traditional risk factors (diabetes mellitus, insulin requirement, hypertension, hypercholesterolemia, smoking habit, and obesity). Detailed clinical examination and electrocardiography were performed in all patients in three consecutive visits before, during, and after Ramadan. Echocardiographic and angiographic findings and medication plans were collected from patient records. Lipid profile, serum leptin, and hs-CRP were assessed before, during, and after Ramadan.
All patients fasted during Ramadan: 80.4% were male, 67.9% were aged >50 years, 71.4% had no change in their symptoms during fasting while 28.6% felt better. No patient has deteriorated. 91.1% of the patients were compliant with medicine during Ramadan, 73.2% after. 89.3% were compliant with diet during Ramadan with no significant change in body weight in the follow-up period. No cardiac or noncardiac morbidity or mortality was reported. High- density lipoprotein-cholesterol (HDL-C) decreased significantly during compared to before fasting (P = 0.012). Low-density lipoprotein-cholesterol (LDL-C) significantly increased during compared to before fasting (P = 0.022). No statistically significant changes were observed in total cholesterol (TC), triglycerides (TG), serum leptin, or hs-CRP. Significant correlation was observed between TC and hs-CRP during fasting (P = 0.036), but not with TG, LDL-C, or HDL-C (P > 0.05). Neither of these correlated with serum leptin (P > 0.05), but significant correlation was observed between hs-CRP and serum leptin (P < 0.05).
Ramadan fasting in stable cardiac patients has no effect on their clinical status, serum leptin, or hs-CRP, but results in decrease in HDL-C, increase in LDL-C, with significant correlation between TC and hs-CRP during Ramadan, but not with TG, LDL-C, or HDL-C, and with significant correlation between hs-CRP and serum leptin before, during, and after fasting.
PMCID: PMC3262481  PMID: 22272070
serum leptin; hs-C-reactive protein; lipid profile; cardiac disease; Ramadan fasting
2.  Insulin Resistance Is an Independent Determinate of ED in Young Adult Men 
PLoS ONE  2013;8(12):e83951.
Insulin resistance (IR) triggers endothelial dysfunction, which contributes to erectile dysfunction (ED) and cardiovascular disease.
To evaluate whether IR was related to ED in young adult patients.
A total of 283 consecutive men complaining of ED at least six months were enrolled, with a full medical history, physical examination, and laboratory tests collected. Quantitative Insulin Sensitivity Check Index (QUICKI) was used to determine IR. The severity of ED was assessed by IIEF-5 questionnaire. Endothelial function was assessed by ultrasonographic examination of brachial artery flow mediated dilation (FMD).
IR was detected in 52% patients. Subjects with IR had significant higher total cholesterol, triglycerides, low density lipoprotein-cholesterol (LDL-c), glycated haemoglobin (HBA1c), high sensitivity C-reactive protein (hs-CRP) and body mass index (BMI), but showed significant lower IIEF-5 score, FMD%, high density lipoprotein -cholesterol (HDL-c), testosterone, sex hormone binding globulin (SHBG) levels than patients without IR. Multiple regression analysis showed QUICKI and testosterone were independent predictors of IIEF-5 score. Furthermore, the incidence of IR was correlated with the severity of ED.
Compared with other CVFs, IR was found as the most prevalent in our subjects. Besides, IR was independently associated with ED and its severity, suggesting an adverse effect of insulin resistance on erectile function.
PMCID: PMC3877124  PMID: 24391852
3.  Lipid Accumulation Product Is Associated with Insulin Resistance, Lipid Peroxidation, and Systemic Inflammation in Type 2 Diabetic Patients 
Endocrinology and Metabolism  2014;29(4):443-449.
Lipid accumulation product (LAP) is a novel biomarker of central lipid accumulation related to risk of diabetes and cardiovascular disease. In this study, we assessed the association of LAP with glucose homeostasis, lipid and lipid peroxidation, and subclinical systemic inflammation in diabetic patients.
Thirty-nine male and 47 female type 2 diabetic patients were assessed for anthropometrics and biochemical measurements. LAP was calculated as [waist circumference (cm)-65]×[triglycerides (mmol/L)] in men, and [waist circumference (cm)-58]×[triglycerides (mmol/L)] in women. Associations of LAP with fasting glucose, insulin, insulin resistance index, lipid and lipoprotein levels, malondialdehyde, and high-sensitive C-reactive protein (hs-CRP) were assessed.
Mean age and LAP index were 53.6±9.6 and 51.9±31.2 years, respectively. After adjustments for age, sex and body mass index status, a significant positive correlation was observed between LAP index and fasting glucose (r=0.39, P<0.001), and homeostasis model assessment of insulin resistance (r=0.31, P<0.05). After additional adjustment for fasting glucose levels, antidiabetic and antilipidemic drugs, the LAP index was also correlated to total cholesterol (r=0.45, P<0.001), high density lipoprotein cholesterol (HDL-C) levels (r=-0.29, P<0.05), triglycerides to HDL-C ratio (r=0.89, P<0.001), malondialdehyde (r=0.65, P<0.001), and hs-CRP levels (r=0.27, P<0.05).
Higher central lipid accumulation in diabetic patients was related to higher insulin resistance, oxidative stress and systemic inflammation.
PMCID: PMC4285040  PMID: 25325262
Diabetes mellitus, type 2; Lipid accumulation product; Subclinical inflammation; Oxidative stress
4.  The Association of the Triglyceride-to-HDL Cholesterol Ratio with Insulin Resistance in White European and South Asian Men and Women 
PLoS ONE  2012;7(12):e50931.
There is recent interest surrounding the use of the triglyceride-to-HDL cholesterol ratio as a surrogate marker of insulin resistance in clinical practice, as it may identify people at high risk of developing diabetes or its complications. However, it has been suggested using this lipid ratio may not be appropriate for measuring insulin resistance in African-Americans, particularly women. We investigated if this inconsistency extended to South Asian women in a UK multi-ethnic cohort of White Europeans and South Asians.
Cross-sectional analysis was done of 729 participants from the ADDITION-Leicester study from 2005 to 2009. The association between tertiles of triglyceride-to-HDL cholesterol ratio to fasting insulin, homeostatic model of assessment for insulin resistance (HOMA1-IR), quantitative insulin sensitivity check index (QUICKI) and glucose: insulin ratio was examined with adjustment for confounding variables.
Incremental tertiles of the triglyceride-to-HDL cholesterol ratio demonstrated a significant positive association with levels of fasting insulin, HOMA1-IR, glucose: insulin ratio and a negative association with QUICKI in White European men (n = 255) and women (n = 250) and South Asian men (n = 124) (all p<0.05), but not South Asian women (n = 100). A significant interaction was demonstrated between sex and triglyceride-to-HDL cholesterol ratio tertiles in South Asians only (p<0.05). The area under the receiver operating characteristic curve for triglyceride-to-HDL cholesterol ratio to detect insulin resistance, defined as the cohort HOMA1-IR≥75th percentile (3.08), was 0.74 (0.67 to 0.81), 0.72 (0.65 to 0.79), 0.75 (0.66 to 0.85) and 0.67 (0.56 to 0.78) in White European men and women, South Asian men and women respectively. The optimal cut-points for detecting insulin resistance were 0.9–1.7 in mmol/l (2.0–3.8 in mg/dl) for the triglyceride-to-HDL ratio.
In South Asian women the triglyceride-to-HDL cholesterol ratio was not associated with insulin resistance; therefore there may be limitations in its use as a surrogate marker in this group.
PMCID: PMC3518473  PMID: 23251403
5.  Association of metabolic syndrome with severity of coronary artery disease 
South Asians are more prone to develop metabolic syndrome (MetS). The additive predictive value of components of MetS for cardiovascular diseases is still debated. We undertook this study to evaluate the association of MetS and its components with severity of coronary artery disease (CAD).
Materials and Methods:
Three hundred patients with known coronary disease above the age of 25 years were included in this study. Blood samples were collected for biochemical markers. Patients were stratified into subjects with and without MetS (International Diabetes Federation, IDF, criteria) and severity of CAD (number of vessel involved).
Mean age of the patient in the study was 60.9 ± 12.4 years (male, M: 72%; female, F: 28%). MetS was present in 64% patients. Patients with MetS had more severe CAD compared to those without MetS. Triple vessel disease (TVD) was present in 62.5% of patients with MetS compared to 34.3% among without MetS (P < 0.0001). The percent number of patients with TVD showed increasing trend with increasing number of components of MetS (0-0%; 1-20%; 2-27.5%; 3-47.8%; 4-72.6%; 5-78.3%; Chi square for trend < 0.0001). Inflammatory markers [interleukin (IL) 6: 77.67 ± 79.48 vs. 41.21 ± 60.72 pg/ml, P < 0.0001; tumor nuclear factor (TNF)-α: 28.0 ± 47.49 vs 20.43 ± 24.5 pg/ml, P < 0.0001; high sensitive C-reactive protein (hsCRP): 14.30 ± 9.91 vs. 7.02 ± 7.18 mg/L, P < 0.0001], insulin resistance [homeostatic model analysis insulin resistance (HOMA-IR): 22.33 ± 23.37 vs. 10.86 ± 13.90, P < 0.0001] were higher and insulin sensitivity [quantitative insulin check index (QUICKI): 0.26 ± 0.03 vs. 0.30 ± 0.04, P < 0.0001] was significantly lower in subjects with MetS compared to subjects without MetS. Among lipids, total cholesterol were comparable but triglyceride (175 ± 42 vs. 179 ± 48 vs. 180 ± 47 mg/dl, P < 0.0001) was high and high-density lipoprotein (HDL; 44.72 ± 7.63 vs. 39.96 ± 8.70 vs. 36.05 ± 8.84, P < 0.0001) was low in subjects with TVD compared to others. Similarly, percentage of patients with diabetes (7.5% vs. 26.3% vs. 63.7%, P < 0.0001) and hypertension (34.3% vs. 56.6% vs. 77.7%, P < 0.0001) were higher in subjects with TVD compared to others.
There is a strong correlation of MetS and its components with severity of CAD.
PMCID: PMC4171897  PMID: 25285291
Coronary artery disease; inflammatory markers; insulin resistance; metabolic syndrome
6.  Anti-tumour necrosis factor alpha therapy improves insulin sensitivity in normal-weight but not in obese patients with rheumatoid arthritis 
Arthritis Research & Therapy  2012;14(4):R160.
Insulin resistance (IR), a risk factor for the development of cardiovascular disease, is common among patients with rheumatoid arthritis (RA). Inflammation, and especially tumour necrosis factor alpha (TNFα), has been associated with IR, and the administration of anti-TNFα agents is suggested to improve insulin sensitivity. However obesity, a potent contributor to IR, may limit the beneficial effects of anti-TNFα medication on IR. The aim of this study is to compare the effects of anti-TNFα therapy on IR between normal-weight and obese patients with RA.
Patients who were normal-weight with IR (N+IR) or obese with IR (O+IR) and had embarked on anti-TNFα treatment, participated. Assessments included body mass index (BMI), insulin sensitivity (Homeostasis Model Assessment of insulin resistance, HOMA and the Quantitative Insulin sensitivity Check Index, QUICKI), and RA disease characteristics before and following six months of anti-TNFα treatment. Their results were compared to matched (for age, gender, BMI, disease duration and smoking status) normal-weight patients without IR (N-IR) and obese without IR (N-IR), respectively. In total, 32 patients were assessed for this study, with 8 in each group.
Following six months of treatment, disease activity was significantly reduced in all groups (P < 0.05) to a similar extent (P for differences between groups > 0.05 in all cases). In the total population, changes in HOMA (mean reduction at 6 m = -0.2 ± 0.1; P = 0.088) and QUICKI (mean increase at 6 m = 0.03 ± 0.022; P = 0.092) after treatment were not statistically significant, though a trend towards improvement was observed. However, N+IR patients showed a significant decrease in HOMA (mean reduction at 6 m = -0.54 ± 0.2; P = 0.002) and increase in QUICKI (mean increase at 6 m = 0.046 ± 0.02; P = 0.011). These changes were significantly different compared to the other groups (P < 0.05 in all cases). Multivariable analyses showed that the change in Erythrocyte Sedimentation Rate (ESR), and the change in C-Reactive Protein (CRP) associated with the improvement in HOMA (ESR: F1-7 = 5.143, P = 0.019; CRP: F1-7 = 3.122, P = 0.022) and QUICKI (ESR: F1-7 = 3.814, P = 0.021; CRP: F1-7 = 2.67; P = 0.041) only in the N+IR group.
Anti-TNFα therapy, through controlling inflammation, seems to improve insulin sensitivity in normal-weight RA patients with insulin resistance, but is not sufficient to achieving the same beneficial effect in obese RA patients with insulin resistance.
PMCID: PMC3580552  PMID: 22765047
7.  Influence of glucocorticoids and disease activity on total and high density lipoprotein cholesterol in patients with rheumatoid arthritis 
Annals of the Rheumatic Diseases  2003;62(9):842-845.
Background: Glucocorticoids induce hypercholesterolaemia, a cardiovascular risk factor, in patients with diseases other than rheumatoid arthritis (RA), but the data in RA are contradictory.
Objective: To determine the effects of antirheumatic treatment, including prednisolone (combination) therapy on total and high density lipoprotein (HDL) cholesterol levels in RA, taking disease activity into account.
Methods: HDL cholesterol and total cholesterol levels were determined in:(a) established RA (b) two cohorts with early active RA, (c) a previously conducted 56 week trial among patients with early RA comparing the value of intensive combination therapy (that included glucocorticoids) with sulfasalazine alone (COBRA trial).
Results: In established RA total cholesterol levels were only slightly raised, irrespective of disease activity. However, HDL cholesterol was significantly higher in patients in remission than in patients with active disease. In contrast, in active early RA at baseline total cholesterol was low normal: between 4.6 and 5.1 mmol/l in the different populations. The level of HDL cholesterol was highly dependent on the duration of storage. In both COBRA groups total cholesterol increased by a mean of 0.6 mmol/l. HDL cholesterol increased by more than 50% after treatment, leading to an improvement of the total cholesterol/HDL ratio (atherogenic index). This increase (and index improvement) was much more rapid in the group receiving combination treatment. A similar pattern was seen in the 2001 cohort with early RA. In all the groups with active disease HDL and total cholesterol levels correlated inversely with disease activity.
Conclusion: In established, but especially in early RA, disease activity is accompanied by atherogenic lipid levels. This dyslipidaemia can be rapidly reversed by aggressive antirheumatic treatment including glucocorticoids.
PMCID: PMC1754645  PMID: 12922956
8.  Lipid screening: is it enough to measure total cholesterol concentration? 
BMJ : British Medical Journal  1990;301(6752):584-587.
OBJECTIVES--To determine whether measurement of total cholesterol concentration is sufficient to identify most patients at lipoprotein mediated risk of coronary heart disease without measurement of triglyceride and high density lipoprotein (HDL) cholesterol concentrations. DESIGN--Cross sectional screening programme. SETTING--Six general practices in Oxfordshire. PATIENTS--1901 Men and 2068 women aged 25-59. MAIN OUTCOME MEASURE--Cardiovascular risk as assessed by fasting venous plasma concentrations of total cholesterol, triglyceride, and HDL cholesterol. RESULTS--2931 Patients (74% of those screened) had a total cholesterol concentration of less than 6.5 mmol/l. If the triglyceride concentration had not been measured in these patients isolated hypertriglyceridaemia (greater than or equal to 2.3 mmol/l) would have remained undetected in 185. Among these 185 patients, however, 123 were overweight or obese and only 18 (0.6% of those screened) had an increased risk associated with both a raised triglyceride concentration (greater than or equal to 2.3 mmol/l) and a low HDL cholesterol concentration (less than 0.9 mmol/l). Conversely, in the 790 patients with predominant hypercholesterolaemia (cholesterol concentration greater than or equal to 6.5 mmol/l and triglyceride concentration less than 2.3 mmol/l) measurement of HDL cholesterol concentration showed that 348 (9% of those screened) had only a moderately increased risk with a ratio of total to HDL cholesterol of less than 4.5 and 104 had a low risk with a ratio of less than 3.5. CONCLUSIONS--Fasting triglyceride and HDL cholesterol concentrations identify few patients at increased risk of coronary heart disease if the total cholesterol concentration is less than 6.5 mmol/l. HDL cholesterol and triglyceride concentrations should, however, be measured in patients with a total cholesterol concentration exceeding this value. Total cholesterol concentration alone may overestimate risk in a considerable number of these patients, and measurement of HDL cholesterol concentration allows a more precise estimate of risk. Measurement of the triglyceride concentration is required to characterise the lipoprotein abnormality. A patient should not be started on a drug that lowers lipid concentrations without having had a full lipoprotein assessment including measurement of HDL cholesterol concentration.
PMCID: PMC1663711  PMID: 2082960
9.  Dyslipidaemia and Intima-Media Thickness of Carotid Arteries in Thirty-Five HIV/AIDS Patients Receiving Highly Active Antiretroviral Therapy 
Highly active antiretroviral therapy (HAART) has being impacted significantly therapies for natural human immunodeficiency virus (HIV) infection, which leads to a remarkable decrease in its morbidity and mortality but it is frequently associated with metabolic complications such as dyslipidaemia and cardiovascular complications. HIV reverse transcriptase (RT) inhibitors can be classified into nucleoside and non-nucleoside types. Mitochondrial dysfunction due to the depletion of mt-DNA is partly responsible for various nucleoside RT inhibitors-associated adverse effects including dyslipidaemia. Efavirenz (EFV) is metabolized primarily by cytochrome P450 2B6 (CYP2B6) and the metabolic effects of EFV have been described previously. All patients in this study received the same HAART treatment regime (Stavudine (d4T) + Lamivudine (3TC) + Efavirenz (EFV)). This study aims to assess incidences for dyslipidaemia and atherosclerosis.
This retrospective study was conducted within outpatients of Shanghai Public Health Center. We selected thirty-five HIV-1 infected patients who receiving highly active antiretroviral therapy. Their mean CD4 cell count was 69.5 (±34.6) copies per micro liter before therapy. Fasting total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol values were respectively compared among patients at present and before therapy. Then the data was statistically analyzed. Twenty-two patients had the intima-media thickness (IMT) of their carotid arteries measured by Philips 5000 Color-Doppler ultrasound tests. Results: After therapy, patients achieved significant changes in levels of triglycerides (1.44 ± 0.35mmol/L Vs. 2.07 ± 0.54mmol/L) (P<0.001), total cholesterol (4.96 ± 0.46 mmol/L Vs. 6.15 ± 0.83mmol/L) (P<0.001) and LDL cholesterol (2.29 ± 0.33 Vs. 3.11 ± 0.29 mmol/L) (P<0.001). In contrast, the level of HDL cholesterol did not significantly change (1.06 ± 0.01 mmol/L Vs. 1.04 ± 0.01 mmol/L) (P>0.5). The mean IMT of twenty-two patients was (0.86 ± 0.14) mm after HAART, which is higher than the norm age-matched value of (0.7 ± 0.2) mm (P<0.05).
After therapy, patients achieved significant changes in levels of triglycerides (1.44 ± 0.35mmol/L Vs. 2.07 ± 0.54mmol/L) (P<0.001), total cholesterol (4.96 ± 0.46 mmol/L Vs. 6.15 ± 0.83mmol/L) (P<0.001) and LDL cholesterol (2.29 ± 0.33 Vs. 3.11 ± 0.29 mmol/L) (P<0.001). In contrast, the level of HDL cholesterol did not significantly change (1.06 ± 0.01 mmol/L Vs. 1.04 ± 0.01 mmol/L) (P>0.5). The mean IMT of twenty-two patients was (0.86 ± 0.14) mm after HAART, which is higher than the norm age-matched value of (0.7 ± 0.2) mm (P<0.05).
These data suggest that HAART is potentially dangerous for hyperlipidaemia and maybe an increase in atherosclerosis.
PMCID: PMC3614766  PMID: 23675126
highly active antiretroviral therapy; dyslipidaemia; intima-media thickness of carotid artery
10.  Atherogenic lipid profile is a feature characteristic of patients with early rheumatoid arthritis: effect of early treatment – a prospective, controlled study 
We investigated lipid profiles and lipoprotein modification after immuno-intervention in patients with early rheumatoid arthritis (ERA). Fifty-eight patients with ERA who met the American College of Rheumatology (ACR) criteria were included in the study. These patients had disease durations of less than one year and had not had prior treatment for it. Smokers or patients suffering from diabetes mellitus, hypothyroidism, liver or kidney disease, Cushing's syndrome, obesity, familiar dyslipidemia and those receiving medications affecting lipid metabolism were excluded from the study. Sixty-three healthy volunteers (controls) were also included. Patients were treated with methotrexate and prednisone. Lipid profiles, disease activity for the 28 joint indices score (DAS-28) as well as ACR 50% response criteria were determined for all patients. The mean DAS-28 at disease onset was 5.8 ± 0.9. After a year of therapy, 53 (91.3%) patients achieved the ACR 20% response criteria, while 45 (77.6%) attained the ACR 50% criteria. In addition, a significant decrease in the DAS-28, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were observed. ERA patients exhibited higher serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides, whereas their serum high-density lipoprotein cholesterol (HDL-C) levels were significantly lower compared to controls. As a consequence, the atherogenic ratio of TC/HDL-C as well as that of LDL-C/HDL-C was significantly higher in ERA patients compared to controls. After treatment, a significant reduction of the atherogenic ratio of TC/HDL-C as well as that of LDL-C/HDL-C was observed, a phenomenon primarily due to the increase of serum HDL-C levels. These changes were inversely correlated with laboratory changes, especially CRP and ESR. In conclusion, ERA patients are characterized by an atherogenic lipid profile, which improves after therapy. Thus, early immuno-intervention to control disease activity may reduce the risk of the atherosclerotic process and cardiovascular events in ERA patients.
PMCID: PMC1526648  PMID: 16646989
11.  Anti-tumor necrosis factor therapy improves insulin resistance, beta cell function and insulin signaling in active rheumatoid arthritis patients with high insulin resistance 
Arthritis Research & Therapy  2012;14(3):R141.
Prevalence of insulin resistance and the metabolic syndrome has been reported to be high in rheumatoid arthritis (RA) patients. Tumor necrosis factor (TNF), a pro-inflammatory cytokine with a major pathogenetic role in RA, may promote insulin resistance by inducing Ser312 phosphorylation (p-Ser312) of insulin receptor substrate (IRS)-1 and downregulating phosphorylated (p-)AKT. We examined whether anti-TNF therapy improves insulin resistance in RA patients and assessed changes in the insulin signaling cascade.
Prospective study of RA patients receiving anti-TNF agents (infliximab, n = 49, adalimumab, n = 11, or etanercept, n = 1) due to high disease activity score in 28 joints (DAS28 > 5.1). A complete biochemical profile was obtained at weeks 0 and 12 of treatment. Insulin resistance, insulin sensitivity and pancreatic beta cell function were measured by the Homeostasis Model Assessment (HOMA-IR), the Quantitative Insulin Sensitivity Check Index (QUICKI) and the HOMA-B respectively. Protein extracts from peripheral blood mononuclear cells were assayed by western blot for p-Ser312 IRS-1 and p-AKT. RA patients treated with abatacept (CTLA4.Ig) were used as a control group for insulin signaling studies.
At study entry, RA patients with high insulin resistance (HOMA-IR above median) had significantly higher mean DAS28 (P = 0.011), serum triglycerides (P = 0.015), and systolic blood pressure levels (P = 0.024) than patients with low insulin resistance. After 12 weeks of anti-TNF therapy, patients with high insulin resistance demonstrated significant reduction in HOMA-IR (P < 0.001), HOMA-B (P = 0.001), serum triglycerides (P = 0.039), and increase in QUICKI (P < 0.001) and serum HDL-C (P = 0.022). Western blot analysis in seven active RA patients with high insulin resistance showed reduction in p-Ser312 IRS-1 (P = 0.043) and increase in p-AKT (P = 0.001) over the study period. In contrast, the effect of CTLA4.Ig on p-Ser312 IRS-1 and p-AKT levels was variable.
Anti-TNF therapy improved insulin sensitivity and reversed defects in the insulin signaling cascade in RA patients with active disease and high insulin resistance. The impact of these biochemical changes in modifying cardiovascular disease burden in active RA patients remains to be seen.
PMCID: PMC3446524  PMID: 22691241
12.  Unacylated Ghrelin is associated with the isolated low HDL-cholesterol obese phenotype independently of insulin resistance and CRP level 
Low plasma high-density lipoprotein-cholesterol (HDL-c) level is commonly present in obesity and represents an independent cardiovascular risk factor. However, obese patients are a very heterogeneous population and the factors and mechanisms that contribute to low HDL-c remain unclear. The aim of this study was to investigate the association between plasma HDL-c levels and plasma hormonal profiles (insulin, adiponectin, resistin, leptin and ghrelin) in subsets of class II and III obese patients.
Fasting plasma levels of glucose, total cholesterol, LDL-c, HDL-c, triglycerides, free fatty acids, apoproteins A-I, B-100, B-48, C-II, C-III, insulin, hs-CRP, adipocytokines (adiponectin, resistin, leptin), unacylated ghrelin, body composition (DXA) and resting energy expenditure were measured in three subsets of obese patients: 17 metabolically abnormal obese (MAO) with metabolic syndrome and the typical metabolic dyslipidaemia, 21 metabolically healthy obese (MHO) without metabolic syndrome and with a normal lipid profile, and 21 isolated low HDL-c obese patients (LHO) without metabolic syndrome, compared to 21 healthy lean control subjects.
Insulin resistance (HOMA-IR) increased gradually from MHO to LHO and from LHO to MAO patients (p < 0.05 between MHO and MAO and between LHO and MAO). In multiple regression analysis, serum unacylated ghrelin levels were only positively and independently associated with HDL-c levels in the LHO group (p = 0.032).
These results suggest that, in class II and III obese patients with an isolated low HDL-c phenotype, unacylated ghrelin is positively associated with HDL-c level independently of insulin resistance and CRP levels, and may contribute to the highly prevalent low HDL-c level seen in obesity.
PMCID: PMC3317856  PMID: 22413940
Adiponectin; Apolipoprotein; Cardiovascular risk; Ghrelin; HDL-cholesterol; Inflammation; Insulin resistance; Lipids; Obesity
13.  Changes in lipid profile during infliximab and corticosteroid treatment in rheumatoid arthritis 
Annals of the Rheumatic Diseases  2007;66(7):958-961.
To evaluate the effects of infliximab and corticosteroid treatment on the lipid profile in patients with active rheumatoid arthritis (RA).
Infliximab infusions were given at weeks 0, 2, 6 and then every 8 weeks. Before each infusion, disease activity parameters (Disease Activity Index 28‐Joint Score (DAS28)) C reactive protein (CRP) and lipid levels (total cholesterol, high‐density lipoprotein (HDL)‐cholesterol, triglycerides, apolipoprotein A1 (apo A1) and apolipoprotein B) were measured in 80 consecutive patients with RA, who completed the study period of 48 weeks. Longitudinal analyses were used to investigate (1) the course of lipid levels over a period of time and (2) the relationship between lipids, prednisone dose and disease activity.
Infliximab treatment causes a significant reduction in disease activity and a concomitant decrease in prednisone dose. Although they initially improved significantly, all lipid levels had returned to baseline levels after 48 weeks, except for apo A1. Longitudinal analyses revealed significant yet opposite associations between lipid levels and disease activity and between lipid levels and prednisone dose. DAS28 improvement by 1 point was associated with an increase of 0.016 mmol/l (0.618 mg/dl) total cholesterol and 0.045 mmol/l (1.737 mg/dl) HDL‐cholesterol. Reduction of 10 mg prednisone was associated with a decrease of 0.04 mmol/l (1.544 mg/dl) total cholesterol and 0.16 mmol/l (6.177 mg/dl) HDL‐cholesterol.
Overall, no changes in serum lipid levels were observed after 48 weeks of infliximab treatment. The initial beneficial effects of infliximab on the lipid profile, by means of a reduction of disease activity, are attenuated by a concomitant decrease in prednisone dose.
PMCID: PMC1955113  PMID: 17314120
14.  Atorvastatin reduces serum HMGB1 levels in patients with hyperlipidemia 
High mobility group box 1 protein (HMGB1) has been identified as a novel pro-inflammatory cytokine in coronary artery disease. This study investigated the effect of atorvastatin on serum HMGB1 levels in patients with hyperlipidemia. In 72 patients with hyperlipidemia, serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and high-sensitivity C-reactive protein (hs-CRP) were compared with the levels in 32 control patients. In hyperlipidemic patients, serum HMGB1 levels were also determined by ELISA before and after a 3-month treatment of atorvastatin (20 mg/day). TC and LDL-C levels in the hyperlipidemic group (6.37±0.94 and 4.99±0.75 mmol/l, respectively) were significantly higher compared to those in the control group (4.34±0.89 and 2.57±0.82 mmol/l, respectively) (both P<0.05). Hs-CRP and HMGB1 levels in the hyperlipidemic group (3.91±1.06 mg/l and 5.42±1.56 ng/ml, respectively) were also significantly higher compared to those in the control group (1.53±0.45 mg/l and 2.11±0.95 ng/ml, respectively) (both P<0.05). After treatment with atorvasatin for three months, TC and LDL-C levels in the hyperlipidemic group were significantly decreased compared to those prior to treatment (TC, 4.67±0.89 vs. 6.37±0.94 mmol/l and LDL-C, 2.75±0.92 vs. 4.99±0.75 mmol/l, respectively) (both P<0.05). HMGB1 and hs-CRP levels in the hyperlipidemic group (3.07±1.24 ng/ml and 1.87±0.79 mg/l, respectively) were also significantly decreased compared to levels prior to treatment (5.42±1.56 ng/ml and 3.91±1.06 mg/l, respectively) (both P<0.05). Serum HMGB1 levels are increased in patients with hyperlipidemia which could be reduced by atorvastatin.
PMCID: PMC3494102  PMID: 23226786
high mobility group box 1 protein; inflammation; atorvastatin; hyperlipidemia
15.  Yi-Qi-Zeng-Min-Tang, a Chinese medicine, ameliorates insulin resistance in type 2 diabetic rats 
AIM: To investigate the effects of the Chinese herbal decoction, Yi-Qi-Zeng-Min-Tang (YQZMT), on insulin resistance in type 2 diabetic rats.
METHODS: Sprague-Dawley rats were divided into two dietary regiments by feeding either normal pellet diet (NPD) or high fat diet (HFD). Four weeks later, the HFD-fed rats were injected intraperitoneally with low-dose streptozotocin (STZ). Rats with non-fasting blood glucose level ≥ 16.67 mmol/L were considered type 2 diabetic and further divided into five subgroups: the type 2 diabetes model group, low-dose, medium-dose and high-dose YQZMT groups, and rosiglitazone group. Age-matched NPD-fed rats served as controls. YQZMT or rosiglitazone were administered for 8 wk. Intraperitoneal glucose and insulin tolerance tests were performed before and after the treatment to measure the glucose tolerance and insulin sensitivity. Serum levels of biochemical parameters, adipocytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), as well as free fatty acids (FFAs), were also analyzed.
RESULTS: There was significant elevation of insulin resistance and serum levels of fasting glucose (12.82 ± 1.08 mmol/L vs 3.60 ± 0.31 mmol/L, P < 0.01), insulin (7197.36 ± 253.89 pg/mL vs 4820.49 ± 326.89 pg/mL, P < 0.01), total cholesterol (TC) (8.40 ± 0.49 mmol/L vs 2.14 ± 0.06 mmol/L, P < 0.01), triglyceride (2.24 ± 0.12 mmol/L vs 0.78 ± 0.05 mmol/L, P < 0.01), low-density lipoprotein cholesterol (LDL-c) (7.84 ± 0.51 mmol/L vs 0.72 ± 0.04 mmol/L, P < 0.01) and decrease in high-density lipoprotein cholesterol (HDL-c) (0.57 ± 0.03 mmol/L vs 1.27 ± 0.03 mmol/L, P < 0.01) in the low-dose STZ and high-fat diet induced type 2 diabetic group when compared with the control group. Administration of YQZMT induced dose- and time-dependent changes in insulin resistance, glucose and lipid profile, and reduced levels of FFA, TNF-α and IL-6 in the type 2 diabetic rats. After the treatment, compared with the diabetic group, the insulin resistance was ameliorated in the high-dose YQZMT (2.82 g/100 g per day) group, with a significant reduction in serum glucose (12.16 ± 1.00 mmol/L vs 17.65 ± 2.22 mmol/L, P < 0.01), homeostasis model assessment of basal insulin resistance (22.68 ± 2.37 vs 38.79 ± 9.02, P < 0.05), triglyceride (0.87 ± 0.15 mmol/L vs 1.99 ± 0.26 mmol/L, P < 0.01), TC (3.31 ± 0.52 mmol/L vs 6.50 ± 1.04 mmol/L, P < 0.01) and LDL-c (2.47 ± 0.50 mmol/L vs 6.00 ± 1.07 mmol/L, P < 0.01), and a significant increase in HDL-c (0.84 ± 0.08 mmol/L vs 0.50 ± 0.03 mmol/L, P < 0.01). But the body weight was not changed significantly.
CONCLUSION: YQZMT, which ameliorates insulin resistance and does not cause increase in body weight, may be a suitable therapeutic adjunct for the treatment of type 2 diabetes.
PMCID: PMC3057160  PMID: 21448349
Yi-Qi-Zeng-Min-Tang; Insulin resistance; Type 2 diabetes; Lipids; Adipocytokines; Free fatty acids
16.  Chinese herbal medicine for impaired glucose tolerance: a randomized placebo controlled trial 
Diabetes remains a major health problem worldwide. Low-risk low-cost alternatives to pharmaceutical interventions are needed where lifestyle modifications have failed. We conducted a double-blind randomised placebo controlled trial to investigate the efficacy of a Chinese herbal formula, Jiangtang Xiaozhi, in treating impaired glucose control and insulin resistance in persons with prediabetes and controlled diabetes.
Seventy-one patients with prediabetes or ‘controlled’ diabetes were randomised to receive 3 capsules of Jiangtang Xiaozhi (n = 39) or placebo (n = 32) three times daily for 16 weeks with a follow up eight weeks later (week 24). The primary outcome was change in glycaemic control as evidenced by fasting blood glucose (FBG), post-prandial plasma glucose and glycosylated haemoglobin (HbA1c). Other measures included change in fasting insulin, insulin resistance and sensitivity, lipids, C-reactive protein (CRP), body mass index (BMI), waist girth, blood pressure (BP), health related quality of life (HRQoL) and safety. Analysis of covariance (ANCOVA) was used to model outcomes at 16 weeks, by treatment group corrected for baseline level of the outcome variable.
In patients receiving Jiangtang Xiaozhi, FBG was not significantly different (p = 0.73) compared to placebo after 16 weeks of treatment (6.3 ± 1.1 mmol/L vs 6.7 ± 1.3 mmol/L). There was a significant difference (p = 0.04) in the mean levels of fasting insulin between the treatment group (11.6 ± 5.5 mmol/L) and the placebo group (22.1 ± 25.9 mmol/L). Insulin resistance slightly decreased in the treatment group (1.58 ± 0.74) compared to that of the placebo group (2.43 ± 1.59) but this change did not reach statistical significance (p = 0.06). Patients taking Jiangtang Xiaozhi had a significant improvement in high-density lipoprotein (HDL) level compared to the placebo group at week 16 (p = 0.03). Mean levels of cholesterol, triglycerides, BMI, waist-girth, HRQoL, BP, CRP and insulin sensitivity were not significantly different between the two groups. The herbal medicine was well tolerated.
In the current study, the 16 week Jiangtang Xiaozhi treatment did not lower fasting blood glucose, but it improved serum insulin and HDL cholesterol in a Western population with prediabetes or controlled diabetes. Our trial may have been underpowered. Dosage needs to be considered before commencing a longer adequately powered trial.
Trial registration
Australian New Zealand Clinical Trials Registry ACTRN12612000128897;
PMCID: PMC3659077  PMID: 23672597
17.  Effect of conjugated linoleic acid, vitamin E and their combination on lipid profiles and blood pressure of Iranian adults with active rheumatoid arthritis 
Vascular Health and Risk Management  2008;4(6):1423-1432.
The aim of this study was to assess the impact of conjugated linoleic acids (CLAs), vitamin E, and combination of these nutrients on serum lipid profiles and blood pressure (BP) in patients with active rheumatoid arthritis (RA). In a randomized, double-blind, placebo-controlled trial, 87 patients with active RA were divided into four groups receiving one of the following daily supplements for three months: Group C: CLAs 2.5 g equivalent to 2 g mixture of cis 9-trans 11 and trans 10-cis12 CLAs in a rate of 50/50; Group E: vitamin E: 400 mg; Group CE: CLAs and vitamin E at above doses: Group P: placebo. After supplementation, SBP levels decreased significantly in the group C in comparison with groups E and P and mean arterial pressure reduced significantly in groups C and CE. There weren’t significant differences in the levels of prostaglandin E2 (PGE2), triglycerides, cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), LDL/HDL, cholesterol/HDL, fasting blood sugar, C-reactive protein (CRP), arylestrase activity, platelet count and body mass index between groups. CRP dropped nonsignificantly in groups P, C, E and CE (19%, 24%, 55%, and 39%, respectively). Erythrocytes sedimentation rate levels decreased in groups C, E and CE (P ≤ 0.05, P ≤ 0.05, P ≤ 0.001, respectively). It is concluded that supplementation of CLAs decreased BP and vitamin E decreased CRP. Therefore cosupplementation of CLAs and vitamin E might be profitable for heart disease prevention in RA patients.
PMCID: PMC2663461  PMID: 19337555
rheumatoid arthritis; lipid profiles; blood pressure; conjugated linoleic acids; vitamin E
18.  High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study 
Arthritis Research & Therapy  2012;14(3):R116.
Higher levels of high density lipoprotein (HDL) subfractions HDL3-chol and particularly HDL2-chol protect against cardiovascular disease (CVD), but inflammation reduces the HDL level and may impair its anti-atherogenic effect. Changed HDL composition through the impact of inflammation on HDL subfractions may contribute to the excess risk of CVD in rheumatoid arthritis (RA). In this study, we investigated whether HDL2-chol and HDL3-chol concentrations differ between RA patients and healthy controls, and whether these levels are related to the level of RA disease activity.
Non-fasting blood samples were collected from 45 RA patients and 45 healthy controls. None of the participants had a history of CVD, diabetes, or used lipid-lowering drugs. HDL2-chol and HDL3-chol concentrations were obtained by ultracentrifugation. Regression modeling was used to compare HDL subfraction levels between RA patients and healthy controls, and to analyze the effect of disease activity on HDL2-chol and HDL3-chol.
HDL2-chol and HDL3-chol were significantly lower in RA patients compared to healthy controls (P = 0.01, P = 0.005, respectively). The HDL2:HDL3 ratio was significantly lower in patients compared to controls (P = 0.04). Reduced HDL2-chol and HDL3-chol levels were primarily present in female RA patients and not in male RA patients. A modest effect of the disease activity score in 28 joins ( DAS28) on HDL2-chol concentrations was found, after correction for disease duration, glucocorticosteroid use and body mass index (BMI), with a 0.06 mmol/L decrease with every point increase in DAS28 (P = 0.05). DAS28 did not significantly affect HDL3-chol concentrations (P = 0.186).
Both HDL subfractions but particularly HDL2-chol concentrations were decreased in RA, primarily in women. This seems to be associated with disease activity and is of clinical relevance. The reduction of the HDL subfraction concentrations, particularly the supposedly beneficial HDL2-chol, may negatively impact the cardiovascular risk profile of women with RA.
PMCID: PMC3446493  PMID: 22584154
19.  Molecular sources of residual cardiovascular risk, clinical signals, and innovative solutions: relationship with subclinical disease, undertreatment, and poor adherence: implications of new evidence upon optimizing cardiovascular patient outcomes 
Residual risk, the ongoing appreciable risk of major cardiovascular events (MCVE) in statin-treated patients who have achieved evidence-based lipid goals, remains a concern among cardiologists. Factors that contribute to this continuing risk are atherogenic non-low-density lipoprotein (LDL) particles and atherogenic processes unrelated to LDL cholesterol, including other risk factors, the inherent properties of statin drugs, and patient characteristics, ie, genetics and behaviors. In addition, providers, health care systems, the community, public policies, and the environment play a role. Major statin studies suggest an average 28% reduction in LDL cholesterol and a 31% reduction in relative risk, leaving a residual risk of about 69%. Incomplete reductions in risk, and failure to improve conditions that create risk, may result in ongoing progression of atherosclerosis, with new and recurring lesions in original and distant culprit sites, remodeling, arrhythmias, rehospitalizations, invasive procedures, and terminal disability. As a result, identification of additional agents to reduce residual risk, particularly administered together with statin drugs, has been an ongoing quest. The current model of atherosclerosis involves many steps during which disease may progress independently of guideline-defined elevations in LDL cholesterol. Differences in genetic responsiveness to statin therapy, differences in ability of the endothelium to regenerate and repair, and differences in susceptibility to nonlipid risk factors, such as tobacco smoking, hypertension, and molecular changes associated with obesity and diabetes, may all create residual risk. A large number of inflammatory and metabolic processes may also provide eventual therapeutic targets to lower residual risk. Classically, epidemiologic and other evidence suggested that raising high-density lipoprotein (HDL) cholesterol would be cardioprotective. When LDL cholesterol is aggressively lowered to targets, low HDL cholesterol levels are still inversely related to MCVE. The efflux capacity, or ability to relocate cholesterol out of macrophages, is believed to be a major antiatherogenic mechanism responsible for reduction in MCVE mediated in part by healthy HDL. HDL cholesterol is a complex molecule with antioxidative, anti-inflammatory, anti-thrombotic, antiplatelet, and vasodilatory properties, among which is protection of LDL from oxidation. HDL-associated paraoxonase-1 has a major effect on endothelial function. Further, HDL promotes endothelial repair and progenitor cell health, and supports production of nitric oxide. HDL from patients with cardiovascular disease, diabetes, and autoimmune disease may fail to protect or even become proinflammatory or pro-oxidant. Mendelian randomization and other clinical studies in which raising HDL cholesterol has not been beneficial suggest that high plasma levels do not necessarily reduce cardiovascular risk. These data, coupled with extensive preclinical information about the functional heterogeneity of HDL, challenge the “HDL hypothesis”, ie, raising HDL cholesterol per se will reduce MCVE. After the equivocal AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With Low HDL/High Triglycerides: Impact on Global Health Outcomes) study and withdrawal of two major cholesteryl ester transfer protein compounds, one for off-target adverse effects and the other for lack of efficacy, development continues for two other agents, ie, anacetrapib and evacetrapib, both of which lower LDL cholesterol substantially. The negative but controversial HPS2-THRIVE (the Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events) trial casts further doubt on the HDL cholesterol hypothesis. The growing impression that HDL functionality, rather than abundance, is clinically important is supported by experimental evidence highlighting the conditional pleiotropic actions of HDL. Non-HDL cholesterol reflects the cholesterol in all atherogenic particles containing apolipoprotein B, and has outperformed LDL cholesterol as a lipid marker of cardiovascular risk and future mortality. In addition to including a measure of residual risk, the advantages of using non-HDL cholesterol as a primary lipid target are now compelling. Reinterpretation of data from the Treating to New Targets study suggests that better control of smoking, body weight, hypertension, and diabetes will help lower residual risk. Although much improved, control of risk factors other than LDL cholesterol currently remains inadequate due to shortfalls in compliance with guidelines and poor patient adherence. More efficient and greater use of proven simple therapies, such as aspirin, beta-blockers, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, combined with statin therapy, may be more fruitful in improving outcomes than using other complex therapies. Comprehensive, intensive, multimechanistic, global, and national programs using primordial, primary, and secondary prevention to lower the total level of cardiovascular risk are necessary.
PMCID: PMC3808150  PMID: 24174878
cardiovascular prevention; low-density lipoprotein; high-density lipoprotein; statin drugs; metabolic syndrome; obesity; diabetes; niacin; AIM-HIGH study; cholesteryl ester transfer protein; endothelial progenitor cells; fibrate drugs
20.  Dietary saturated fat/cholesterol, but not unsaturated fat or starch, induces C-reactive protein associated early atherosclerosis and ectopic fat deposition in diabetic pigs 
Diabetes is thought to accelerate cardiovascular disease depending on the type of diet. This study in diabetic subjects was performed to investigate the metabolic, inflammatory and cardiovascular effects of nutritional components typically present in a Western, Mediterranean or high glycaemic diet.
Streptozotocin-diabetic pigs (~45 kg) were fed for 10 weeks supplemental (40% of dietary energy) saturated fat/cholesterol (SFC), unsaturated fat (UF) or starch (S) in an eucaloric dietary intervention study.
Fasting plasma total, LDL and HDL cholesterol concentrations were 3-5 fold higher (p < 0.01) in SFC compared to UF and S pigs. Fasting plasma NEFA concentrations (mmol/L) were highest (p < 0.05) in SFC (1.09 ± 0.17), intermediate in UF (0.80 ± 0.14) and lowest in S pigs (0.58 ± 0.14) whereas plasma glucose (~13 mmol/L), triglyceride (~0.5 mmol/L) and insulin (~24 pmol/L) concentrations were comparable among SFC, UF and S pigs. The postprandial response area under the curves (AUC, 0-4 h) for glucose but not for insulin and triglyceride responses were intermediate in SFC (617 ± 144) and lowest (p < 0.05) in UF (378 ± 157) compared to S pigs (925 ± 139). Fasting hepatic glucose production, hepatic and peripheral insulin sensitivity and blood pressure were not different among pigs. C-reactive protein (CRP) concentrations (mg/L) were highest (p < 0.05) in SFC (25 ± 4), intermediate in S (21 ± 3) and lowest in UF pigs (14 ± 2). Liver weights, liver and muscle triglyceride concentrations, and the surface area of aorta fatty streaks were highest (p < 0.01) in SFC pigs. A positive correlation between postprandial plasma CRP and aorta fatty streaks was observed in SFC pigs (R2 = 0.95). Retroperitoneal fat depot weight (g) was intermediate in SFC (260 ± 72), lowest in S (135 ± 51) and highest (p < 0.05) in UF (571 ± 95) pigs.
Dietary saturated fat/cholesterol induces inflammation, atherosclerosis and ectopic fat deposition whereas an equally high dietary unsaturated fat load does not induce these abnormalities and shows beneficial effects on postprandial glycaemia in diabetic pigs.
PMCID: PMC3143922  PMID: 21756316
Diabetes; Insulin; Diet; Unsaturated fat; Saturated fat; Cholesterol; Inflammation; C-reactive protein; Atherosclerosis; Pigs
21.  Lipid Profile of Type 2 Diabetic and Hypertensive Patients in the Jamaican Population 
Previous studies have shown that diabetes mellitus (DM) increases the risk of cardiovascular diseases in females to a greater extent than in males. In this cross-sectional study, we evaluated the lipid profiles of type 2 diabetic males and females.
Materials and Methods:
The study included 107 type 2 diabetic patients (41 males and 66 females), and 122 hypertensive type 2 diabetic patients (39 males and 83 females), aged 15 years and older. Total cholesterol (TC), triglycerides (TG), low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDL-C) and high density lipoprotein-cholesterol (HDL-C) concentrations were assayed for each group using standard biochemical methods.
The mean TC, TG, VLDL-C, HDL-C and LDL-C concentrations, TG/HDL and LDL/HDL ratios were higher in type 2 diabetic and hypertensive type 2 diabetic patients compared with non-diabetic, and hypertensive non-diabetic control subjects, although these were not significant (P > 0.05). Hypertensive type 2 diabetic females had significantly higher serum TC (7.42 ± 1.63 mmol/L) than hypertensive non-diabetic males (5.76±1.57 mmol/L; P < 0.05). All the other lipid and lipoprotein parameters except HDL-C were non-significantly higher in females with type 2 DM and those with hypertension and type 2 DM, compared with type 2 diabetic and hypertensive type 2 diabetic males, respectively (P > 0.05).
This study demonstrated that dyslipidemia exists in our type 2 diabetic population with greater TC in hypertensive type 2 diabetic females compared with hypertensive type 2 diabetic males. This suggests that hypertensive type 2 diabetic females are exposed more profoundly to risk factors including atherogenic dyslipidemia compared with males.
PMCID: PMC3147082  PMID: 21814403
Females; hypertension; lipids; lipoprotein; males; type 2 diabetes mellitus
22.  Effects of Growth Hormone Deficiency on Body Composition and Biomarkers of Cardiovascular Risk after Definitive Therapy for Acromegaly 
Clinical endocrinology  2012;77(3):430-438.
Both growth hormone (GH) excess and GH deficiency are associated with body composition and biomarkers of cardiovascular risk in patients with pituitary disorders. However, the effects of developing GH deficiency after definitive treatment of acromegaly are largely unknown.
To determine whether development of GH deficiency after definitive therapy for acromegaly is associated with increased visceral adiposity and biomarkers of cardiovascular risk compared to GH sufficiency after definitive therapy for acromegaly.
We studied three groups of subjects, all with a history of acromegaly (n=76): subjects with subsequent GH deficiency (GHD; n=31), subjects with subsequent GH sufficiency (GHS; n=25), and subjects with active acromegaly (AA; n=20). No study subjects were receiving somatostatin analogues, dopamine agonists or hGH.
Body composition (by DXA), abdominal adipose tissue depots (by cross-sectional CT), total body water (by bioimpedance analysis) and carotid intima-media thickness (IMT) were measured. Fasting morning serum was collected for high-sensitivity C-reactive protein (hsCRP), lipids and lipoprotein levels. An oral glucose tolerance test was performed, and homeostasis model of assessment-insulin resistance (HOMA-IR) was calculated.
Abdominal visceral adipose tissue, total adipose tissue, and total body fat were higher in subjects with GHD than GHS or AA (p < 0.05). Subcutaneous abdominal fat was higher, and fibrinogen and IMT were lower in GHD (but not GHS) than AA (p < 0.05). Patients with GHD had the highest hsCRP, followed by GHS, and hsCRP was lowest in AA (p < 0.05). Fasting glucose, 120-minute glucose, fasting insulin, HOMA-IR, and percent total body water were lower in GHD and GHS than AA (p < 0.05). Triglycerides were higher in GHS than AA (p < 0.05). Lean body mass, mean arterial pressure, total cholesterol, HDL, and LDL were comparable among groups.
Development of GHD after definitive treatment of acromegaly may adversely affect body composition and inflammatory biomarkers of cardiovascular risk but does not appear to adversely affect glucose homeostasis, lipids and lipoproteins, or other cardiovascular risk markers.
PMCID: PMC3366162  PMID: 22315983
Acromegaly; Growth hormone; Growth hormone deficiency
23.  Moderate diet-induced weight loss is associated with improved insulin sensitivity in middle-aged healthy obese Korean women 
Nutrition Research and Practice  2014;8(4):469-475.
The goal of the present study was to investigate the effects of moderate caloric restriction on β-cell function and insulin sensitivity in middle-aged obese Korean women.
Fifty-seven obese pre-menopausal Korean women participated in a 12-week calorie restriction program. Data on total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides (TG), and fasting serum levels of glucose, insulin, C-peptide, blood pressure, leptin and anthropometrics were collected. A dietary intake assessment was based on three days of food recording. Additionally, β-cell function [homeostasis model assessment of β-cell (HOMA-β), insulinogenic index (ISI), C-peptide:glucose ratio, and area under curve insulin/glucose (AUCins/glu)] and insulin sensitivity [homeostasis model assessment for insulin resistance (HOMA-IR), Quantitative insulin-sensitivity check index (QUICKI) and Matsuda index (MI)] were recorded.
When calories were reduced by an average of 422 kcal/day for 12 weeks, BMI (-2.7%), body fat mass (-10.2%), and waist circumference (-5%) all decreased significantly (P < 0.05). After calorie restriction, weight, body fat percentage, hip circumference, BP, TC, HDL-C, LDL-C, plasma glucose at fasting, insulin at fasting and 120 min, AUCglu and the insulin area under the curve all decreased significantly (all P < 0.05), while insulin sensitivity (HOMA-IR, QUICKI and Matsuda index) measured by OGTT improved significantly (P < 0.01).
Moderate weight loss due to caloric restriction with reduction in insulin resistance improves glucose tolerance and insulin sensitivity in middle-aged obese women and thereby may help prevent the development of type 2 diabetes mellitus.
PMCID: PMC4122721  PMID: 25110569
Oderate weight loss; β-cell function and insulin sensitivity
24.  Effect of Exercise Therapy on Lipid Parameters in Patients with End-Stage Renal Disease on Hemodialysis 
Dyslipidemia has been established as a well-known traditional risk factor for cardiovascular disease in chronic kidney disease patients.
This study investigated the impact of Hatha yoga exercise on lipid parameters in patients with end-stage renal disease (ESRD) on hemodialysis.
Materials and Methods:
This prospective randomized study consisted of 33 ESRD patients in the Hatha yoga exercise group that was matched with 35 ESRD patients in the control group. Serum total cholesterol, triglycerides, low-density lipoprotein (LDL)-cholesterol, and high-density lipoprotein (HDL)-cholesterol were determined at baseline (0 month) and after 4 months.
Comparing values after 4 months versus baseline in the prehemodialysis Hatha yoga exercise group, there was found a significant decrease in total cholesterol from 5.126 ± 0.092 mmol/l to 4.891 ± 0.072 mmol/l (-4.58%; P = 0.0001), triglycerides from 2.699 ± 0.078 mmol/l to 2.530 ± 0.063 mmol/l (-6.26%; P = 0.0001), LDL-cholesterol from 2.729 ± 0.083 mmol/l to 2.420 ± 0.066 mmol/l (-11.32%; P = 0.0001), and total cholesterol/HDL-cholesterol ratio from 5.593 ± 0.119 mmol/l to 4.907 ± 0.116 mmol/l (-12.26%; P = 0.047). For patients in the Hatha yoga exercise group, 51.5% had normal total cholesterol at 0 month while 70.0% had normal total cholesterol (P < 0.05) after 4 four months and 54.5% of patients had normal LDL-cholesterol at 0 month while 84.9% had normal LDL-cholesterol after 4 months (P < 0.05).
These findings suggest that Hatha yoga exercise has preventive and beneficial effects and may be a safe therapeutic modality in ESRD patients.
PMCID: PMC3425259  PMID: 22923917
Cardiovascular; end-stage renal disease; hatha yoga exercise; total cholesterol
25.  Effects of patient‐tailored atorvastatin therapy on ameliorating the levels of atherogenic lipids and inflammation beyond lowering low‐density lipoprotein cholesterol in patients with type 2 diabetes 
Recently, patient‐tailored statin therapy was proven effective for achieving target low‐density lipoprotein (LDL) cholesterol levels. It is unclear, however, whether this therapeutic modality would be effective for atherogenic lipid profiles and inflammation in patients with type 2 diabetes.
Materials and Methods
The present study was an 8‐week, multicenter, single‐step titration trial of patient‐tailored atorvastatin therapy (10, 20 and 40 mg) according to baseline LDL cholesterol levels in 440 patients with type 2 diabetes. We measured the LDL particle size by polyacrylamide gel electrophoresis, and used high‐sensitivity C‐reactive protein (hsCRP) and adiponectin as surrogate markers of inflammation.
In the intention‐to‐treat analysis, 91% of the patients achieved their LDL cholesterol targets (<2.6 mmol/L) at week 8. There were significant reductions at week 8 in total cholesterol, triglycerides, non‐high‐density lipoprotein cholesterol (HDL) cholesterol, and the total cholesterol:HDL cholesterol ratio compared with the baseline values for all of the doses. The mean LDL particle size was significantly increased, and the small, dense LDL cholesterol levels were decreased in a dose‐dependent manner over the study period. In addition, the hsCRP levels were decreased in those high‐risk patients with baseline hsCRP levels over 3 mg/L (P < 0.001), and the adiponectin levels tended to increase with all of the doses (P = 0.004) at 8 weeks.
Patient‐tailored atorvastatin therapy based on LDL cholesterol at baseline was effective in ameliorating atherogenic LDL particle size and inflammation, in addition to achieving the target LDL cholesterol level without an undesirable effect on glycemic control in patients with type 2 diabetes. This trial was registered with (no. NCT01239849).
PMCID: PMC4025110  PMID: 24843697
Atorvastatin; Low‐density lipoprotein cholesterol; Type 2 diabetes mellitus

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