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1.  Inflammatory Adipokines, High Molecular Weight Adiponectin, and Insulin Resistance: A Population-Based Survey in Prepubertal Schoolchildren 
PLoS ONE  2011;6(2):e17264.
The aim of this study was to investigate sex differences and associations of high molecular weight (HMW) adiponectin, leptin and proinflammatory adipokines, individually or in combinations, with adiposity and insulin resistance (IR) measures in prepubertal childhood.
We studied 305 prepubertal children (boys/girls: 144/161; Tanner stage 1; age: 5-13 yr), included in a cohort of 44,231 adolescents who participated in an extensive Italian school-based survey. According to Cole's criteria, 105 individuals were lean (L; boys/girls: 59/46), 60 overweight (OW; boys/girls: 32/28) and 140 obese (OB; boys/girls: 70/70). Measurements comprised total and HMW adiponectin, leptin, as well as a panel of proinflammatory adipokines/chemokines associated with diabetes risk.
Principal Findings
Leptin-, and the leptin-to-HMW adiponectin ratio (L/HMW)-, increased progressively (p<0.0001) from L to OW to OB boys and girls. When compared with L peers, OW and OB girls exhibited lower (p<0.001) HMW adiponectin levels, while in boys the HMW multimers did not differ significantly across the BMI-stratified groups. OB girls displayed higher (p<0.05) IL-8, IL-18, monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion molecule-1 levels (sICAM-1) than L girls, whereas increased macrophage migration inhibitory factor (MIF) concentrations in OB vs OW boys were seen. HMW adiponectin (negatively), leptin or inflammatory markers (positively) correlated with adiposity and IR measures. In multivariate models, leptin represented a strong and independent determinant of HOMA-IR (R2 0.378; p<0.01). Adjustment for age, BMIz-score, lipids and inflammatory mediators abolished the association between leptin and HOMA-IR in boys, while in girls leptin remained still a significant predictor of IR (R2 0.513; p<0.01). Finally, in both sexes, the joint effect of the L/HMW did not improve the prediction of basal IR as compared with leptin levels alone, which were mainly explained by the BMIz-score.
In prepubertal children, leptin emerges as a sex-independent discrimination marker of adiposity degree and as a useful, sex-associated predictor of the systemic insulin resistance.
PMCID: PMC3041818  PMID: 21365005
2.  Ghrelin, adipokines, metabolic factors in relation with weight status in school-children and results of a 1-year lifestyle intervention program 
Overweight in Guadeloupe is a public health matter affecting children and adults. In the present study we evaluated the metabolic profile, including serum ghrelin, leptin and adiponectin levels, in normal weight, overweight and obese school children and we analyzed the potential changes in anthropometric and metabolic risk factors after a 1-year lifestyle intervention program.
Parameters were assessed at baseline and at 1 year. Three groups (G) were defined according the International Obesity Task Force reference values, G1: normal weight / G2: overweight / G3: obese. The lifestyle intervention included dietary counseling, regular physical activity and family support.
A total of 120 children (G1: n = 44, G2: n = 39, G3: n = 37), aged 11– 15 years and 59 % girls were enrolled. Obese children showed significant lower HDL-C, adiponectin and ghrelin concentrations, higher triglycerides, fasting blood glucose, insulin and leptin levels and also higher frequencies of abdominal obesity (G1: 2.3 %, G2: 28.2 %, G3: 73 %) and insulin resistance (GI: 39 %, G2: 72 %, G3: 89 %) than the other groups. In the overall sample, the linear regressions exploring the associations of ghrelin, adiponectin and leptin with age, gender, BMI z-score, HOMA-IR and tanner stage as independent variables showed strong associations of leptin levels with weight status and insulin resistance at baseline. The models accounted for 58 % of variability in leptin levels compared with 26 and 15 % for adiponectin and ghrelin levels respectively.
In 83 children who completed the program, significant decreases in BMI z-score in overweight and obese children were noted. Leptin levels decreased significantly only in the obese group whereas adiponectin concentrations increased significantly in the three groups,
In obese children, a significant correlation was found between changes in BMI Z-score, and changes in leptin levels (r = 0.39; P = 0.049) but not with changes in adiponectin levels.
Abdominal obesity and insulin resistance were highly prevalent in obese children highlighting their risk of metabolic complications in adulthood. A 1-year long lifestyle intervention was associated with improvement in BMI z-score and metabolic parameters.
PMCID: PMC4650925  PMID: 26581745
Adolescents; Obesity; Adipokines; Ghrelin; Lifestyle intervention
3.  Exploring the Developmental Overnutrition Hypothesis Using Parental–Offspring Associations and FTO as an Instrumental Variable 
PLoS Medicine  2008;5(3):e33.
The developmental overnutrition hypothesis suggests that greater maternal obesity during pregnancy results in increased offspring adiposity in later life. If true, this would result in the obesity epidemic progressing across generations irrespective of environmental or genetic changes. It is therefore important to robustly test this hypothesis.
Methods and Findings
We explored this hypothesis by comparing the associations of maternal and paternal pre-pregnancy body mass index (BMI) with offspring dual energy X-ray absorptiometry (DXA)–determined fat mass measured at 9 to 11 y (4,091 parent–offspring trios) and by using maternal FTO genotype, controlling for offspring FTO genotype, as an instrument for maternal adiposity. Both maternal and paternal BMI were positively associated with offspring fat mass, but the maternal association effect size was larger than that in the paternal association in all models: mean difference in offspring sex- and age-standardised fat mass z-score per 1 standard deviation BMI 0.24 (95% confidence interval [CI]: 0.22 to 0.26) for maternal BMI versus 0.13 (95% CI: 0.11, 0.15) for paternal BMI; p-value for difference in effect < 0.001. The stronger maternal association was robust to sensitivity analyses assuming levels of non-paternity up to 20%. When maternal FTO, controlling for offspring FTO, was used as an instrument for the effect of maternal adiposity, the mean difference in offspring fat mass z-score per 1 standard deviation maternal BMI was −0.08 (95% CI: −0.56 to 0.41), with no strong statistical evidence that this differed from the observational ordinary least squares analyses (p = 0.17).
Neither our parental comparisons nor the use of FTO genotype as an instrumental variable, suggest that greater maternal BMI during offspring development has a marked effect on offspring fat mass at age 9–11 y. Developmental overnutrition related to greater maternal BMI is unlikely to have driven the recent obesity epidemic.
Using parental-offspring associations and theFTO gene as an instrumental variable for maternal adiposity, Debbie Lawlor and colleagues found that greater maternal BMI during offspring development does not appear to have a marked effect on offspring fat mass at age 9-11.
Editors' Summary
Since the 1970s, the proportion of children and adults who are overweight or obese (people who have an unhealthy amount of body fat) has increased sharply in many countries. In the US, 1 in 3 adults is now obese; in the mid-1970s it was only 1 in 7. Similarly, the proportion of overweight children has risen from 1 in 20 to 1 in 5. An adult is considered to be overweight if their body mass index (BMI)—their weight in kilograms divided by their height in meters squared—is between 25 and 30, and obese if it is more than 30. For children, the healthy BMI depends on their age and gender. Compared to people with a healthy weight (a BMI between 18.5 and 25), overweight or obese individuals have an increased lifetime risk of developing diabetes and other adverse health conditions, sometimes becoming ill while they are still young. People become unhealthily fat when they consume food and drink that contains more energy than they need for their daily activities. It should, therefore, be possible to avoid becoming obese by having a healthy diet and exercising regularly.
Why Was This Study Done?
Some researchers think that “developmental overnutrition” may have caused the recent increase in waistline measurements. In other words, if a mother is overweight during pregnancy, high sugar and fat levels in her body might permanently affect her growing baby's appetite control and metabolism, and so her offspring might be at risk of becoming obese in later life. If this hypothesis is true, each generation will tend to be fatter than the previous one and it will be very hard to halt the obesity epidemic simply by encouraging people to eat less and exercise more. In this study, the researchers have used two approaches to test the developmental overnutrition hypothesis. First, they have asked whether offspring fat mass is more strongly related to maternal BMI than to paternal BMI; it should be if the hypothesis is true. Second, they have asked whether a genetic indicator of maternal fatness—the “A” variant of the FTO gene—is related to offspring fat mass. A statistical association between maternal FTO genotype (genetic make-up) and offspring fat mass would support the developmental nutrition hypothesis.
What Did the Researchers Do and Find?
In 1991–1992, the Avon Longitudinal Study of Parents and Children (ALSPAC) enrolled about 14,000 pregnant women and now examines their offspring at regular intervals. The researchers first used statistical methods to look for associations between the self-reported prepregnancy BMI of the parents of about 4,000 children and the children's fat mass at ages 9–11 years measured using a technique called dual energy X-ray absorptiometry. Both maternal and paternal BMI were positively associated with offspring fat mass (that is, fatter parents had fatter children) but the effect of maternal BMI was greater than the effect of paternal BMI. When the researchers examined maternal FTO genotypes and offspring fat mass (after allowing for the offspring's FTO genotype, which would directly affect their fat mass), there was no statistical evidence to suggest that differences in offspring fat mass were related to the maternal FTO genotype.
What Do These Findings Mean?
Although the findings from first approach provide some support for the development overnutrition hypothesis, the effect of maternal BMI on offspring fat mass is too weak to explain the recent obesity epidemic. Developmental overnutrition could, however, be responsible for the much slower increase in obesity that began a century ago. The findings from the second approach provide no support for the developmental overnutrition hypothesis, although these results have wide error margins and need confirming in a larger study. The researchers also note that the effects of developmental overnutrition on offspring fat mass, although weak at age 9–11, might become more important at later ages. Nevertheless, for now, it seems unlikely that developmental overnutrition has been a major driver of the recent obesity epidemic. Interventions that aim to improve people's diet and to increase their physical activity levels could therefore slow or even halt the epidemic.
Additional Information.
Please access these Web sites via the online version of this summary at
See a related PLoS Medicine Perspective article
The MedlinePlus encyclopedia has a page on obesity (in English and Spanish)
The US Centers for Disease Control and Prevention provides information on all aspects of obesity (in English and Spanish)
The UK National Health Service's health Web site (NHS Direct) provides information about obesity
The International Obesity Taskforce provides information about preventing obesity and on childhood obesity
The UK Foods Standards Agency, the United States Department of Agriculture, and Shaping America's Health all provide useful advice about healthy eating for adults and children
The ALSPAC Web site provides information about the Avon Longitudinal Study of Parents and Children and its results so far
PMCID: PMC2265763  PMID: 18336062
4.  Adipokines and Body Fat Composition in South Asians: Results of the Metabolic syndrome and Atherosclerosis in South Asians Living in America (MASALA) Study 
To investigate whether leptin and adiponectin are associated with body fat composition in a South Asian population independent of metabolic variables.
Cross-sectional study
150 South Asian men and women, between the ages of 45–79 years, in the San Francisco Bay Area without pre-existing clinical cardiovascular disease.
Blood samples were obtained to measure glucose metabolism variables, lipid profiles and adipokines. Total body fat was determined using dual-energy x-ray absorptiometry. Abdominal computed tomography was used to measure subcutaneous, visceral, and hepatic fat.
Average body mass index (BMI) was overweight at 26.1±4.6 kg/m2 and did not differ by sex. However, women had significantly more total body fat (p<0.001) and subcutaneous fat (p<0.001) than men, while men had significantly more visceral fat (p<0.001) and hepatic fat (p=0.04) than women. Women had significantly higher levels of adiponectin (p<0.01) and leptin (p<0.01). In sex-stratified analyses, leptin was strongly associated with all body composition measures in women (p<0.05) as well as in men (p<0.05 except for hepatic fat) while there was an insignificant trend towards an inverse association between adiponectin and body composition in both women and men which was significant in combined bivariate analyses. In multivariate analyses, leptin was strongly associated with all measures of adiposity, including BMI (p<0.001), total body fat (p<0.001), visceral fat (p<0.001), and hepatic fat (p=0.01). However, adiponectin’s inverse association with adiposity was significantly attenuated by high-density lipoprotein (HDL), triglycerides, and insulin resistance. The association between adipokines and diabetes was markedly attenuated after adjusting for body composition.
Despite only modestly elevated BMI, South Asians have elevated levels of total and regional adiposity. Leptin is strongly associated with adiposity while adiponectin’s association with adiposity is attenuated by metabolic variables in South Asians. Adipokines in association with adiposity play an important role in the development of diabetes.
PMCID: PMC3224670  PMID: 21863003
South Asians; body composition; sex differences in adiposity; adiponectin and leptin; hepatic fat
5.  The impact of gestational diabetes mellitus on pubertal changes in adiposity and metabolic profiles in Latino offspring 
The Journal of pediatrics  2012;162(4):741-745.
To examine the impact of maternal gestational diabetes mellitus (GDM) status on longitudinal changes in adiposity and metabolic variables in overweight Latino offspring (from age 8– 20 years) across puberty.
Study design
This is a longitudinal cohort of 210 overweight Latino children who were measured annually for 3 ± 1 years for: Tanner stage via physical examination, adiposity via dual-energy X-ray absorptiometry and magnetic resonance imaging, lipids, glucose and insulin action via oral glucose tolerance test and frequently sampled intravenous glucose tolerance test. Linear mixed-effects modeling estimated the impact of maternal GDM status on baseline and changes in adiposity and metabolic variables across puberty.
Twenty-two percent of offspring were from GDM pregnancies. At baseline, GDM offspring were heavier at birth, had more family history of type 2 diabetes, and were less likely to have been breastfeed (any duration). GDM offspring compared with non-GDM offspring had greater increases in total body fat (+6.5% vs +4.5%; p=0.03) and steeper declines in acute insulin response (−39% vs. −17%; p<0.001) and disposition index (−57% vs. −35%; p<0.001) across Tanner stages, independent of ethnicity, sex, breastfeeding status, family history of diabetes, and baseline and changes in body composition.
These findings confirm the elevated risk for excess adiposity and type 2 diabetes in GDM offspring, and further highlight the need for interventions targeting Latino GDM and their offspring.
PMCID: PMC3578029  PMID: 23149173
Longitudinal study; Hispanics; overweight and obesity; Gestional diabetes; type 2 diabetes risk; puberty
6.  Correlation of Adiponectin and Leptin with Insulin Resistance: A Pilot Study in Healthy North Indian Population 
The increasing incidence of obesity, leading to metabolic complications is now recognized as a major public-health problem. Insulin resistance is a central abnormality of the metabolic syndrome, or syndrome X, originally hypothesized by Reaven Insulin resistance is more strongly linked to intra abdominal fat than to fat in other depots. Adipose tissue secretes numerous factors (adipokines) known to markedly influence lipid and glucose/insulin metabolism, oxidative stress, and cardiovascular integrity. Some of these adipokines have been shown to directly or indirectly affect insulin sensitivity through modulation of insulin signaling and the molecules involved in glucose and lipid metabolism. A pilot study was conducted with 80 healthy subjects who were non diabetic, non hypertensive and having no family history of hypertension, the aim was to evaluate the correlation of adiponectin and leptin levels with obesity and insulin resistance markers in healthy north Indian adult population. Serum leptin, adiponectin and insulin was estimated by sandwich ELISA method. In our study, Leptin correlated significantly with BMI (P value of 0.0000), WC (P value = 0.007), and HC (P value = 0.000). leptin showed significant positive correlation with fasting insulin (P value 0.002), post prandial insulin (P value = 0.000) and HOMA-IR (P value = 0.002). Adiponectin showed significant positive correlation with triglycerides (P value = 0.038), strong negative correlation with HDL-cholesterol (P value = 0.017). Serum concentrations of leptin are associated with central body fat distribution. Insulin resistance and adiponectin is associated with dyslipidemia and these all disorders may ultimately lead to metabolic syndrome.
PMCID: PMC3107404  PMID: 22468049
Adiponectin; Leptin; Insulin resistance; Cytokines
7.  Effects of diabetes family history and exercise training on the expression of adiponectin and leptin and their receptors 
Metabolism  2011;60(2):206-214.
Daughters of diabetes patients have lower insulin sensitivity than women with no diabetes family history, but increase insulin sensitivity to a greater extent with exercise training. This study aimed to determine whether differences in circulating concentrations of adiponectin and leptin, and adipose tissue expression of their genes and receptors played a role. Women offspring of patients with type 2 diabetes mellitus (n = 34; age, 35.6 ± 7.0 years; body mass index, 28.1 ± 5.1 kg/m2) and matched controls with no diabetes family history (n = 36; age, 33.6 ± 6.1 years; body mass index, 27.3 ± 4.7 kg/m2) participated. Blood and abdominal subcutaneous adipose tissue samples were obtained at baseline and after a controlled 7-week endurance-type exercise intervention (sessions were performed at 65%-80% of maximum heart rate). At baseline, no significant differences were observed between groups in circulating leptin or adiponectin concentrations, or expression of their genes or receptors. In response to exercise, plasma leptin decreased more in offspring than controls (−32.2% vs −7.3%, P = .005 for interaction); and the long isoform of the leptin receptor messenger RNA (mRNA) increased significantly only in the offspring (+39.4%, P = .026 vs +7.7%, P = .892). Leptin mRNA decreased similarly in both groups (−24.7% vs −25.0%, P < .05 for both). Furthermore, changes in plasma leptin (r = −0.432, P < .001) and leptin mRNA (r = −0.298, P = .019) correlated significantly with changes in insulin sensitivity. Plasma adiponectin decreased similarly in both groups (−12.1% vs −15.2%, P < .01 for both), but no significant changes were observed in adiponectin-related gene expression. This work shows that exercise training has differing effects on leptin-related variables between women with and without a diabetes family history and suggests that these molecular differences may contribute to the differential effects of exercise training on insulin sensitivity between these 2 groups.
PMCID: PMC3032051  PMID: 20153489
8.  Adiponectin and Leptin Metabolic Biomarkers in Chinese Children and Adolescents 
Journal of Obesity  2010;2010:892081.
Objective. To evaluate leptin and adiponectin as biomarkers of metabolic syndrome (MS) risk factors even in nonobese children/adolescents. Methods. Serum leptin, adiponectin, leptin:adiponectin ratio, lipids, glucose, and insulin concentrations as well as body size parameters and pubertal development were evaluated in a large population of Chinese children/adolescents (n = 3505, 6–18 years, 1722 girls and 1783 boys). Results. Leptin concentration increased while adiponectin decreased with obesity, both were influenced by pubertal development. Central obesity had an additive effect on leptin levels (above obesity alone). Leptin/adiponectin increased 8.4-fold and 3.2-fold in overweight/obesity, and 15.8- and 4.5-fold with obesity plus MS, in early and late puberty, respectively. Even in normal weight children/adolescents, higher leptin and lower adiponectin concentrations associated with increased risk profile. Conversely, overweight/obese with lower leptin or higher adiponectin concentrations had a less compromised metabolic profile. Conclusion. Leptin, adiponectin, and leptin:adiponectin ratio are informative biomarkers for obesity, central obesity, MS, and abnormal metabolic profile even in normal weight children/adolescents.
PMCID: PMC2968118  PMID: 21052532
9.  CRP Is Related to Higher Leptin Levels in Minority Peripubertal Females Regardless of Adiposity Levels 
Obesity (Silver Spring, Md.)  2011;20(3):512-516.
Overweight is related to higher levels of C-reactive protein (CRP) and leptin, which have been independently associated with increased risk for diabetes, cardiovascular disease, and the metabolic syndrome. Elevated CRP may trigger leptin resistance by inhibiting the binding of leptin to its receptors. We cross-sectionally examined the relationship between CRP, leptin, BMI z-score, percent body fat (%BF) assessed by air plethysmography (BodPod), and insulin sensitivity (SI) and acute insulin response (AIRg) measured by intravenous glucose tolerance test in 51 Latina and African-American females (77% Latina), mean age 9.2 (±0.9) years, at either Tanner Pubertal Stage (TPS) 1 (n = 25) or TPS 2 (n = 26). Females at TPS 2 had higher BMI z-scores, %BF (23% ± 10.1 vs. 30% ± 10.0, P = 0.02), AIRg (976.7 ± 735.2 vs. 1555.3 ± 1,223 µIU/ml, P = 0.05), fasting insulin (11.0 ± 10.8 vs. 17.2 ± 13.6 µlU/ml, P = 0.00) and leptin levels (11.0 ± 7.1 vs. 19.6 ± 10.9 ng/ml, P < 0.001) than those at TPS 1. There were no ethnic differences in any of the measured variables. CRP was positively correlated with BMI z-score (P = 0.001), %BF (P = 0.006), fasting insulin and AIRg (P = 0.02), and fasting leptin (P = 0.00), and negatively correlated with SI (P = 0.05). A linear regression model showed that CRP independently explained 10% (P = 0.00) of the variance in leptin after adjusting %BF, TPS, ethnicity, habitual physical activity and SI. Hence, low-grade inflammation may contribute to prolonged leptin exposure and leptin resistance, even in healthy children.
PMCID: PMC3200494  PMID: 21436796
10.  Association of polymorphism in adiponectin (+45 T/G) and leptin (–2548 G/A) genes with type 2 diabetes mellitus in male Egyptians 
Archives of Medical Science : AMS  2015;11(5):937-944.
Adiponectin is an adipose tissue-specific protein with insulin-sensitizing properties. Many investigators have explored the association between adiponectin single nucleotide polymorphisms (SNPs) and type 2 diabetes mellitus (T2DM) in different ethnic populations from different regions. Leptin is a protein hormone constituting an important signal in the regulation of adipose tissue mass and body weight. The aim of this study was to explore potential associations between SNP +45 T>G of the adiponectin gene and SNP 2548G/A of leptin with T2DM and the effect of SNPs on serum adiponectin and leptin levels.
Material and methods
From the Egyptian population, we enrolled 110 T2DM patients and 90 non-diabetic controls. Serum lipid profile, blood glucose, serum adiponectin, and leptin were measured. Genotyping for two common SNPs of the adiponectin and leptin genes was performed by polymerase chain reaction–restriction fragment length polymorphism.
The G allele and TG/GG genotype of SNP 45 occurred more frequently than the T allele and TT genotype in T2DM patients compares to the controls. Subjects with the GG + TG genotype of SNP 45 were at increased risk for T2DM (OR = 6.476; 95% CI: 3.401–12.33) and associated with a low serum adiponectin level compared with the TT genotype. The serum leptin concentration of GA + AA genotype carriers was not significantly different from that of the GG genotype in the diabetic group.
The G allele carriers who have reduced plasma concentrations of adiponectin may have an association with T2DM, while leptin SNP 2548 G/A is not associated with the risk of development of T2DM in the Egyptian population.
PMCID: PMC4624740  PMID: 26528333
single nucleotide polymorphism; polymerase chain reaction–restriction fragment length polymorphism
11.  Relation of Absolute or Relative Adiposity to Insulin Resistance, Retinol Binding Protein-4, Leptin, and Adiponectin in Type 2 Diabetes 
Diabetes & Metabolism Journal  2012;36(6):415-421.
Central fat mass (CFM) correlates with insulin resistance and increases the risk of type 2 diabetes and cardiovascular complications; however, peripheral fat mass (PFM) is associated with insulin sensitivity. The aim of this study was to investigate the relation of absolute and relative regional adiposity to insulin resistance index and adipokines in type 2 diabetes.
Total of 83 overweighted-Korean women with type 2 diabetes were enrolled, and rate constants for plasma glucose disappearance (KITT) and serum adipokines, such as retinol binding protein-4 (RBP4), leptin, and adiponectin, were measured. Using dual X-ray absorptiometry, trunk fat mass (in kilograms) was defined as CFM, sum of fat mass on the lower extremities (in kilograms) as PFM, and sum of CFM and PFM as total fat mass (TFM). PFM/TFM ratio, CFM/TFM ratio, and PFM/CFM ratio were defined as relative adiposity.
Median age was 55.9 years, mean body mass index 27.2 kg/m2, and mean HbA1c level 7.12±0.84%. KITT was positively associated with PMF/TFM ratio, PMF/CFM ratio, and negatively with CFM/TFM ratio, but was not associated with TFM, PFM, or CFM. RBP4 levels also had a significant relationship with PMF/TFM ratio and PMF/CFM ratio. Adiponectin, leptin, and apolipoprotein A levels were related to absolute adiposity, while only adiponectin to relative adiposity. In correlation analysis, KITT in type 2 diabetes was positively related with HbA1c, fasting glucose, RBP4, and free fatty acid.
These results suggest that increased relative amount of peripheral fat mass may aggravate insulin resistance in type 2 diabetes.
PMCID: PMC3530712  PMID: 23275935
Adiponectin; Adiposity; Insulin resistance; Leptin; Retinol binding protein-4
12.  Serum adiponectin and leptin in relation to risk for preeclampsia: results from a large case-control study 
Metabolism: clinical and experimental  2011;60(11):1539-1544.
Conditions resulting in insulin resistance, as well as metabolic, immune and angiogenic perturbations, have been associated with an increased risk of preeclampsia (PE). Our purpose was to assess whether the adipose tissue secreted hormones: adiponectin, which has immune modulating, metabolic and angiogenic properties, and leptin, which reflects overall fat mass, are associated with PE risk.
We performed a case-control design study within a hospital-based cohort of 368 pregnant women (106 with PE and 262 controls; mean age: 26.6 ± 6.8 years; mean gestational age at admission: 38.2 ± 2.8 weeks) between March 2005 and August 2007 at the Hospital of Pennsylvania University. Serum adiponectin and leptin were measured by radioimmunoassay. Statistical analysis of data was performed using simple and multiple regression analyses.
No significant differences in adiponectin or leptin levels between pre-eclamptic and control pregnant women emerged in univariate analyses (p=0.57 and p=0.15 respectively). Among pre-eclamptic women, there were also no differences in adipokines between those with mild and severe disease. Serum adiponectin and leptin were not associated with higher risk of PE before and after adjustment for maternal age, race, primigravida, smoking status, body mass index at screening, gestational age at admission, history of preeclampsia, chronic hypertension and gestational diabetes (OR: 0.93, 95% C.I.: 0.83–1.04 and OR: 1, 95% C.I.0.97–1.03, respectively).
Maternal serum adiponectin and leptin levels, drawn at the time of PE diagnosis, were not associated with PE.
PMCID: PMC3178730  PMID: 21632080
Adiponectin; Adipokine; Hypertension; Leptin; Preeclampsia
13.  Association of serum adipocytokine levels with cardiac autonomic neuropathy in type 2 diabetic patients 
Cardiac autonomic neuropathy (CAN) is a common complication of diabetes associated with poor prognosis. In addition, the autonomic imbalance is associated with cardiovascular disease (CVD) in diabetes. It is thought that adipocytokines contribute to the increased risk of vascular complications in patients with type 2 diabetes mellitus (T2DM). However, literature data on the association between CAN with adipocytokines such as leptin, tumor necrosis factor-alpha (TNF-alpha), adiponectin in subjects with T2DM is limited.
Therefore, in the present study, we examined the relationship between fasting serum leptin, TNF- alpha and adiponectin and CAN in Korean T2DM patients.
A total of 142 T2DM patients (94 males, 48 females) were recruited. CAN was assessed by the five tests according to the Ewing's protocol and the time and frequency domain of the heart rate variability (HRV) was evaluated. Serum TNF-alpha and adiponectin levels were measured using enzyme-linked immunosorbent assay and serum leptin levels were measured using radioimmunoassay.
Although, the mean levels of leptin, TNF-alpha and adiponectin were not significantly different between the groups with and without CAN, the levels of leptin and adiponectin had a tendency to increase as the score of CAN increased (p = 0.05, p = 0.036). Serum leptin levels demonstrated a negative correlation with low frequency (LF) in the upright position (p = 0.037). Regarding TNF-alpha, a significant negative correlation was observed with SDNN and RMSSD in the upright position (p = 0.023, p = 0.019). Adiponectin levels were not related to any HRV parameters. Multivariate logistic regression analysis demonstrated that the odds of CAN increased with a longer duration of diabetes (1.25, [1.07-1.47]) and higher homeostatic model of assessment-insulin resistance (HOMA-IR) (5.47, [1.8-16.5]). The relative risks for the presence of CAN were 14.1 and 51.6 for the adiponectin 2nd, 3rd tertiles when compared with first tertile (p-value for trend = 0.022).
In the present study, the higher serum adiponectin levels and HOMA-IR were associated with an increased risk for the presence of CAN. Also, the CAN score correlated with the serum adiponectin. Serum adipocytokines such as leptin and TNF-alpha were significantly correlated with parameters of HRV, representative markers of CAN. Future prospective studies with larger number of patients are required to establish a direct relationship between plasma adipocytokine concentrations and the development or severity of CAN.
PMCID: PMC3353195  PMID: 22413919
Cardiac autonomic neuropathy; heart rate variability; leptin; TNF- alpha; adiponectin; type 2 diabetes mellitus
14.  Association of serum leptin and adiponectin with anthropomorphic indices of obesity, blood lipids and insulin resistance in a Sub-Saharan African population 
There is little data on the metabolic effects of adipokines in sub-Saharan African populations. This study aimed to explore the potential relationship of leptin and adiponectin, with obesity, plasma lipids and insulin resistance in a Cameroonian population.
We enrolled 167 men and 309 women aged ≥18 years from the general population in Cameroon. Data were collected on waist circumference (WC), body mass index (BMI), waist-to-hip ratio (WHR), body fat (BF%), fasting blood glucose, plasma lipids, adiponectin, leptin, insulin and homeostasis model for assessment of insulin resistance (HOMA-IR). Pearson’s correlation and multiple stepwise linear regression analyses were used to determine correlates of leptin and adiponectin serum levels.
The prevalence of obesity was higher in women compared to men (p < 0.0001), and Central obesity which is more prevalent particularly in women (WC = 42.4 %, WHR = 42.3 %), is almost for 90 % comparable to %BF (42.7 %).
Adiponectin negatively with BMI (r = −0.294, p < 0.0001), WC (r = −0.294, p < 0.0001), %BF (r = −0.122, p = 0.028), WHR (r = −0.143, p = 0.009), triglycerides (r = −0.141, p = 0.011), HOMA-IR (r = −0.145, p = 0.027) and insulin (r = −0.130, p = 0.048). Leptin positively correlated with BMI (r = 0.628), WC (r = 0.530), BF% (r = 0.720), (all p < 0.0001); with DBP (r = 0.112, p = 0.043), total cholesterol (r = 0.324, p < 0.0001), LDL-cholesterol (r = 0.298, p < 0.0001), insulin (r = 0.320, p < 0.001 and HOMA-IR (r = 0.272, p < 0.0001).
In multiple stepwise regression analysis, adiponectin was negatively associated with WC (β = −0.38, p = 0.001) and BF% (β = 0.33, p < 0.0001), while leptin was positively associated with BF% (β = 0.60, p < 0.0001), total cholesterol (β = 0.11, p = 0.02) and HOMA-IR (β = 0.11, p = 0.02). When controlled for gender, HOMA-IR was found significantly associated to adiponectin (β = 0.13, p = 0.046), but not BF%, while the association previously found between leptin and HOMA-IR disappeared; BMI and WC were significantly associated with leptin (β = 0.18, p = 0.04 & β = 0.19, p = 0.02 respectively).
This study, which includes a population who was not receiving potentially confounding medications, confirms the associations previously observed of adiponectin with reduced adiposity especially central adiposity and improved insulin sensitivity. Confirmatory associations were also observed between leptin and obesity, blood lipids and insulin resistance for the first time in an African population. Gender was significant covariate interacting with insulin sensitivity/insulin resistance and obesity indexes associations in this population.
PMCID: PMC4869296  PMID: 27189377
Adipokines; Adiponectin; Leptin; Blood lipids; Insulin resistance; Insulin sensitivity; Obesity indices
15.  Plasma Adiponectin Does Not Correlate With Insulin Resistance and Cardiometabolic Variables in Nondiabetic Asian Indian Teenagers  
Diabetes Care  2008;31(12):2374-2379.
OBJECTIVE—The objectives of this study were to determine age- and sex-specific concentrations of adiponectin in Asian Indian teenagers and adults and to assess whether its blood levels correlated with insulin resistance and other cardiometabolic parameters.
RESEARCH DESIGN AND METHODS—We studied 196 teenagers (94 boys, 102 girls) 12–18 years of age, selected from a cohort of 2,640 individuals from a cross-sectional school-based survey in Chennai, India. For comparison, adiponectin and plasma insulin were measured in 84 healthy adults. Correlation of adiponectin with plasma levels of insulin, proinsulin, insulin resistance, anthropometry, and family history of diabetes were studied.
RESULTS—Adiponectin showed a sex dimorphism, with girls having higher values (in μg/ml) (10.3 ± 5.0) than boys (8.4 ± 3.5) (P < 0.0001), and it showed a positive correlation with HDL cholesterol in boys only and not with other lipid parameters, insulin resistance, proinsulin, anthropometry, and family history of diabetes. In the adults, adiponectin correlated with fasting glucose and inversely with triglycerides.
CONCLUSIONS—In Asian Indian adults and teenagers, adiponectin did not correlate directly with measures of insulin sensitivity, overweight, and other cardiometabolic variables. This was at variance with several reports in other populations showing an inverse association of adiponectin with insulin resistance, proinsulin, and BMI, suggesting ethnic differences in the relationship of adiponectin with insulin sensitivity. The role of adiponectin in relation to action of insulin needs more detailed studies in Asian Indians.
PMCID: PMC2584198  PMID: 18809626
16.  Lifestyle-Induced Decrease in Fat Mass Improves Adiponectin Secretion in Obese Adults 
Several studies have identified relationships between weight loss and adipokine levels; however none have looked at the combined effect of aerobic exercise training with consumption of a low, or high glycemic diet. We examined the effects of 12-weeks of aerobic exercise combined with either a low- (GI: ~40, LoGIX) or high-glycemic (GI: ~80, HiGIX) diet on plasma leptin and adiponectin (total and high molecular weight - HMW) in 27 older obese adults (age 65±0.5 years; BMI 34.5±0.7 kg/m2).
Insulin sensitivity was calculated from an oral glucose tolerance test (ISIOGTT). Fasting HMW adiponectin and leptin were quantified from plasma samples obtained prior to the ISIOGTT. Glucose and insulin measures were obtained before and every 30 min during the test. Dual-energy X-ray absorptiometry and computerized tomography was used to determine body composition and to quantify subcutaneous and visceral abdominal adiposity, respectively.
Fasting leptin was significantly decreased in both groups (LoGIX, pre: 33.8±4.7, post: 19.2±4.5; HiGIX, pre: 27.9±4.2, post: 11.9±2.2 ng/ml, P=0.004), and HMW adiponectin was significantly increased (LoGIX, pre: 1606.9±34.6, post: 3502.3±57; HiGIX, pre: 3704.8±38.1, post: 4284.3±52.8 pg/ml; P=0.003) following the 12-week intervention. Total body fat was reduced after both interventions, and visceral fat mass was inversely correlated with HMW adiponectin, while subcutaneous fat correlated with leptin.
The data suggest that exercise training, independent of dietary GI, favorably alters HMW adiponectin and leptin secretion, and that a reduction in visceral fat mass is a key factor regulating HMW adiponectin in older obese persons.
PMCID: PMC3991752  PMID: 24614337
adiponectin; leptin; aerobic exercise; glycemic diet
17.  Prognostic Effect of Circulating Adiponectin in a Randomized 2 × 2 Trial of Low-Dose Tamoxifen and Fenretinide in Premenopausal Women at Risk for Breast Cancer 
Journal of Clinical Oncology  2011;30(2):151-157.
Adipokines are linked to obesity and insulin sensitivity and have recently been related to breast cancer risk and prognosis. We investigated the associations of plasma leptin and adiponectin with mammographic density and disease status and assessed their prognostic effect on recurrence-free survival in premenopausal women at risk for breast cancer.
Patients and Methods
We measured circulating lipids, insulin-like growth factor 1, glucose, insulin and insulin sensitivity (calculated by homeostasis model assessment [HOMA] index), leptin, adiponectin, and leptin-to-adiponectin ratio in 235 premenopausal women with pT1mic/pT1a breast cancer (n = 21), intraepithelial neoplasia (n = 160), or 5-year Gail risk of 1.3% or greater (n = 54) who participated in a 2 × 2 trial of low-dose tamoxifen, fenretinide, both agents, or placebo over a 2-year period.
At baseline, adiponectin levels were directly associated with mammographic density and HDL cholesterol and negatively associated with leptin, leptin-to-adiponectin ratio, body mass index (BMI), and HOMA index. Median adiponectin levels were lower in affected than in unaffected women (P = .006). After a median of 7.2 years and total of 57 breast neoplastic events, there was a 12% reduction in the risk of breast neoplastic events per unit increase of adiponectin (adjusted hazard ratio, 0.88; 95% CI, 0.81 to 0.96; P = .03). There was no interaction between treatment and adiponectin levels.
Low adiponectin levels are associated with a history of prior intraepithelial neoplasia or pT1mic/pT1a breast cancer and higher risk of second breast neoplastic events in premenopausal women. The associations are independent of BMI, mammographic density, and treatment. Our findings support the role of adiponectin as a potential target for premenopausal breast cancer prevention and treatment.
PMCID: PMC3255561  PMID: 22162577
18.  Testing the fetal overnutrition hypothesis; the relationship of maternal and paternal adiposity to adiposity, insulin resistance and cardiovascular risk factors in Indian children 
Public health nutrition  2012;16(9):1656-1666.
We aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children.
Children from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9·5 years of age. Detailed anthropometric measurements were recorded for mothers (at 30 ± 2 weeks’ gestation) and fathers (5 years following the index pregnancy).
Holdsworth Memorial Hospital, Mysore, India.
Children (n 504), born to mothers with normal glucose tolerance during pregnancy.
Twenty-eight per cent of mothers and 38 % of fathers were overweight/obese (BMI ≥ 25·0 kg/m2), but only 4 % of the children were overweight/obese (WHO age- and sex-specific BMI ≥ 18·2 kg/m2). The children’s adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child’s sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child’s current adiposity.
In this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intrauterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.
PMCID: PMC3622715  PMID: 22895107
Adiposity; Cardiovascular risk factors; Children; India; Insulin resistance; Intergeneration; Maternal and paternal effects
19.  Change of Body Composition and Adipokines and Their Relationship with Insulin Resistance across Pubertal Development in Obese and Nonobese Chinese Children: The BCAMS Study 
A transient increase in insulin resistance (IR) is a component of puberty. We investigated the impact of body composition and adipokines on IR during puberty in Chinese children. This study included 3223 schoolchildren aged 6–18 years. IR was calculated using homeostasis model assessment (HOMA-IR). We revealed that body mass index (BMI) and waist circumference increased gradually during puberty in both genders, while fat-mass percentage (FAT%) increased steadily only in girls. Change of leptin showed striking sexual dimorphisms: in girls leptin increased steadily during puberty, whereas in boys, after a transient rise at the beginning of puberty, leptin declined by Tanner staging even in those overweight or obese. Inversely, adiponectin level decreased significantly during puberty. In both genders, HOMA-IR started to increase at the beginning of puberty, peaked in the middle, and revised at late puberty in overweight/obesity boys while it stayed high till the end of puberty in girls and normal weight boys. Multivariate regression analysis revealed that leptin presented a stronger indicator of HOMA-IR than anthropometric measures during puberty. Our results demonstrated that gender-specific FAT% and leptin changed with pubertal development. Leptin emerged as a stronger predictor of IR than traditional anthropometric indices, suggesting a prominent role in the development of pubertal IR.
PMCID: PMC3534211  PMID: 23316228
20.  Altered distribution of adiponectin isoforms in children with Prader–Willi syndrome (PWS): association with insulin sensitivity and circulating satiety peptide hormones 
Clinical endocrinology  2007;67(6):944-951.
Prader–Willi syndrome (PWS) is a genetic syndrome characterized by relative hypoinsulinaemia and normal or increased insulin sensitivity despite profound obesity. We hypothesized that this increased insulin sensitivity is mediated by increased levels of total and high molecular weight adiponectin and associated with changes in levels of satiety hormones.
Design, patients and measurements
We measured total adiponectin and its isoforms [high molecular weight (HMW), middle molecular weight (MMW) and low molecular weight (LMW) adiponectin] and satiety hormones in 14 children with PWS [median age 11.35 years, body mass index (BMI) Z-score 2.15] and 14 BMI-matched controls (median age 11.97 years, BMI Z-score 2.34).
Despite comparable BMI Z-scores and leptin levels, the PWS children exhibited lower fasting insulin and HOMA-IR (homeostasis model assessment of insulin resistance) scores compared to obese controls. For any given BMI Z-score, the PWS children showed higher concentrations of fasting total and HMW adiponectin and higher HMW/total adiponectin ratios. The HMW/total adioponectin ratio was preserved in children with PWS at high degrees of obesity. In PWS children, fasting plasma total adiponectin, HMW adiponectin and HMW/total adiponectin ratio correlated negatively with age (P < 0.05), HOMA-IR (P < 0.01), BMI Z-score (P < 0.05), insulin (P < 0.01) and leptin (P < 0.05). In addition to higher fasting ghrelin concentrations, the PWS children showed significantly higher fasting levels of total peptide YY (PYY) and gastric inhibitory polypeptide (GIP) compared to obese controls.
Relative to controls of similar age and BMI Z-score, the PWS children had significantly higher levels of total and HMW adiponectin, and increased ratios of HMW/total adiponectin. These findings may explain in part the heightened insulin sensitivity of PWS children relative to BMI-matched controls.
PMCID: PMC2605973  PMID: 17666087
21.  Effects of individual and combined dietary weight loss and exercise interventions in postmenopausal women on adiponectin and leptin levels 
Journal of internal medicine  2013;274(2):163-175.
Excess body weight and a sedentary lifestyle are associated with the development of several diseases, including cardiovascular disease, diabetes, and cancer in women. One proposed mechanism linking obesity to chronic diseases is an alteration in adipose-derived adiponectin and leptin levels. We investigated the effects of 12-month reduced calorie, weight loss and exercise interventions on adiponectin and leptin concentrations.
Overweight/obese postmenopausal women (n=439) were randomized as follows: 1) a reduced calorie, weight loss diet (diet; N=118); 2) moderate-to-vigorous intensity aerobic exercise (exercise; N=117); 3) a combination of a reduced calorie, weight loss diet and moderate-to-vigorous intensity aerobic exercise (diet+exercise; N=117); or 4) control (N=87). The reduced calorie diet had a 10% weight loss goal. The exercise intervention consisted of 45 minutes of moderate-to-vigorous aerobic activity 5 days/week. Adiponectin and leptin levels were measured at baseline and after 12 months of intervention using a radioimmunoassay.
Adiponectin increased by 9.5 % in the diet group and 6.6 % in the diet+exercise group (both p≤0.0001 vs. control). Compared with controls, leptin decreased with all interventions (diet+exercise, −40.1%, p<0.0001; diet, −27.1%, p<0.0001; exercise, −12.7%, p=0.005). The results were not influenced by the baseline body mass index (BMI). The degree of weight loss was inversely associated with concentrations of adiponectin (diet, p-trend=0.0002; diet+exercise, p-trend=0.0005) and directly associated with leptin (diet, p-trend<0.0001; diet+exercise, p-trend<0.0001).
Weight loss through diet or diet+exercise increased adiponectin concentrations. Leptin concentrations decreased in all of the intervention groups, but the greatest reduction occurred with diet+exercise. Weight loss and exercise exerted some beneficial effects on chronic diseases via effects on adiponectin and leptin.
PMCID: PMC3738194  PMID: 23432360
adiponectin; leptin; randomized controlled trial; diet and exercise intervention
22.  Effects of Sugar-sweetened Beverages on plasma Acylation Stimulating Protein, Leptin & Adiponectin and Metabolic Parameters 
Obesity (Silver Spring, Md.)  2013;21(12):10.1002/oby.20437.
We determined the effects of fructose and glucose consumption on plasma acylation stimulating protein (ASP), adiponectin, and leptin concentrations relative to energy intake, body weight, adiposity, circulating triglycerides, and insulin sensitivity.
Design and Methods
32 overweight/obese adults consumed glucose- or fructose-sweetened beverages (25% energy requirement) with their ad libitum diets for 8 weeks, followed by sweetened beverage consumption for 2 weeks with a standardized, energy-balanced diet. Plasma variables were measured at baseline, 2, 8 and 10 weeks, and body adiposity and insulin sensitivity at baseline and 10 weeks.
Fasting and postprandial ASP concentrations increased at 2 and/or 8 weeks. ASP increases correlated with changes in late-evening triglyceride concentrations. At 10 weeks, fasting adiponectin levels decreased in both groups, and decreases were inversely associated with baseline intra-abdominal fat volume. Sugar consumption increased fasting leptin concentrations; increases were associated with body weight changes. 24-h leptin profiles increased during glucose consumption and decreased during fructose consumption. These changes correlated with changes of 24-h insulin levels.
The consumption of fructose and glucose beverages induced changes in plasma concentrations of ASP, adiponectin and leptin. Further study is required to determine if these changes contribute to the metabolic dysfunction observed during fructose consumption.
PMCID: PMC3732502  PMID: 23512943
fructose; glucose; obesity; acylation stimulating protein; leptin; adiponectin
23.  Grand Multiparity Is Associated With Type 2 Diabetes in Filipino American Women, Independent of Visceral Fat and Adiponectin 
Diabetes Care  2009;33(2):385-389.
To determine whether multiparity is associated with type 2 diabetes, independent of visceral adipose tissue (VAT) and adipokines.
Participants were from the University of California San Diego Filipino Women's Health Study with at least one live birth. A 2-h 75-g oral glucose tolerance test was administered; adiponectin, leptin, ghrelin, reproductive history, family history of diabetes, VAT, and lifestyle behaviors were measured between 1995 and 2002.
Among 152 women, mean age was 59.5 years (range 48–73 years) and mean parity was 4.3 (range 1–12 births). Type 2 diabetes prevalence increased by parity group (low parity, 1–2 births, 25%; medium parity, 3–5 births, 30.3%; and grand multiparity: 6–12 births, 50%; P = 0.048). Family history of diabetes, exercise, insulin resistance, and leptin and ghrelin levels did not differ by parity group. Compared with women in the low parity group, women with ≥6 births were significantly older (62 vs. 57 years), had lower college completion (22 vs. 58%, P = 0.006), more hypertension (72 vs. 55%), higher VAT (74.9 vs. 58.4 cm3), and lower adiponectin concentration (5.79 vs. 7.61 μg/ml). In multivariate analysis adjusting for adiponectin, VAT, family history of diabetes, age, education, hypertension, and estrogen use, grand multiparous women had a threefold higher odds of type 2 diabetes (adjusted odds ratio 3.40 [95% CI 1.13–10.2]) compared with low parity women. No differences were observed in the odds of diabetes between women in the medium (1.10 [0.41–2.91]) and low parity groups.
Having ≥6 children was associated with type 2 diabetes, independent of adiponectin, VAT, family history, and other measured diabetes risk factors.
PMCID: PMC2809288  PMID: 19918009
24.  Differential effects of leptin on adiponectin expression with weight gain versus obesity 
Adiponectin exerts beneficial effects by reducing inflammation, and improving lipid metabolism and insulin-sensitivity. Although adiponectin is lower in obese individuals, whether weight gain reduces adiponectin expression in humans is controversial. We sought to investigate the role of weight gain, and consequent changes in leptin, on altering adiponectin expression in humans.
Forty four normal-weight healthy subjects were recruited (mean age 29 years; 14 women) and randomized to either gain 5% of body weight by 8-weeks of overfeeding (n=34) or maintain weight (n=10). Modest weight gain of 3.8 ± 1.2 kg resulted in increased adiponectin (p=0.03) while weight maintenance resulted in no changes in adiponectin. Further, changes in adiponectin correlated positively with changes in leptin (p=0.0085). In-vitro experiments using differentiated human white preadipocytes showed that leptin increased adiponectin mRNA and protein expression, while a leptin-antagonist had opposite effects. To understand the role of leptin in established obesity, we compared adipose tissue samples obtained from normal weight versus obese subjects. We noted, first, that leptin activated cellular signaling pathways and increased adiponectin mRNA in adipose tissue from normal-weight participants, but did not do so in adipose tissue from obese participants; and second, that obese subjects had increased caveolin-1 expression, which attenuates leptin-dependent increases in adiponectin.
Modest weight gain in healthy individuals is associated with increases in adiponectin, which correlate positively with changes in leptin. In-vitro, leptin induces adiponectin expression which is attenuated by increased caveolin-1 expression. Additionally, adipose tissue from obese subjects shows increased caveolin-1 expression, and impaired leptin signaling. This leptin signal impairment may prevent concordant increases in adiponectin in obese subjects despite their high levels of leptin. Therefore, impaired leptin signaling may contribute to low adiponectin expression in obesity and may provide a target for increasing adiponectin expression, hence improving insulin sensitivity and cardio-metabolic profile in obesity.
PMCID: PMC4747836  PMID: 26374448
25.  Waist circumference, ghrelin and selected adipose tissue-derived adipokines as predictors of insulin resistance in obese patients: Preliminary results 
The aim of the study was to estimate the association between anthropometric obesity parameters, serum concentrations of ghrelin, resistin, leptin, adiponectin and homeostasis model assessment (HOMA-IR) in obese non-diabetic insulin-sensitive and insulin-resistant patients.
Study subjects included 37 obese (body mass index [BMI] ≥30 kg/m2) out-clinic patients aged 25 to 66 years. Insulin resistance was evaluated by HOMA-IR. Serum fasting concentrations of glucose, insulin, ghrelin, adiponectin, resistin and leptin were measured by using the ELISA method. Body weight, waist and hip circumferences were measured to calculate BMI and waist-to-hip ratio (WHR) values for all the patients. According to HOMA-IR, patients were divided into two groups: A, insulin sensitive (n=19); and B, insulin resistant (n=18).
Patients with insulin resistance have greater mean waist circumference (WC) higher mean serum insulin level and leptin concentration, but lower concentrations of adiponectin and ghrelin. In the insulin-sensitive patient group we observed positive correlations between BMI and HOMA-IR, WC and HOMA-IR, and adiponectin and leptin, and negative correlations between ghrelin and HOMA-IR, WC and adiponectin, and WHR and adiponectin. In the insulin-resistant group, there was a positive correlation between resistin and ghrelin and a negative correlation between WHR and leptin.
Waist circumference, adiponectin, leptin and ghrelin are associated with insulin resistance and may be predictors of this pathology.
PMCID: PMC3539504  PMID: 22037753
adipokines; ghrelin; insulin resistance; obese patients; waist circumference

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