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1.  Angiotensin II-Superoxide Signaling and Arterial Baroreceptor Function in Type-1 Diabetes Mellitus 
Journal of diabetes & metabolism  2013;Suppl 12:1-6.
Diabetes is a major world health problem. Growing evidence from both clinical trials and animal experiments has clearly confirmed that arterial baroreflex dysfunction is a feature of type 1 diabetes, which links to prognosis and mortality of the type 1 diabetic patients. The arterial baroreflex normally regulates the blood pressure and heart rate through sensing changes of arterial vascular tension by the arterial baroreceptors in the aortic arch and carotid sinus. The aortic baroreceptor neuron located in the nodose ganglia is a primary afferent component of the arterial baroreflex. The functional changes of these neurons are involved in the arterial baroreflex dysfunction in the type 1 diabetes. Type 1 diabetes causes the overexpression and hyperactivation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels and further reduces cell excitability of the aortic baroreceptor neurons. The alterations of the HCN channels are regulated by angiotensin II-NADPH oxidase-superoxide signaling in the aortic baroreceptor neurons. From the present review, we can understand the possible mechanisms responsible for the attenuated arterial baroreflex in the type 1 diabetes. These findings are beneficial for improving quality of life and prognosis in patients with the type 1 diabetes mellitus.
doi:10.4172/2155-6156.S12-001
PMCID: PMC3932051  PMID: 24567847
Baroreflex; Baroreceptor; Ion channels; Angiotensin II; Superoxide; Diabetes
2.  Dynamic Stress Factor (DySF): A Significant Predictor of Severe Hypoglycemic Events in Children with Type 1 Diabetes 
Journal of diabetes & metabolism  2012;3:10.4172/2155- 6156.1000177.
Hemoglobin A1c (HbA1c) is the current standard used in the clinical treatment of patients with diabetes. However, it has been shown that patients with similar HbA1c values may have widely different fluctuations in blood glucose values over the same period of time, including time spent in hyper- and/or hypo-glycemia. Hence, there exists a need for quantitative measures that can supplement HbA1c in managing patients with diabetes. We introduce and compare the Dynamic Stress Factor, DySF, a newly developed metric that quantifies glycemic volatility based on patient-specific glucose transition density profiles with HbA1c and with currently used glucose variability metrics in predicting severe hypoglycemia in children with type 1 diabetes. DySF, the daily weighted number of large monotonic glycemic transitions that occur within one hour, was calculated for 441 total subjects with type 1 diabetes (146 children, aged 8-14 yrs) to assess the magnitude and frequency of glucose transitions per day. Severe hypoglycemic episodes (HE) were quantified for all subjects and evaluated against HbA1c and existing measures of glucose variability, including SD, MAGE, MODD, and CONGA using logistic regression models. DySF was found to be a predictor of severe HE in children (p = 0.018) with the likelihood of a child, aged 8-14 yrs, experiencing severe hypoglycemia increasing by up to 20% with decreasing values of up to 60% of DySF. Patients of any age who had one or multiple severe hypoglycemic episodes had on average a lower DySF when compared to those with no HE. Additionally, when considering mean glucose levels, DySF/mean was a preliminary predictor of severe HE in patients with HbA1c ≤ 6.5% (p = 0.062). DySF is a dynamic, quantitative, measure of daily glucose “volatility” that separates patients, within the same strata of HbA1c, into visually distinct patient profiles. DySF can be used as a preliminary predictor of clinically severe hypoglycemia in children and “well-controlled” patients with HbA1c ≤ 6.5%.
PMCID: PMC3869027  PMID: 24349871
3.  Dynamic Stress Factor (DySF): A Significant Predictor of Severe Hypoglycemic Events in Children with Type 1 Diabetes 
Hemoglobin A1c (HbA1c) is the current standard used in the clinical treatment of patients with diabetes. However, it has been shown that patients with similar HbA1c values may have widely different fluctuations in blood glucose values over the same period of time, including time spent in hyper- and/or hypo-glycemia. Hence, there exists a need for quantitative measures that can supplement HbA1c in managing patients with diabetes. We introduce and compare the Dynamic Stress Factor, DySF, a newly developed metric that quantifies glycemic volatility based on patient-specific glucose transition density profiles with HbA1c and with currently used glucose variability metrics in predicting severe hypoglycemia in children with type 1 diabetes. DySF, the daily weighted number of large monotonic glycemic transitions that occur within one hour, was calculated for 441 total subjects with type 1 diabetes (146 children, aged 8-14 yrs) to assess the magnitude and frequency of glucose transitions per day. Severe hypoglycemic episodes (HE) were quantified for all subjects and evaluated against HbA1c and existing measures of glucose variability, including SD, MAGE, MODD, and CONGA using logistic regression models. DySF was found to be a predictor of severe HE in children (p = 0.018) with the likelihood of a child, aged 8-14 yrs, experiencing severe hypoglycemia increasing by up to 20% with decreasing values of up to 60% of DySF. Patients of any age who had one or multiple severe hypoglycemic episodes had on average a lower DySF when compared to those with no HE. Additionally, when considering mean glucose levels, DySF/mean was a preliminary predictor of severe HE in patients with HbA1c ≤ 6.5% (p = 0.062). DySF is a dynamic, quantitative, measure of daily glucose “volatility” that separates patients, within the same strata of HbA1c, into visually distinct patient profiles. DySF can be used as a preliminary predictor of clinically severe hypoglycemia in children and “well-controlled” patients with HbA1c ≤ 6.5%.
doi:10.4172/2155-6156.1000177
PMCID: PMC3859451  PMID: 24349871
4.  Comparison of the Development Diabetic Induced Renal Disease in Strains of Goto-Kakizaki Rats 
Journal of diabetes & metabolism  2013;Suppl 9(5):S9-005.
This study compared temporal changes in renal hemodynamics, proteinuria and the development of renal disease in Goto-Kakizaki (GK) type II diabetic rats that are resistant to the development of diabetic nephropathy and a genetically modified GK substrain (T2DN) carrying the mitochondrial genome and other alleles from Fawn hooded-hypertensive (FHH) rats is more susceptible to the development of renal injury. Both GK and T2DN rats were diabetic (>250 mg/ dL) and blood glucose levels were not significantly different at 3, 6 and 18 months of age. Blood pressure was also similar in both strains at all 3 ages. Renal blood flow (RBF) was 45% higher in 3 month old T2DN rats than GK rats but glomerular filtration rate (GFR) was similar. T2DN rats exhibited a progressive increase in proteinuria from 41 ± 2 to 524 ± 50 mg/day and 57% fall in GFR as they aged from 3 to 18 months of age. In contrast, proteinuria only increased to 162 ± 31 mg/day in GK rats and GFR remained unaltered. The kidneys from 18 month old T2DN rats exhibited severe glomerulosclerosis, interstitial fibrosis and tubular necrosis while kidneys from GK rats did not. Plasma creatinine levels were 2.4 fold higher in 18 month old T2DN than in GK rats. These data demonstrate that T2DN rats develop most of the features of diabetic nephropathy including progressive proteinuria and chronic kidney disease whereas the closely related GK strain does not, even though blood pressure and the level of hyperglycemia are similar.
doi:10.4172/2155-6156.S9-005
PMCID: PMC3853344  PMID: 24319624
Diabetic nephropathy; GK rats; Type II diabetes; Renal hemodynamics; Renal disease
5.  The IL-6 Paradox: Context Dependent Interplay of SOCS3 and AMPK 
Journal of diabetes & metabolism  2013;Suppl 13:10.4172/2155-6156.S13-003.
Insulin resistance is the principle step towards the progression of type 2 diabetes, and has been linked to increased circulating levels of cytokines, leading to chronic low-grade inflammation. Specifically, in chronic disease states increased IL-6 is thought to play a critical role in the regulation of insulin resistance in the peripheral tissues, and has been used as a marker of insulin resistance. There is also an endogenous up-regulation of IL-6 in response to exercise, which has been linked to improved insulin sensitivity. This leads to the question “how can elevated IL-6 lead to the development of insulin resistance, and yet also lead to increased insulin sensitivity?” Resolving the dual role of IL-6 in regulating insulin resistance/sensitivity is critical to the development of potential therapeutic interventions. This review summarizes the literature on the seemingly paradoxical role of elevated IL-6 on insulin signalling, including the activation of AMPK and the involvement of leptin and SOCS3.
doi:10.4172/2155-6156.S13-003
PMCID: PMC3828628  PMID: 24244888
Type 2 diabetes; Insulin resistance; Insulin sensitivity; Chronic low-grade inflammation; SOCS3; AMPK; Leptin signalling
6.  Thrombospondin-1 Deficiency Exacerbates the Pathogenesis of Diabetic Retinopathy 
Journal of diabetes & metabolism  2013;Suppl 12:10.4172/2155-6156.S12-005.
Diabetic retinopathy is a leading cause of blindness in the United States. Access to new animal models that exhibit retinal vasculopathies with short duration of diabetes, are vital for understanding the underlying mechanisms and examining the efficacy of new treatment modalities. Our previous studies demonstrated decreased expression of Thrombospondin-1 (TSP1), an endogenous inhibitor of angiogenesis, in eyes from both patients and rodents with diabetes. Here we examined whether TSP1 deficiency could exacerbate diabetic retinal vasculopathies. Akita/+ male mice reproducibly develop diabetes by 4 weeks of age. These mice demonstrated the early non-proliferative stages of diabetic retinopathy, including decreased numbers of pericytes and increased glial cell activation. However, Akita/+ male mice deficient in TSP1 (Akita/+; TSP1−/−) demonstrated more advanced stages of diabetic retinopathy with a 4-fold increase in acellular capillaries and increased fibronectin and GFAP expression. These vascular changes were not attributable to aberrant retinal vascular development in the absence of TSP1, since down-regulation of TSP1 postnatally in the endothelium also resulted in more severe retinopathy. In addition, lack of another endogenous inhibitor of angiogenesis, pigment epithelium derived factor (PEDF), also enhanced diabetic retinopathy in Akita/+ mice. Akita/+; PEDF−/− male mice demonstrated increased numbers of acellular capillaries compared to controls but at a level lower than that observed in Akita/+; TSP1−/− mice. Thus, the exacerbation of diabetic retinopathy in Akita/+; TSP1−/− mice will allow the study of retinal vasculopathies with a shorter duration of diabetes and facilitate future testing of treatment modalities that protect the retinal vasculature and preserve sight.
doi:10.4172/2155-6156.S12-005
PMCID: PMC3818794  PMID: 24224119
Angiogenesis inhibitors; Diabetic retinopathy; Thrombospondin-1; PEDF
7.  Vitamin D Deficiency and Cardio-Metabolic Risk in a North Indian Community with Highly Prevalent Type 2 Diabetes 
Journal of diabetes & metabolism  2012;3:10.4172/2155-6156.1000213.
Objective
The purpose of this investigation was to examine serum vitamin D status in a population of Punjabi ancestry from Northern India with a high prevalence of type 2 diabetes (T2D) and evaluate the effects of 25(OH)D levels on cardio-metabolic traits.
Research design and methods
We assessed cardiovascular risk factors and 25(OH)D levels in 1,765 participants (887 T2D cases, 878 normoglycemic controls).
Results
76% of individuals were deficient (<50 nmol/L) in vitamin D. A higher percentage of T2D participants(83%) were vitamin D deficient compared to normoglycemic controls (68%)(p<0.0001).The prevalence of vitamin D deficiency increased progressively with body mass index (BMI) categories (p<0.0001): BMI<23 kg/m2, 65%; BMI 23–27.5 kg/m2, 75%; and BMI>27.5 kg/m2, 81%. T2D participants had significantly decreased serum 25(OH)D levels (β=−0.41, p=2.8 × 10−20). Individuals with low serum 25(OH)D had elevated fasting glucose(β=−0.18, p=0.022), BMI (β=-0.71, p=1.4 × 10−7) and systolic blood pressure (β=−1.68, p=0.006). A positive association of increased 25(OH)D with HOMA-B (β=0.17, p=8.0×10−6), and C-peptide (β=0.09, 0.017) was observed. Non-medicated, normoglycemic, non-hypertensive individuals classified as vitamin D deficient (n=289) exhibited a significant increase in fasting glucose (p=0.02) and BMI (p<0.0001) as well as a significant decrease in C-peptide (p<0.0001) and amylin (p<0.0001) compared to vitamin D sufficient controls (n=150).
Conclusions
Vitamin D deficiency appears to be a significant risk factor for T2D severity and associated cardio-metabolic risk. Early intervention may be considered to improve prevention of T2D related cardiovascular complications.
doi:10.4172/2155-6156.1000213
PMCID: PMC3817265  PMID: 24199029
8.  Involvement of SIRT1 in Zn2+, Streptozotocin, Non-Obese Diabetic, and Cytokine-Mediated Toxicities of β-cells 
Journal of diabetes & metabolism  2012;3(4):1000193.
Zn2+ toxicity is implicated in pancreatic β-cell death that occurs secondarily to: streptozotocin exposure in vitro; and both autoimmune attack or streptozotocin in vivo models of T1DM. This is demonstrated by reduced β-cell death or diabetic incidence in vitro or in NOD mice after treatment with Zn2+ preferring chelators, pyruvate, nicotinamide, a reduced zinc diet, sirtuin inhibitors, or zinc transporter knockout. These therapeutics are also demonstrated to be efficacious against Zn2+ neurotoxicity.
Aims
To determine if the sirtuin pathway is involved in Zn2+-, streptozotocin-, or cytokine-mediated β-cell death in vitro, and streptozotocin-, or NOD induced T1DM in vivo.
Methods
Sensitivity of MIN6 cells expressing empty vector, sirtuin protein-1 (SIRT1) or its siRNA, to Zn2+, streptozotocin, or cytokines, and effects on NAD+ levels were determined. Covariance of manipulating SIRT1 levels with diabetic incidence was tested in vivo.
Results
1) sirtuin pathway inhibition or SIRT1 knockdown attenuated Zn2+-, STZ-, and cytokine-mediated toxicity and NAD+ loss in β-cells, 2) SIRT1 overexpression potentiated these toxicities, 3) young SIRT1 β-cell transgenic mice have improved glucose tolerance under basal conditions, but upon aging showed increased sensitivity to streptozotocin compared to SIRT1 +/− mice, and 4) SIRT1 +/− mice in an NOD background or exposed to streptozotocin trended toward reduced diabetic incidence and mortality compared to wildtype.
Conclusions
These results have implicated SIRT1-mediated NAD+ loss in Zn2+, STZ, or cytokine toxicities of MIN6, and in NOD or streptozotocin T1DM animal models. Modulation of β-cell Zn2+ and NAD+ levels, and the sirtuin pathway could be novel therapeutic targets for T1DM.
doi:10.4172/2155-6156.1000193
PMCID: PMC3615451  PMID: 23565341
Sirtuins; NAD+; MIN6; SIRT1 knockout
9.  Contributions of the Insulin/Insulin-Like Growth Factor-1 Axis to Diabetic Osteopathy 
Recent studies in diabetic humans and rodent models of diabetes have identified osteopathy as a serious complication of type 1 (T1D) and type 2 (T2D) diabetes. Accumulating evidence suggests that disruption of insulin and insulin-like growth factor 1 (IGF-1) homeostasis in the diabetic condition may be responsible for the observed skeletal deficits. Indeed, replacement of insulin or IGF-1 in rodent models of T1D results in significant improvement in bone healing despite ongoing moderate to severe hyperglycemia. Insulin and IGF-1 act through distinct receptors. Mice in which the receptor for insulin or IGF-1 is selectively deleted from osteoblast lineages show skeletal deficits. Despite acting through distinct receptors, insulin and IGF-1 exert their cellular activities via conserved intracellular signaling proteins. Genetic manipulation of these signaling proteins, such as insulin receptor substrate (IRS)-1 and -2, Protein Kinase B (Akt), and MAPK/ERK kinase (MEK), has uncovered a significant role for these signal transduction pathways in skeletal homeostasis. In addition to effects on skeletal physiology via canonical signaling pathways, insulin and IGF-1 may crosstalk with wingless-int. (Wnt) and bone morphogenic protein 2 (BMP-2) signaling pathways in cells of the osteoblast lineage and thereby promote skeletal development. In this review, a discussion is presented regarding the role of insulin and IGF-1 in skeletal physiology and disruptions of this axis that occur in the diabetic condition which could underlie many of the skeletal pathologies observed.
doi:10.4172/2155-6156.S1-003
PMCID: PMC3593087  PMID: 23484069
10.  Relationship between Depression and Treatment Satisfaction among Patients with Type 2 Diabetes 
Journal of diabetes & metabolism  2012;3(7):1000210.
Background
Depression has been shown to adversely affect glycemic control. The purpose of this study is to examine the association between depression and treatment satisfaction in patients with diabetes.
Materials and methods
Baseline data was collected on 545 patients with poorly controlled type 2 diabetes enrolled in a study that examined the effectiveness of diabetes nurse case managers. Depression was measured using the Center for Epidemiologic Studies Depression (CES-D) questionnaire, and treatment satisfaction, using the Diabetes Treatment Satisfaction Questionnaire (DTSQ).
Results
The majority of participants (59%) were female, with a high percentage (41%) of Hispanic/Latino participants with a mean HbA1C of 8.4%. The prevalence of depression in this population was 35.6%. High CES-D scores were associated with elevated levels of HbA1C and LDL cholesterol (p<0.001). The relationship between depression and treatment satisfaction was significant (p<0.001), indicating that as depression increases, treatment satisfaction decreases.
Discussion
We identified a significant relationship between depression and treatment satisfaction in this group of poorly controlled type 2 diabetes patients. Although causation cannot be determined, it is possible that patients who are depressed are less likely to be satisfied with their treatment. This could lead to decreased patient adherence, ultimately resulting in poor glycemic control.
doi:10.4172/2155-6156.1000210
PMCID: PMC3521162  PMID: 23243556
Depression; Treatment satisfaction; Type 2 diabetes
11.  Type 2 Diabetes Genetics: Beyond GWAS 
The global epidemic of type 2 diabetes mellitus (T2D) is one of the most challenging problems of the 21st century leading cause of and the fifth death worldwide. Substantial evidence suggests that T2D is a multifactorial disease with a strong genetic component. Recent genome-wide association studies (GWAS) have successfully identified and replicated nearly 75 susceptibility loci associated with T2D and related metabolic traits, mostly in Europeans, and some in African, and South Asian populations. The GWAS serve as a starting point for future genetic and functional studies since the mechanisms of action by which these associated loci influence disease is still unclear and it is difficult to predict potential implication of these findings in clinical settings. Despite extensive replication, no study has unequivocally demonstrated their clinical role in the disease management beyond progression to T2D from impaired glucose tolerance. However, these studies are revealing new molecular pathways underlying diabetes etiology, gene-environment interactions, epigenetic modifications, and gene function. This review highlights evolving progress made in the rapidly moving field of T2D genetics that is starting to unravel the pathophysiology of a complex phenotype and has potential to show clinical relevance in the near future.
doi:10.4172/2155-6156.1000198
PMCID: PMC3521576  PMID: 23243555
12.  Examination of Rare Variants in HNF4 α in European Americans with Type 2 Diabetes 
Journal of diabetes & metabolism  2011;2(145):1000145.
The hepatocyte nuclear factor 4-α (HNF4α) gene codes for a transcription factor which is responsible for regulating gene transcription in pancreatic beta cells, in addition to its primary role in hepatic gene regulation. Mutations in this gene can lead to maturity-onset diabetes of the young (MODY), an uncommon, autosomal dominant, non-insulin dependent form of diabetes. Mutations in HNF4α have been found in few individuals, and infrequently have they segregated completely with MODY in families. In addition, due to similarity of phenotypes, it is unclear what proportion of type 2 diabetes (T2DM) in the general population is due to MODY or HNF4α mutations specifically. In this study, 27 documented rare and common variants were genotyped in a European American population of 1270 T2DM cases and 1017 controls from review of databases and literature implicating HNF4α variants in MODY and T2DM. Seventeen variants were found to be monomorphic. Two cases and one control subject had one copy of a 6-bp P2 promoter deletion. The intron 1 variant (rs6103716; MAF = 0.31) was not significantly associated with disease status (p>0.8) and the missense variant Thr130Ile (rs1800961; MAF = 0.027) was also not significantly different between cases and controls (p>0.2), but showed a trend consistent with association with T2DM. Four variants were found to be rare as heterozygotes in small numbers of subjects. Since many variants were infrequent, a pooled chi-squared analysis of rare variants was used to assess the overall burden of variants between cases and controls. This analysis revealed no significant difference (P=0.22). We conclude there is little evidence to suggest that HNF4α variants contribute significantly to risk of T2DM in the general population, but a modest contribution cannot be excluded. In addition, the observation of some mutations in controls suggests they are not highly penetrant MODY-causing variants.
doi:10.4172/2155-6156.1000145
PMCID: PMC3515062  PMID: 23227446
Type 2 Diabetes; HNF4A; Rare variants
13.  Elevated angiotensin II in rat nodose ganglia primes diabetes-blunted arterial baroreflex sensitivity: involvement of NADPH oxidase-derived superoxide 
Journal of diabetes & metabolism  2011;2(6):1000135.
Clinical trials and experimental animal studies have confirmed the contribution of arterial baroreflex impairment in causing excess morbidity and mortality in type-1 diabetes. Our previous study has shown that angiotensin II (Ang II)-NADPH oxidase-superoxide signaling is associated with the reduced cell excitability in the aortic baroreceptor neurons (a primary afferent limb of the arterial baroreflex) from diabetic rats. In this study, we examined whether above-mentioned signaling might contribute to the blunted baroreflex sensitivity in streptozotocin-induced diabetic rats. Using Ang II 125I radioimmunoassay and lucigenin chemiluminescence method, we found Ang II concentration, NADPH oxidase activity, and superoxide production in the nodose ganglia were enhanced in diabetic rats, compared to sham rats. As an index of the arterial baroreflex sensitivity, the reflex decreases in blood pressure and heart rate evoked by unilateral steady-frequency aortic depressor nerve stimulation were attenuated in diabetic rats. Local microinjection (50 nl) of losartan (an AT1 receptor antagonist, 1 nmol), apocynin (a NADPH oxidase inhibitor, 1 nmol), and tempol (a superoxide dismutase mimetic, 10 nmol) into the nodose ganglia significantly improved the arterial baroreflex sensitivity in diabetic rats. In addition, these three chemicals also normalized exogenous Ang II-attenuated arterial baroreflex sensitivity in sham rats. These results indicate that overactivation of the Ang II-NADPH oxidase-superoxide signal pathway in the nodose ganglia contributes to the blunted baroreflex sensitivity in diabetes.
doi:10.4172/2155-6156.1000135
PMCID: PMC3269316  PMID: 22308229
Angiotensin II; Baroreflex; Diabetes; NADPH oxidase; Superoxide
14.  Low Plasma Hdl Cholesterol and Elevated C Reactive Protein further Increase Cardiovascular Disease Risk in Latinos with Type 2 Diabetes 
The purpose of this study was to determine whether low plasma HDL and high C reactive protein (CRP) concentrations would further increase cardiovascular disease (CVD) risk in Latinos with poorly controlled type-2 diabetes, already at high risk for CVD. Subjects (n = 68) were grouped into High-HDL (≥ or 1.03 or 1.3 mmol/L) or Low-HDL (<1.03 or 1.3 mmol/L) for men and women, respectively. Following classification, risk factors for CVD including apolipoproteins, lipoprotein size and subfraction distribution were assesed. Similarly, participants were divided according to their CRP levels (≥ or < 3mg/L) and key inflammatory markers as well as leptin and adiponectin were analyzed. The Low-HDL group had higher concentrations of the atherogenic particles, large and medium VLDL and the smaller LDL subfractions compared to the High-HDL group (p<0.001). Consistently, VLDL diameter was larger and LDL diameter smaller in the Low HDL group (p<0.001). The High-CRP group had larger waist circumference (p<0.001) and body mass index (p<0.001) than the Low-CRP group. Leptin was also higher in the High- CRP group (p< 0.01). These data suggest that Latinos with type-2 diabetes having either Low-HDL or High-CRP concentrations are at a higher risk for atherosclerosis and CVD than their counterparts who have High-HDL or Low-CRP.
PMCID: PMC3296281  PMID: 22407331
Type 2 diabetes; Latinos; Heart disease risk; HDL; CRP; Inflammatory markers; Apolipoproteins
15.  Prieurianin Causes Weight Loss in Diet-Induced Obese Mice and Inhibits Adipogenesis in Cultured Preadipocytes 
Journal of diabetes & metabolism  2010;1(101):1000101.
The global increase in the incidence of obesity has emerged as one of the most serious public health risks in recent years. Despite the enormity of the obesity pandemic, there are currently only two FDA-approved therapies for its treatment and these drugs exhibit modest efficacy and have limiting side effects. Prieurianin is a plant limonoid product that deters feeding in insect larvae. We investigated in this study the effects of prieurianin on weight loss and adipogenesis. Our results showed that prieurianin causes weight loss by reducing energy intake in obese mice on high-calorie diet. We also found that prieurianin is anti-adipogenic in cultured preadipocytes and adipocytes by inhibiting proliferation and differentiation of preadipocytes into adipocytes, and induces either dedifferentiation or delipidation of mature adipocytes. Whether prieurianin can potentially be used for obesity treatment in human warrants further investigation.
PMCID: PMC3093537  PMID: 21572918
Prieurianin; Obesity; Appetite; Adipogenesis; Weight loss; Tolerance; Preadipocytes; Adipocytes

Results 1-15 (15)