Plasma Resistin Concentrations Research Articles

Control by Reproduction-related Hormones of Resistin Expression and Plasma Concentration

Although not simultaneously, resistin expression in white adipose tissue (WAT) and resistin plasma concentration have been shown to increase in pregnant rats. To clarify the involvement of sex hormones in such increases, we administered for 3-5 days progesterone, estradiol, or human chorionic gonadotropin (hCG) to female rats in dioestrus II. Progesterone increased resistin expression retroperitoneal WAT but lacked effect in parametrial or subcutaneous depots. It also increased resistin plasma concentration. Estradiol decreased resistin expression in both parametrial and inguinal WAT but was without effect on retroperitoneal depots. It did not alter plasma resistin. Human hCG increased resistin expression in all the visceral depots examined - parametrial, inguinal and retroperitoneal - but did not change plasma resistin. These results show that hormonal influences in resistin expression are depot-dependent and can run separately from changes in its plasma concentration. Besides, the locally restricted effect of progesterone in resistin expression compared with that of hCG suggests it is not the only hormone enhancing resistin expression in early pregnancy. However, it could enhance resistin release in late pregnancy. Estradiol could be involved in the decrease of resistin expression in late pregnancy. Finally, since hCG acts through LH receptors, our results suggest that they are present in WAT and that they control resistin expression.

Plasma resistin is increased in patients with unstable angina

Resistin, a novel adipokine linked to insulin resistance and obesity in rodents, which is derived mainly from macrophages and identified in atheromas in human, has been shown to play a potential role in atherosclerosis. Resistin levels were reported to increase in coronary artery disease (CAD), while data concerning resistin in different stages of CAD in Chinese people are lacking. The aim of this study was to assess whether plasma concentrations of resistin differed between patients with unstable and stable angina pectoris. Plasma resistin levels were determined by means of enzyme-linked immunosorbent assay (ELISA) in 46 patients with unstable angina (UAP), 37 with stable angina (SAP) and 31 control subjects. Plasma concentrations of resistin were significantly increased in UAP group (geometric mean (interquartile range) 12.09 ng/ml (8.40, 18.08)) in comparison with SAP (9.04 ng/ml (7.09, 11.44)) and control groups (8.71 ng/ml (6.58, 11.56)). No differences in resistin levels were found between patients with SAP and controls. We also found that plasma resistin positively correlated with leukocyte counts (r = 0.21, P = 0.027), high sensitive C-reactive protein (hs-CRP) (r = 0.25, P = 0.008), and endothelin-1 (r = 0.21, P = 0.025) after adjustment for age, sex and BMI. Resistin may be involved in the development of CAD by influencing systemic inflammation and endothelial activation.

Effects of rosiglitazone and metformin on inflammatory markers and adipokines: decrease in interleukin‐18 is an independent factor for the improvement of homeostasis model assessment‐beta in type 2 diabetes mellitus

We examined the individual pharmacological effects of the addition of rosiglitazone and metformin to glimepiride on inflammatory markers and adipokines in patients with type 2 diabetes mellitus. We analysed the relationships between these variables, the measurements of insulin sensitivity and beta-cell function in patients treated with rosiglitazone plus glimepiride. One hundred twenty (120) patients with type 2 diabetes mellitus were randomized and treated with glimepiride plus rosiglitazone or glimepiride plus metformin for 12 weeks. The plasma concentrations of the inflammatory markers and adipokines were measured at baseline and after 12 weeks. Markers of insulin sensitivity and beta-cell function were determined by the quantitative insulin sensitivity check index (QUICKI) and the homeostasis model assessment of beta-cell function (HOMA-beta), respectively. Plasma concentrations of adiponectin were measured by radioimmunoassay. Plasma concentrations of resistin, tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-18 (IL-18) were measured using ELISA. Improvements in fasting insulin level, QUICKI and HOMA-beta were noted in the rosiglitazone-treated group. Only the QUICKI value improved in the metformin-treated group. Adiponectin concentrations significantly increased in the rosiglitazone-treated group after 12 weeks. Significant decreases in resistin, C-reactive protein, TNF-alpha, IL-6 and IL-18 were seen in the rosiglitazone-treated patients but not in the metformin-treated patients. The independent risk factor for the HOMA-beta change according to stepwise multivariate regression analysis was a change in IL-18. Rosiglitazone, but not metformin, improved the plasma concentrations of inflammatory markers and adipokines in patients with type 2 diabetes mellitus. A decrease in IL-18 is an independent factor for the improvement of HOMA-beta in type 2 diabetes mellitus.

Resistin: a hormone which induces insulin resistance is increased in normal pregnancy

Resistin, a newly discovered adipokine, is thought to play a key role in the regulation of insulin resistance. The objectives of this study were to develop a nomogram of maternal plasma concentrations of resistin from 11 weeks of gestation to term and to determine whether resistin concentrations differ between normal and overweight pregnant women. In this cross-sectional study, plasma concentrations of resistin were determined in normal pregnant women of normal body mass index (BMI 18.5-24.9; n=261), overweight pregnant women (BMI > or =25; n=140), and non-pregnant women of normal BMI (n=40). Blood samples were collected once from each woman between the first trimester and term. Percentiles for resistin concentration were determined for five pre-specified windows of gestational age. Plasma resistin concentration was determined by immunoassay. Non-parametric statistics were used for analysis. The median maternal plasma concentration of resistin between 11 to 14 weeks of gestation in women of normal weight was significantly higher than non-pregnant women; the plasma concentration of resistin increased with gestational age. Normal pregnant women have a higher median plasma concentration of resistin than non-pregnant women and the concentration of this adipokine increases with advancing gestation. Alterations in the maternal plasma concentration of resistin during pregnancy could contribute to metabolic changes of pregnancy.

Plasma Adiponectin and Resistin Levels in Type 2 Diabetic Obese Female Patients With and Without Hypertension and Retinopathy

Background: In the past, adipose tissue was largely regarded as a depot for fuel storage in the form of triglyceride. However, adipose tissue is an active endocrine organ that secretes a variety of metabolically important substances including adipokines. The adipocyte is now known to secrete a variety of proteins such as tumour necrosis factor (TNF)- , adipsin, plasminogen activator inhibitor-1, leptin, resistin, and adiponectin. Adipose tissue regulates insulin sensitivity via the circulating adipocytokines, resistin and adiponectin. These factors affect insulin sensitivity and may represent a link between obesity, insulin resistance and type 2 diabetes (DM). The objective of this study was to compare the levels of resistin and adiponectin in type 2 diabetic obese female patients with and without hypertension and retinopathy. Subjects and Methods: In this study the plasma adiponectin and resistin concentrations were investigated, in 20 control obese non-diabetic females and 40 obese female patients with type 2 diabetes mellitus. The diabetic females were divided into 2 groups. GI included 20 controlled uncomplicated diabetics & GII included 20 diabetic patients with hypertension and retinopathy. Results: The plasma concentration of adiponectin was significantly lower (P< 0.01) in diabetic females in GΙ & GΠ than non-diabetic control females. In diabetic patients with hypertension and retinopathy ( GII) there was a significant decrease in plasma adiponectin levels (P< 0.01) as compared to their levels in diabetic females in GΙ and control females. Our results also show that there were non-significant changes in plasma resistin in diabetic patients in both groups GΙ & GII as compared to their levels in control group. Conclusion: These results suggest that adiponectin may play a key role in pathophysiology of type 2 diabetes mellitus and its microangiopathy and macrovascular complications. Key words: diabetes mellitus . obesity Introduction

High Plasma Resistin Level Is Associated with Enhanced Highly Sensitive C-Reactive Protein and Leukocytes

Resistin is a newly described hormone with a suggested role in insulin resistance. In humans, inflammatory cells seem to be the major source of resistin. The aim of this study was to find out whether plasma resistin concentration associates with carotid artery atherosclerosis and the risk factors of atherosclerosis. Plasma resistin concentrations were measured in 525 Finnish middle-aged subjects among our population-based cohort. Intima-media thickness was measured from the internal carotid artery, the bifurcation enlargement, and the common carotid artery. Among all the subjects, the median resistin concentration was 7.07 ng/ml (interquartile range, 5.82-8.84), women having higher levels than men (P < 0.001) with median values of 7.56 ng/ml (6.18-9.19) and 6.67 ng/ml (5.63-8.31), respectively. Resistin level correlated negatively with mean intima-media thickness, internal carotid artery, and common carotid artery, but the association did not remain significant after adjustments. Plasma resistin concentration was associated positively with leukocytes (P < 0.001), highly sensitive C-reactive protein (P = 0.009), and IGF binding protein 1 (P < 0.001), but not with plasma insulin or glucose levels in analysis of covariance after adjustments for age, sex, and body mass index. The results imply that inflammatory factors are more important in the determination of plasma resistin concentration than plasma insulin or glucose values. Resistin is associated with proatherogenic inflammatory markers but not independently with early atherosclerosis.

Plasma resistin concentration, and steatosis and insulin sensitivity in hepatitis C virus‐infected patients

Plasma resistin concentration, and steatosis and insulin sensitivity in hepatitis C virus‐infected patients

Roles of adipocyte derived hormone adiponectin and resistin in insulin resistance of type 2 diabetes

To detect plasma levels of new adipocyte derived hormone adiponectin and resistin in type 2 diabetes patients and to explore their potential roles in insulin resistance in type 2 diabetes. According to the body mass index (BMI), 60 type 2 diabetes patients were divided into two groups, one group was non-obese diabetes patients with BMI<25Kg/M(2) (30 cases) and the other group was obese diabetes patients with BMI>25Kg/M(2) (30 cases). There were 28 healthy persons in the control group. ELISA technique was employed to determine the plasma adiponectin and resistin concentrations. The fasting blood glucose, insulin and blood lipid were detected respectively by electrocheminescence immunoassay and immunoturbidimetric assay. Insulin resistance index and insulin sensitive index were calculated by the homeostasis model assessment (HOMO). The levels of plasma adiponectin were decreased significantly in diabetes group compared to that in control group (non-obese: 8.58+/-0.86, obese: 6.22+/-1.34 vs 10.53+/-1.47 P<0.05); moreover, adiponectin concentration in obese diabetes group was significantly decreased compared to that in non-obese diabetes group (6.22+/-1.34 vs 8.58+/-0.86, P<0.05). The levels of plasma resistin were increased significantly in diabetes group compared to that in control group (obese: 18.64+/-4.65, non-obese: 24.05+/-9.07 vs 14.16+/-5.25, P<0.05, P<0.05); furthermore, the levels of resistin in obese diabetes group were increased significantly compared to that in non-obese diabetes group (P<0.05). Plasma adiponectin was correlated negatively with BMI, blood glucose, insulin resistance index and triglyceride (respectively, r=-0.55, P<0.01; r=-0.51, P<0.05; r=-0.52, P<0.05ûr=-0.39, P<0.05), while it was positively correlated with insulin sensitive index (r=0.45, P<0.05). Conversely, plasma resistin correlated positively with BMI, blood glucose, triglyceride and insulin resistance index (respectively, r=0.40, P<0.05; r=0.52, P<0.05; r=0.46, P<0.01; r=0.27, P<0.05), and negatively correlated with insulin sensitive index (r=-0.32, P<0.05). Plasma adiponectin and resistin are associated with the disorder of metabolism of glucose and lipid in diabetes. The relationship between these hormone and insulin sensitivity suggests that they may take part in the development of insulin resistance of type 2 diabetes.

Resistin in Preterm and Term Newborns: Relation to Anthropometry, Leptin, and Insulin

This study aimed to investigate 1) the plasma resistin concentration at birth, 2) the relationship of resistin with leptin and insulin, and 3) the association of resistin with anthropometric indexes in newborn infants. Blood samples for hormonal assay were obtained from preterm and term newborns within the first 2 h of life and before milk feeding or energy intake. Although these infants required blood sampling for clinical reasons, all were proved to be noninfected. Plasma resistin was significantly higher in term than in preterm infants. It was also significantly correlated with serum leptin, and both hormones were significantly associated with gestational age and anthropometric indexes. Infants who were born vaginally were found to have significantly higher plasma resistin levels compared with those who were born by cesarean section. In the multivariate forward stepwise regression models, resistin was found to be significantly associated with the mode of delivery and gestational age or birth weight. The association among resistin, leptin, and anthropometric indexes suggested that both hormones might be gestation related. A high circulating resistin level at term gestation could be advantageous to the infant by promoting hepatic glucose production and preventing hypoglycemia after birth. Infants who were born vaginally had significantly higher plasma resistin levels, suggesting that this hormone might also be associated with stress or inflammation induced by the birth process.

Prevention of hepatic steatosis and hepatic insulin resistance in mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 knockout mice

In order to investigate the role of mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 (mtGPAT1) in the pathogenesis of hepatic steatosis and hepatic insulin resistance, we examined whole-body insulin action in awake mtGPAT1 knockout (mtGPAT1(-/-)) and wild-type (wt) mice after regular control diet or three weeks of high-fat feeding. In contrast to high-fat-fed wt mice, mtGPAT1(-/-) mice displayed markedly lower hepatic triacylglycerol and diacylglycerol concentrations and were protected from hepatic insulin resistance possibly due to a lower diacylglycerol-mediated PKC activation. Hepatic acyl-CoA has previously been implicated in the pathogenesis of insulin resistance. Surprisingly, compared to wt mice, mtGPAT1(-/-) mice exhibited increased hepatic insulin sensitivity despite an almost 2-fold elevation in hepatic acyl-CoA content. These data suggest that mtGPAT1 might serve as a novel target for treatment of hepatic steatosis and hepatic insulin resistance and that long chain acyl-CoA's do not mediate fat-induced hepatic insulin resistance in this model.

Resistin expression and plasma concentration peak at different times during pregnancy in rats

Resistin has been proposed as both an anti-adipogenic factor and an inducer of insulin resistance. During late pregnancy, white adipose tissue mass increases and insulin sensitivity decreases. To check for the involvement of resistin in these processes, we measured plasma resistin in pregnant and non-pregnant rats and in lactating dams. Plasma resistin increased by day 15 of pregnancy and remained high 5 days post partum. The simultaneous increase in plasma resistin concentration and the decrease in insulin sensitivity is compatible with resistin depressing maternal insulin sensitivity. Resistin expression increased 5-15 times in visceral white adipose tissue depots by day 8 of pregnancy but was similar to pre-pregnancy values by day 19. Resistin expression in the placenta and mammary gland was similar to that in the parametrial adipose depot by day 8 but was almost null by day 19. There was therefore a time-lag between the peaks in expression and in plasma concentration. White adipose tissue mass increased without changes in adipocyte size once peaks in resistin expression had passed, which is compatible with an anti-adipogenic role for enhanced resistin expression. A bolus injection of chorionic gonadotrophin - which peaks in early pregnancy - to non-pregnant rats increased resistin expression in white adipose tissue, indicating that this hormone is involved in controlling resistin expression. Resistin was not detected in cerebrospinal fluid. Our results have suggested a role for resistin in pregnancy.

Regulation of human resistin gene expression in cell systems: an important role of stimulatory protein 1 interaction with a common promoter polymorphic site

Resistin is an adipokine that might link obesity and insulin resistance. A common polymorphism of the human resistin gene, -420C >G, is a major determinant of plasma resistin concentrations as well as resistin mRNA expression in human adipose tissue. In this study, we investigated the regulatory mechanism by which this polymorphism affects resistin expression. Electrophoretic mobility shift assay was performed to identify the transcription factors binding to the -420G region. Transient transfection and reporter assay were used to measure promoter activities of the resistin gene. The binding ability of stimulatory protein 1 (Sp1) in response to adipocyte differentiation or high glucose concentrations was also measured. Sp1 and stimulatory protein 3 (Sp3) specifically bound to the region around -420G of the human resistin gene. Overexpression of Sp1 increased the promoter activity regardless of -420 genotypes, while the promoter activity of the -420G construct was two-fold higher than that of the -420C construct. In contrast, overexpression of Sp3 scarcely increased the promoter activity. The binding ability of Sp1 to the -420G region was increased in response to adipocyte differentiation. Mithramycin A, an inhibitor of DNA binding of Sp1, reduced the effect of high glucose on transcription induction of the resistin gene in adipocytes. These results suggest that Sp1 is an important factor regulating transcription of human resistin gene. A common polymorphism of the human resistin promoter, -420C >G, is critical for the binding of Sp1 and modulates the transcriptional activity of the resistin gene by changing the binding ability of Sp1. In addition, Sp1 may be involved in the increase of resistin expression by hyperglycaemia.

W08-P-014 Effect of acute hyperinsulinaemia andat-I receptor blockade on resistin plasma concentration and expression in adipose tissue in healthy subjects

W08-P-014 Effect of acute hyperinsulinaemia andat-I receptor blockade on resistin plasma concentration and expression in adipose tissue in healthy subjects

Adipocytokines and VLDL Metabolism

We investigated the relationship of plasma adipocytokine concentrations with VLDL apolipoprotein B (apoB)-100 kinetics in men. Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). VLDL apoB kinetics were determined using an intravenous infusion of 1-[(13)C]leucine, gas chromatography-mass spectrometry, and compartmental modeling. Visceral and subcutaneous adipose tissue mass (ATM) were determined using magnetic resonance imaging, and total ATM was measured by bioelectrical impedance. In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). Leptin was not an independent predictor of VLDL apoB kinetics. In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics.

The effects of rosiglitazone and metformin on the plasma concentrations of resistin in patients with type 2 diabetes mellitus

Resistin is a protein secreted from adipose tissue that is thought to play a role in insulin sensitivity. We examined the effects of rosiglitazone and metformin on the plasma resistin levels in individuals with type 2 diabetes mellitus. Patients with type 2 diabetes mellitus who showed poor glycemic control with glimepiride (4 mg/d) were randomized to rosiglitazone (4 mg/d) and metformin (500 mg bid) treatment groups. All subjects continued glimepiride treatment as well. The plasma concentrations of resistin were measured at baseline and at 6 months of treatment for both groups. The anthropometric parameters, fasting plasma glucose, HbA1c, total cholesterol, triglyceride, high-density lipoprotein cholesterol, free fatty acids, and adiponectin concentrations were also measured. After 6 months of treatment, the reduction in plasma glucose levels was similar between the 2 groups. There were no significant changes in the lipid profiles of either group during the study period. The plasma resistin levels decreased in the rosiglitazone group (2.49 ± 1.93 vs 1.95 ± 1.59 ng/ml; P < .05) but increased in the metformin group (2.61 ± 1.69 vs 5.13 ± 2.81 ng/ml; P < .05). The plasma adiponectin concentrations were increased in the rosiglitazone group (2.91 ± 1.46 vs 4.23 ± 1.77 μg/ml; P < .05) but were unchanged in the metformin group. In summary, rosiglitazone treatment decreased the plasma resistin levels whereas metformin treatment increased them in patients with type 2 diabetes mellitus showing poor glycemic control with sulfonylurea therapy. These results suggest that the observed changes in plasma resistin levels are not the consequences of improved insulin resistance, nor are they consequences of glycemic control. Considering the potential role of resistin in insulin resistance, decrease in resistin levels may contribute to improving insulin action with rosiglitazone treatment.

Effect of medical and surgical weight loss on endothelial vasomotor function in obese patients

We prospectively examined brachial artery endothelial function using vascular ultrasound in 41 obese subjects treated with medical or surgical (gastric bypass) weight loss interventions. Surgical intervention produced greater weight loss and more pronounced improvement in endothelial function than medical treatment alone. Improved endothelial function with weight loss correlated strongly with fasting glucose but not with alteration in blood pressure, lipids, degree of weight loss, or plasma resistin concentrations. These data demonstrate that weight loss in markedly obese patients improves endothelial function and glycemic control that may represent important mechanisms of the cardiovascular benefit associated with weight reduction.

Association of adiponectin and resistin with adipose tissue compartments, insulin resistance and dyslipidaemia

In this study, we investigated the association of plasma adiponectin and resistin concentrations with adipose tissue compartments in 41 free-living men with a wide range of body mass index (22-35 kg/m(2)). Using enzyme immunoassays, plasma adiponectin and resistin were measured. Intraperitoneal, retroperitoneal, subcutaneous abdominal and posterior subcutaneous abdominal adipose tissue masses (IPATM, RPATM, SAATM and PSAATM, respectively) were determined using magnetic resonance imaging. Total adipose tissue mass (TATM) was measured using bioelectrical impedance. Insulin resistance was estimated with the help of homeostasis model assessment (HOMA) score. In univariate regression, plasma adiponectin levels were inversely related to IPATM (r = -0.389, p < 0.05), SAATM (r = -0.500, p < 0.001), PSAATM (r = -0.502, p < 0.001), anterior SAATM (r = -0.422, p < 0.01) and TATM (r = -0.421, p < 0.01). In multiple regression models, adiponectin was chiefly correlated with PSAATM. Plasma adiponectin concentrations were also inversely correlated with HOMA score (r = -0.540, p < 0.001) and triglyceride (r = -0.632, p < 0.001), and positively correlated with high-density lipoprotein cholesterol (r = 0.508, p < 0.001). There were no significant correlations between resistin levels and adipose tissue masses, insulin resistance or dyslipidaemia. In men, total body fat is significantly correlated with plasma adiponectin, but not with plasma resistin levels. Low plasma adiponectin levels appear to be chiefly determined by the accumulation of posterior subcutaneous abdominal fat mass, as opposed to intra-abdominal fat, and are strongly predictive of insulin resistance and dyslipidaemia.

Plasma Ghrelin and Resistin Concentrations Are Suppressed in Infants of Insulin-Dependent Diabetic Mothers

This study aimed to investigate 1) the effect of maternal diabetes mellitus on ghrelin, resistin, leptin, and insulin in term newborns; 2) the interrelationship of these metabolic hormones in the early postnatal period; and 3) the association of the hormones with anthropometric parameters at birth. A total of 120 term newborns were prospectively enrolled and categorized into three groups: 40 were infants of nondiabetic mothers (group N), 42 were infants born to mothers with gestational diabetes on low energy dietary treatment (group D), and 38 were infants born to mothers with preexisting or severe gestational diabetes who required exogenous insulin for stabilization of blood sugar during pregnancy (group I). Plasma ghrelin and resistin were significantly lower in group I than in either group N or group D infants (P < 0.048). Plasma ghrelin and subscapular skinfold thickness were significantly higher in female than in male infants [plasma ghrelin: median (interquartile range), 3.8 (3.0-4.8) vs. 3.0 (2.4-4.0) ng/ml in females and males, respectively; P = 0.003; subscapular skinfold thickness: 4.9 (4.2-5.6) vs. 4.6 (3.9-5.2) mm; P = 0.03]. In group N, plasma ghrelin was significantly, but negatively, associated with birth weight (r = -0.31; P = 0.05) and body length (r = -0.33; P = 0.04), whereas in group I, plasma ghrelin was negatively correlated with plasma resistin (r = -0.37; P = 0.02). Plasma ghrelin and resistin are suppressed in infants of insulin-dependent diabetic mothers, suggesting that the metabolic hormonal system is probably operational in fetal and early postnatal life. A low circulating ghrelin concentration may be advantageous to these infants, because a reduction in appetite may prevent excessive weight gain postnatally and counterbalances the in utero anabolic effect of hyperinsulinism in poorly controlled diabetic mothers. The suppressive effect of insulin on resistin may partially explain the excess accumulation of adipose tissue in infants of diabetic mothers by reducing the inhibitory effect of resistin on adipogenesis. Female infants have significantly higher plasma ghrelin levels than male infants, suggesting that sexual dimorphism exists in utero. This study has also shown an association between some of the metabolic hormones in specific groups of infants and thus suggests that these hormones could have interacted in utero to regulate growth and fat storage during this critical period.

Erratum to: Common genetic polymorphisms in the promoter of resistin gene are major determinants of plasma resistin concentrations in humans

Erratum to: Common genetic polymorphisms in the promoter of resistin gene are major determinants of plasma resistin concentrations in humans

Plasma resistin concentration, hepatic fat content, and hepatic and peripheral insulin resistance in pioglitazone-treated type II diabetic patients.

To study the effect of pioglitazone (PIO) on plasma resistin concentration, endogenous glucose production (EGP), and hepatic fat content (HFC) in patients with type II diabetes (T2DM). A total of 13 T2DM patients (age=51+/-2 y, BMI=29.7+/-1.1 kg/m(2), HbA(1c)=8.0+/-0.5%). HFC (magnetic resonance spectroscopy) and basal plasma resistin concentration were quantitated before and after PIO treatment (45 mg/day) for 16 weeks. Subjects received a 3 h euglycemic insulin (100 mU/m(2)/min) clamp with 3-[(3)H] glucose to determine rates of EGP and tissue glucose disappearance (Rd) before and after PIO. PIO reduced fasting plasma glucose (10.3+/-0.7 to 7.6+/-0.6 mmol/l, P<0.001) and HbA(1c) (8.0+/-0.4 to 6.8+/-0.3%, P<0.001) despite increased body weight (83.2+/-3.4 to 86.3+/-3.4 kg, P<0.001). PIO improved Rd (4.9+/-0.4 to 6.6+/-0.5 mg/kg/min, P<0.005) and reduced EGP (0.22+/-0.04 to 0.06+/-0.02 mg/kg/min, P<0.01) during the insulin clamp. Following PIO, HFC decreased from 21.1+/-3.5 to 11.2+/-2.1% (P<0.005), and plasma resistin decreased from 5.3+/-0.6 to 3.5+/-0.3 ng/ml (P<0.01). Plasma resistin concentration correlated positively with HFC before (r=0.58, P<0.05) and after (r=0.55, P<0.05) PIO treatment. Taken collectively, plasma resistin concentration, before and after PIO treatment, correlated positively with hepatic fat content (r=0.66, P<0.001) and EGP during the insulin clamp (r=0.41, P<0.05). However, the plasma resistin concentration did not correlate with whole body glucose disposal (Rd) during the insulin clamp either before (r=-0.18, P=NS) or after (r=-0.13, P=NS) PIO treatment. PIO treatment in T2DM causes a significant decrease in plasma resistin concentration. The decrease in plasma resistin is positively correlated with the decrease in hepatic fat content and improvement in hepatic insulin sensitivity.