Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance

Silha, Josef V.; Kršek, Michal; Škrha, J; Sucharda, P; Nyomba, B. L. Grégoire; Murphy, Liam

doi:10.1530/eje.0.1490331

Cited by 530 publications

(448 citation statements)

References 25 publications

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“…1,2 Recent studies do not suggest a major role of resistin in the regulation of glucose metabolism and insulin resistance in humans. Circulating resistin was reported to be elevated in human obesity in some, [3][4][5] but not in all studies. [6][7][8] Positive correlations of circulating resistin and insulin resistance 9,10 could not be confirmed in other studies.…”

Section: Introductionmentioning

confidence: 96%

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

et al. 2006

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Objective: Human resistin has been stated to influence preadipocyte cell numbers and to stimulate adipocyte triglyceride lipolysis in vivo and in vitro. However, its role in human obesity remains unclear. Design: Cross-sectional study for comparisons of lean and obese subjects, and subsequent longitudinal 4-month weight loss intervention study in obese subjects. Subjects: Healthy subjects, lean (n ¼ 20, BMIo25) and overweight (n ¼ 43, BMIX25). Measurements: Serum resistin, body weight, body fat, waist-to-hip ratio, as well as markers of insulin resistance and lipid metabolism at baseline and after 4 months of intervention. Results: Serum resistin was positively correlated to HOMA-IR (partial r ¼ 0.288; P ¼ 0.055), serum fructosamines (partial r ¼ 0.280; P ¼ 0.062), serum NEFA (partial r ¼ 0.276; P ¼ 0.066) and negatively to age (partial r ¼ À0.349; P ¼ 0.019) and serum apolipoprotein A-1 (partial r ¼ À0.363; P ¼ 0.014). During the intervention, serum resistin increased significantly (Po0.001). The increase was inversely related to changes in waist-to-hip ratio (P ¼ 0.025) and positively to serum apolipoprotein B (P ¼ 0.011). In males only, the increase in resistin during weight loss was predicted by total serum cholesterol at baseline (r ¼ 0.703, P ¼ 0.007). No relation was observed between changes in resistin and changes in HOMA-IR. Conclusion: The present study indicates an association between serum resistin and markers of abdominal fat distribution as well as the regulation of lipid metabolism. However, human resistin is unlikely to play an independent role in the regulation of glucose metabolism.

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Section: Introductionmentioning

confidence: 96%

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

et al. 2006

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“…2,3 Studies in humans are even more controversial. 4,5 In crosssectional studies in adulthood, serum resistin was reported to be related to fat mass [6][7][8] and to insulin resistance, [9][10][11][12] while other reports reveal no correlations to BMI, percent body fat 11,[13][14][15] or to insulin sensitivity. 13,14,16,17 Longitudinal data are necessary to analyze the relationships between resistin, obesity, and insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Resistin concentrations before and after weight loss in obese children

et al. 2005

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Objective: The influences of gender, puberty, and obesity on resistin levels and the longitudinal relationships between insulin resistance, weight loss, and resistin have not yet been studied in childhood. Methods: Age, pubertal stage, gender, weight status (standard deviation score-body mass index (SDS-BMI)), resistin levels, and insulin resistance index calculated by homeostasis model assessment (HOMA) were evaluated in 63 obese children and compared to 36 lean children of same age, gender, and pubertal stage. Furthermore, we analyzed the changes of weight status (SDS-BMI, percentage body fat based on skinfold measurements), waist-to-hip ratio, resistin, and HOMA over a 1-year period in 38 obese children. Results: The resistin levels did not significantly (P ¼ 0.079) differ between obese (median resistin 8.7 ng/ml) and lean children (median resistin 9.7 ng/ml). Resistin concentrations were independent of age and pubertal stage, but girls demonstrated significantly higher resistin levels than boys (P ¼ 0.021). There were no significant correlations between changes of resistin and changes of SDS-BMI (r ¼ 0.14, P ¼ 0.198), changes of percentage body fat (r ¼ À0.01, P ¼ 0.466), changes of waist-to-hip ratio (r ¼ 0.17, P ¼ 0.141), and changes of insulin resistance index (r ¼ 0.01, P ¼ 0.472) over the 1-year period. The weight loss of X0.5 SDS-BMI in 16 children was associated with a significant decrease in HOMA (P ¼ 0.030), while there was no significant change in resistin levels (P ¼ 0.878). Conclusions: Girls demonstrated higher resistin concentrations than boys. Our data do not support a relationship between resistin, insulin resistance index, and weight status in childhood.

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“…[1][2][3] Although the pathophysiological role of resistin remains obscure in the setting of human cardiovascular diseases, accumulating evidence support that it promotes endothelial dysfunction and proinflammatory activation, leading to acceleration of subclinical atherosclerosis. [4][5][6][7][8] In these lines, augmented levels of resistin characterize patients with abdominal obesity, 9 type 2 diabetes mellitus 10 as well as essential hypertension 11,12 suggesting involvement of this protein in multiple vascular disease states.…”

Section: Introductionmentioning

confidence: 99%

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

et al. 2009

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Resistin, a newly discovered protein, promotes endothelial dysfunction and proinflammatory activation, contributing to subclinical atherosclerosis in different clinical settings. In this study we sought to investigate the relationship of increased resistin levels with estimated glomerular filtration rate (eGFR), the most established marker of kidney impairment, in hypertensive subjects. Our population consisted of 132 untreated non-diabetic subjects with stage I-II essential hypertension (49 males, mean age ¼ 54 years, office blood pressure (BP) ¼ 159/100 mm Hg). In all patients eGFR was assessed by the Modification in Renal Disease equation and venous blood sampling was performed for estimation of resistin concentrations. The distribution of resistin was split by the median (4.63 ng ml À1 ) and accordingly subjects were stratified into those with high and low values. Hypertensive patients with high (n ¼ 66) compared to those with low resistin (n ¼ 66) exhibited lower eGFR values (77.1±9.4 vs 89.1±12.2 ml min À1 per 1.73m 2 , Po0.0001), even after adjustment for established confounders. In the total population, resistin was associated with 24-h systolic BP (r ¼ 0.244, Po0.05), serum creatinine (r ¼ 0.311, P ¼ 0.007) and eGFR (r ¼ À0.519, Po0.0001). Multiple regression analysis revealed that age (b ¼ 0.379, P ¼ 0.01), body mass index (b ¼ 0.158, P ¼ 0.022), 24-h systolic BP (b ¼ 0.284, P ¼ 0.006) and resistin (b ¼ 0.429, Po0.0001) were independent predictors of eGFR (R 2 ¼ 0.436, Po0.0001). In essential hypertensive subjects, higher resistin levels are associated with renal function impairment, as reflected by decreased eGFR. Moreover, the independent association of resistin with eGFR suggests involvement of resistin in the progression of kidney damage in the early stages of hypertension.

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Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance

Cited by 530 publications

References 25 publications

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism

Resistin concentrations before and after weight loss in obese children

Independent association of circulating resistin with glomerular filtration rate in the early stages of essential hypertension

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