Plasma bile acids more closely align with insulin resistance, visceral and hepatic adiposity than total adiposity

2020 ◽  
Author(s):  
Ramy H Bishay ◽  
Katherine T Tonks ◽  
Jacob George ◽  
Dorit Samocha-Bonet ◽  
Gideon Meyerowitz-Katz ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Subcutaneous Fat ◽  
Academic Research ◽  
Fat Distribution ◽  
Fat Free Mass ◽  
Liver Fat ◽  
Fibroblast Growth Factor 21 ◽  
Insulin Resistant ◽  
Adult Volunteers

Abstract Context The etiological mechanism of bile acid (BA) effects on insulin resistance and obesity is unknown. Objective To determine if plasma BA are elevated in human obesity and/or insulin resistance. Design Observational study. Setting Academic research center. Participants 71 adult volunteers formed four groups: lean insulin-sensitive (BMI≤25kg/m 2, HOMA-IR<2.0, n=19), overweight/obese non-diabetic who were either insulin-sensitive (Obsensitive, BMI>25kg/m 2, HOMA-IR<1.5, n=11), or insulin-resistant (Obresistant, BMI>25kg/m 2, HOMA-IR>3.0, n=20), and type 2 diabetes (T2D, n=21). Main Outcome Measures Insulin sensitivity by hyperinsulinemic-euglycemic clamp, body composition by dual energy x-ray absorptiometry, abdominal fat distribution and liver density by CT and plasma BA. Results In the Obresistant group, glucose infusion rate/fat free mass (GIR/FFM, an inverse measure of insulin resistance) was significantly lower, and visceral and liver fat higher, compared to lean and Obsensitive subjects, despite similar total adiposity in Obresistant and Obsensitive. Total BA concentrations were higher in Obresistant (2.62±1.5mmol/L, p=0.03) and T2D (3.36±2.26mmol/L, p=0.0004) versus Obsensitive (1.16±0.47mmol/L), but were similar between Obsensitive and lean (2.31±1.43mmol/L). Total BA were positively associated with waist circumference (R=0.245, p=0.041), visceral fat (R=0.360, p=0.002) and fibroblast growth factor 21 (R=0.341, p=0.004) and negatively associated with insulin sensitivity (R=-0.395, p=0.001), abdominal subcutaneous fat (R=-0.352, p=0.003), adiponectin (R=-0.375, P=0.001) and liver fat (Hounsfield units, an inverse marker of liver fat, R=-0.245, p=0.04). Conjugated BA were additionally elevated in T2D individuals (p<0.001). Conclusions BA concentrations correlated with abdominal, visceral and liver fat in humans, though an etiological role in insulin resistance remains to be verified.

scholarly journals Pioglitazone improves insulin resistance and decreases blood pressure in adult patients with congenital adrenal hyperplasia

2009 ◽  
Vol 161 (6) ◽  
pp. 887-894 ◽  
Author(s):  
Jeanne Margot Kroese ◽  
Christiaan F Mooij ◽  
Marinette van der Graaf ◽  
Ad R M M Hermus ◽  
Cees J Tack
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Matched Control ◽  
Fat Distribution ◽  
Body Fat Distribution ◽  
Adrenal Hyperplasia ◽  
Insulin Resistant ◽  
Steroid Profiles

ContextPatients with congenital adrenal hyperplasia (CAH) are chronically treated with supraphysiological doses of glucocorticoids, which are known to induce insulin resistance. Thiazolidinediones might reverse this effect and improve insulin sensitivity.ObjectivesTo assess insulin sensitivity in CAH patients and the effect of pioglitazone treatment on insulin sensitivity in CAH patients. Secondary objectives were the effects of treatment with pioglitazone on blood pressure, body fat distribution, lipid, and steroid profiles.DesignRandomized placebo controlled crossover trial.ParticipantsTwelve CAH patients and 12 body mass and age-matched control subjects.InterventionSixteen-week treatment with pioglitazone (45 mg/day) or placebo.Main outcome measureInsulin sensitivity measured by euglycemic clamp and oral glucose tolerance test. Further measures were 24-h blood pressure profiles, body fat distribution measured by magnetic resonance imaging, dual energy x-ray absorptiometry (DEXA) and bioimpedance procedures, liver fat by magnetic resonance spectroscopy, lipid, and steroid profiles.ResultsCAH patients were insulin resistant compared with healthy controls. Treatment with pioglitazone significantly improved insulin sensitivity in CAH patients (glucose infusion rate (GIR) from 28.5±11.6 to 38.9±11.0 μmol/kg per min, P=0.000, GIR in controls 46.2±23.4 μmol/kg per min, P<0.05 versus CAH). Treatment with pioglitazone decreased blood pressure (systolic: 124.0±13.6 vs 127.0±14.9 mmHg, P<0.001, diastolic: 72.8±11.5 vs 77.4±12.6 mmHg, P<0.001). No changes in body fat distribution, lipid, and steroid profiles were observed.ConclusionsCAH patients are insulin resistant compared with matched control subjects. Treatment with pioglitazone improves insulin sensitivity and decreases blood pressure in CAH patients.

Acquired obesity is associated with increased liver fat, intra-abdominal fat, and insulin resistance in young adult monozygotic twins

2005 ◽  
Vol 288 (4) ◽  
pp. E768-E774 ◽  
Author(s):  
Kirsi Hannele Pietiläinen ◽  
Aila Rissanen ◽  
Jaakko Kaprio ◽  
Sari Mäkimattila ◽  
Anna-Maija Häkkinen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Monozygotic Twins ◽  
Fat Distribution ◽  
Population Based ◽  
Abdominal Fat ◽  
Liver Fat ◽  
Whole Body ◽  
Fasting Insulin ◽  
Impaired Insulin

We determined whether acquired obesity is associated with increases in liver or intra-abdominal fat or impaired insulin sensitivity by studying monozygotic (MZ) twin pairs discordant and concordant for obesity. We studied nineteen 24- to 27-yr-old MZ twin pairs, with intrapair differences in body weight ranging from 0.1 to 24.7 kg [body mass index (BMI) range 20.0–33.9 kg/m2], identified from a population-based FinnTwin16 sample. Fat distribution was determined by magnetic resonance imaging, percent body fat by dual-energy X-ray absorptiometry, liver fat by proton spectroscopy, insulin sensitivity by measuring the fasting insulin concentration, and whole body insulin sensitivity by the euglycemic insulin clamp technique. Intrapair differences in BMI were significantly correlated with those in intra-abdominal fat ( r = 0.82, P < 0.001) and liver fat ( r = 0.57, P = 0.010). Intrapair differences in fasting insulin correlated with those in subcutaneous abdominal ( r = 0.60, P = 0.008), intra-abdominal ( r = 0.75, P = 0.0001) and liver ( r = 0.49, P = 0.048) fat. Intrapair differences in whole body insulin sensitivity correlated with those in subcutaneous abdominal ( r = −0.72, P = 0.001) and intra-abdominal ( r = −0.55, P = 0.015) but not liver ( r = −0.20, P = 0.20) fat. We conclude that acquired obesity is associated with increases in intra-abdominal and liver fat and insulin resistance, independent of genetic factors.

scholarly journals Changes in FGF21 Serum Concentrations and Liver mRNA Expression in an Experimental Model of Complete Lipodystrophy and Insulin-Resistant Diabetes

2014 ◽  
pp. 483-490 ◽  
Author(s):  
A. ŠPOLCOVÁ ◽  
M. HOLUBOVÁ ◽  
B. MIKULÁŠKOVÁ ◽  
V. NAGELOVÁ ◽  
A. ŠTOFKOVÁ ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mrna Expression ◽  
Plasma Levels ◽  
Glucose Transporter ◽  
Liver Fat ◽  
Fibroblast Growth Factor 21 ◽  
Glucose Transporter 1 ◽  
Insulin Resistant

Patients with obesity and type 2 diabetes often display high levels of the anti-diabetic factor fibroblast growth factor-21 (FGF21), suggesting that the overproduction of FGF21 may result from increased adiposity in an attempt by white adipose tissue (WAT) to counteract insulin resistance. However, the production of FGF21 diabetes in the absence of WAT has not been examined. In this study, we investigated the effects of lipodystrophy in A-ZIP F-1 mice on FGF21 production in relation to diabetes. A-ZIP F-1 mice displayed high FGF21 plasma levels resulting from enhanced FGF21 mRNA expression in the liver. Concomitant enhancement of FGF21 receptor (FGFR1) and glucose transporter 1 (GLUT-1) mRNA expression was observed in the muscles of A-ZIP F-1 mice. Furthermore, the activation of hypothalamic NPY and AgRP mRNA expression positively correlated with plasma levels of FGF21 but not active ghrelin. Our study demonstrates that an increased FGF21 plasma level in lipodystrophic A-ZIP F-1 mice results mainly from up-regulated liver production but does not suffice to overcome the lipodystrophy-induced severe type 2-diabetes and insulin resistance in the liver linked to the augmented liver fat deposition.

Increased intrahepatic triglyceride is associated with peripheral insulin resistance: in vivo MR imaging and spectroscopy studies

2007 ◽  
Vol 293 (6) ◽  
pp. E1663-E1669 ◽  
Author(s):  
Jong-Hee Hwang ◽  
Daniel T. Stein ◽  
Nir Barzilai ◽  
Min-Hui Cui ◽  
Julia Tonelli ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Magnetic Resonance ◽  
Subcutaneous Fat ◽  
Liver Fat ◽  
Whole Body ◽  
Glucose Disposal ◽  
Resonance Spectroscopy ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Triglyceride Accumulation

Recent studies have indicated that the mass/content of intramyocellular lipid (IMCL), intrahepatic triglyceride (IHTG), visceral fat (VF), and even deep abdominal subcutaneous fat (SF) may all be correlated with insulin resistance. Since simultaneous measurements of these parameters have not been reported, the relative strength of their associations with insulin action is not known. Therefore, the goals of this study were 1) to simultaneously measure IMCL, IHTG, VF, and abdominal SF in the same nondiabetic individuals using noninvasive 1H-magnetic resonance spectroscopy (MRS) and magnetic resonance imaging (MRI) and 2) to examine how these fat stores are correlated with systemic insulin sensitivity as measured by whole body glucose disposal (Rd) during euglycemic-hyperinsulinemic clamp studies. Positive correlations were observed among IMCL, IHTG, and VF. There were significant inverse correlations between whole body Rd and both IMCL and VF. Notably, there was a particularly tight inverse correlation between IHTG and whole body Rd ( r = −0.86, P < 0.001), consistent with an association between liver fat and peripheral insulin sensitivity. This novel finding suggests that hepatic triglyceride accumulation has important systemic consequences that may adversely affect insulin sensitivity in other tissues.

scholarly journals Does metformin reduce excess birthweight in offspring of obese pregnant women? A randomised controlled trial of efficacy, exploration of mechanisms and evaluation of other pregnancy complications

2016 ◽  
Vol 3 (7) ◽  
pp. 1-800 ◽  
Author(s):  
Carolyn A Chiswick ◽  
Rebecca M Reynolds ◽  
Fiona C Denison ◽  
Amanda J Drake ◽  
Shareen Forbes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Pregnant Women ◽  
Controlled Trial ◽  
Fat Distribution ◽  
Glycogen Storage ◽  
Fat Free Mass ◽  
Secondary Outcome ◽  
Myometrial Contractility ◽  
Randomised Controlled

BackgroundMaternal obesity is associated with high birthweight, obesity and premature mortality in adult offspring, probably as a result of maternal hyperglycaemia and insulin resistance. We present the results of a trial designed to test the hypothesis that metformin will improve insulin sensitivity in obese pregnant women, thereby reducing the incidence of high-birthweight babies.ObjectiveTo determine the efficacy of metformin (up to 2500 mg daily) given to obese pregnant women in reducing the gestational age-, parity- and sex-adjusted birthweight centile of the baby.DesignDouble-blind, placebo-controlled, randomised controlled trial with embedded substudies.SettingFifteen NHS hospitals in the UK.ParticipantsPregnant women aged ≥ 16 years with a singleton fetus and a body mass index of ≥ 30 kg/m2.InterventionMetformin tablets (or placebo) administered between 12 and 16 weeks’ gestation until delivery of the baby.Main outcome measuresThe primary outcome measure was z-score corresponding to the gestational age-, parity- and sex-adjusted birthweight centile of live-born babies delivered at ≥ 24 weeks’ gestation. The main secondary outcome was maternal insulin resistance at 36 weeks’ gestation. Embedded substudies were included to assess the effect of metformin on insulin sensitivity using the hyperinsulinaemic–euglycaemic clamp; endothelial function; maternal and fetal fat distribution using magnetic resonance imaging; placental expression of 11β-hydroxysteroid dehydrogenase types 1 and 2 and glucocorticoid receptor; and myometrial contractility and glycogen storage.ResultsWe randomised 449 women to either placebo (n = 223) or metformin (n = 226), of whom 434 were included in the final intention-to-treat analysis. Mean birthweight at delivery was 3463 g [standard deviation (SD) 660 g] in the placebo group and 3462 g (SD 548 g) in the metformin group. The estimated effect size of metformin on the primary outcome was non-significant [adjusted mean difference in z-score –0.029, 95% confidence interval (CI) –0.217 to 0.158;p = 0.7597]. There was no evidence of a reduction in the main secondary outcome of homeostatic model assessment – insulin resistance (HOMA-IR) at 36 weeks’ gestation (mean HOMA-IR 5.98 and 6.30 molar units in the placebo and metformin groups, respectively; adjusted mean ratio 0.974, 95% CI 0.865 to 1.097). Metformin had no effect on the combined adverse outcome of miscarriage, termination of pregnancy, stillbirth or neonatal death. Subjects taking metformin demonstrated increased insulin sensitivity [glucose disposal per unit plasma insulin difference between means during high-dose insulin 0.02 mg/kg, 95% CI 0.001 to 0.03 mg/kg (fat-free mass)/minute/µIU/l;p = 0.04] compared with those taking placebo and enhanced endogenous glucose production [difference between means 0.54 mg/kg, 95% CI 0.08 to 1.00 mg/kg (fat-free mass)/minute;p = 0.02]. There were no differences in endothelial function, maternal or fetal body fat distribution, placental expression of 11β-hydroxysteroid dehydrogenase types 1 and 2 and glucocorticoid receptor, or myometrial contractility and glycogen storage.ConclusionsMetformin has no clinically significant effect on birthweight centile in obese pregnant women. Follow-up studies of the children born to participants in the trial are required to determine whether or not there are any longer-term benefits or harms of maternal metformin for offspring weight, fat mass or metabolism.Trial registrationCurrent Controlled Trials ISRCTN51279843.FundingThis project was funded by the Efficacy and Mechanism Evaluation programme, a Medical Research Council and National Institute for Health Research partnership.

scholarly journals Hepatic Insulin Extraction in NAFLD Is Related to Insulin Resistance Rather Than Liver Fat Content

2018 ◽  
Vol 104 (5) ◽  
pp. 1855-1865 ◽  
Author(s):  
Kristina M Utzschneider ◽  
Steven E Kahn ◽  
David C Polidori
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Subcutaneous Fat ◽  
Insulin Clearance ◽  
Liver Fat ◽  
Glucose Disposal ◽  
Oral Glucose ◽  
Cross Sectional ◽  
Hepatic Insulin Extraction

Abstract Context Total insulin clearance is decreased in nonalcoholic fatty liver disease (NAFLD), but the relationship between liver fat and hepatic insulin extraction (HIE) is unknown. Objective This cross-sectional study addresses the hypothesis that HIE is reduced in NAFLD and investigates metabolic and/or anthropometric characteristics most closely associated with insulin clearance. Participants Nondiabetic subjects with NAFLD (n = 13) and age- and body mass index (BMI)-matched controls with normal liver enzymes (n = 15) underwent abdominal CT, dual-energy X-ray absorptiometry, oral glucose tolerance test (OGTT), and labeled two-step hyperinsulinemic-euglycemic clamps. Outcome Measurements Liver fat was estimated by the CT liver/spleen ratio. Hepatic and extrahepatic insulin clearances were modeled using clamp and OGTT data. Results Extrahepatic insulin clearance and HIE were not different between NAFLD and controls and did not correlate with liver fat. HIE was positively correlated with insulin sensitivity [rate of glucose disposal (Rd; low r = +0.7, P &lt; 0.001; high r = +0.6, P = 0.001), adiponectin (r = +0.55, P = 0.004), and insulin-mediated suppression of clamp nonesterified free fatty acid (NEFA; r = +0.67, P &lt; 0.001)] but was not associated with fasting NEFA, insulin-mediated suppression of glucose production, or measures of adiposity. Extrahepatic insulin clearance was positively associated with percent body fat (r = +0.44, P = 0.02) and subcutaneous fat (r = +0.42, P = 0.03) but not BMI, intra-abdominal fat, liver fat, Rd, adiponectin, or NEFA. Conclusions HIE is not directly associated with hepatic steatosis but is associated with muscle and adipose tissue insulin resistance. The data suggest differential regulation of insulin clearance with extrahepatic insulin clearance being associated with body fat and not insulin sensitivity.

Transthyretin contributes to insulin resistance and diminishes exercise-induced insulin sensitivity in obese mice by inhibiting AMPK activity in skeletal muscle

2021 ◽  
Author(s):  
Yingzi He ◽  
Ruojun Qiu ◽  
Beibei Wu ◽  
Weiwei Gui ◽  
Xihua Lin ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Inhibitory Effect ◽  
Quadriceps Femoris ◽  
Treadmill Training ◽  
C2c12 Cells ◽  
Obese Mice ◽  
Insulin Resistant ◽  
Ampk Activity ◽  
Exercise Induced

Exercise improves obesity-induced insulin resistance and metabolic disorders via mechanisms that remain unclear. Here, we show that the levels of the hepatokine transthyretin (TTR) in circulation are elevated in insulin-resistant individuals including high-fat diet (HFD)-induced obese mice, db/db mice, and patients with metabolic syndrome. Liver Ttr mRNA and circulating TTR levels were reduced in mice by treadmill training, as was the TTR levels in quadriceps femoris muscle; however, AMPK signalling activity was enhanced. Transgenic overexpression of TTR or injection of purified TTR triggered insulin resistance in mice fed on regular chow (RC). Furthermore, TTR overexpression reduced the beneficial effects of exercise on insulin sensitivity in HFD-fed mice. TTR was internalized by muscle cells via the membrane receptor Grp78 and the internalization into the quadriceps femoris was reduced by treadmill training. The TTR/Grp78 combination in C2C12 cells was increased, whereas the AMPK activity of C2C12 cells was decreased as the TTR concentration rose. Additionally, Grp78 silencing prevented the TTR internalization and reversed its inhibitory effect on AMPK activity in C2C12 cells. Our study suggests that elevated circulating TTR may contribute to insulin resistance and counteract the exercise-induced insulin sensitivity improvement; the TTR suppression might be an adaptive response to exercise through enhancing AMPK activity in skeletal muscles.

scholarly journals Hepatokine ERAP1 impairs skeletal muscle insulin sensitivity via ADRB2/PKA pathway

2020 ◽  
Author(s):  
Feifan Guo ◽  
Yuguo Niu ◽  
Haizhou Jiang ◽  
Hanrui Yin ◽  
Fenfen Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Neutralizing Antibodies ◽  
Leptin Receptor ◽  
Whole Body ◽  
C2c12 Myotubes ◽  
Insulin Resistant ◽  
Skeletal Muscle Insulin Sensitivity ◽  
Pka Pathway

Abstract The current study aimed to investigate the role of endoplasmic reticulum aminopeptidase 1 (ERAP1), a novel hepatokine, in whole-body glucose metabolism. Here, we found that hepatic ERAP1 levels were increased in insulin-resistant leptin-receptor-mutated (db/db) and high-fat diet (HFD)-fed mice. Consistently, hepatic ERAP1 overexpression attenuated skeletal muscle (SM) insulin sensitivity, whereas knockdown ameliorated SM insulin resistance. Furthermore, serum and hepatic ERAP1 levels were positively correlated, and recombinant mouse ERAP1 or conditioned medium with high ERAP1 content (CM-ERAP1) attenuated insulin signaling in C2C12 myotubes, and CM-ERAP1 or HFD-induced insulin resistance was blocked by ERAP1 neutralizing antibodies. Mechanistically, ERAP1 reduced ADRB2 expression and interrupted ADRB2-dependent signaling in C2C12 myotubes. Finally, ERAP1 inhibition via global knockout or the inhibitor thimerosal improved insulin sensitivity. Together, ERAP1 is a hepatokine that impairs SM and whole-body insulin sensitivity, and its inhibition might provide a therapeutic strategy for diabetes, particularly for those with SM insulin resistance.

scholarly journals Prevalence and Clinical Characteristics of Children and Adolescents with Metabolically Healthy Obesity: Role of Insulin Sensitivity

Life ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 127 ◽  
Author(s):  
Federica Vinciguerra ◽  
Andrea Tumminia ◽  
Roberto Baratta ◽  
Alfredo Ferro ◽  
Salvatore Alaimo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Children And Adolescents ◽  
Metabolic Phenotype ◽  
Sensitivity Index ◽  
Insulinogenic Index ◽  
Model Assessment ◽  
Insulin Resistant ◽  
Metabolically Healthy

Obesity represents a major risk factor for metabolic disorders, but some individuals, “metabolically healthy” (MHO), show less clinical evidence of these complications, in contrast to “metabolically unhealthy” (MUO) individuals. The aim of this cross-sectional study is to assess the prevalence of the MHO phenotype in a cohort of 246 overweight/obese Italian children and adolescents, and to evaluate their characteristics and the role of insulin resistance. Homeostasis model assessment–insulin resistance (HOMA-IR), insulin sensitivity index (ISI), insulinogenic index (IGI) and disposition index (DI) were all calculated from the Oral Glucose Tolerance Test (OGTT). MHO was defined by either: (1) HOMA-IR < 2.5 (MHO-IRes), or (2) absence of the criteria for metabolic syndrome (MHO-MetS). The MHO prevalence, according to MHO-MetS or MHO-IRes criteria, was 37.4% and 15.8%, respectively. ISI was the strongest predictor of the MHO phenotype, independently associated with both MHO-IRes and MHO-MetS. The MHO-MetS group was further subdivided into insulin sensitive or insulin resistant on the basis of HOMA-IR (either < or ≥ 2.5). Insulin sensitive MHO-MetS patients had a better metabolic profile compared to both insulin resistant MHO-MetS and MUO-MetS individuals. These data underscore the relevance of insulin sensitivity to identifying, among young individuals with overweight/obesity, the ones who have a more favorable metabolic phenotype.

scholarly journals Insulin Sensitivity Is Correlated with Subcutaneous but Not Visceral Body Fat in Overweight and Obese Prepubertal Children

2008 ◽  
Vol 93 (6) ◽  
pp. 2122-2128 ◽  
Author(s):  
Claudio Maffeis ◽  
Riccardo Manfredi ◽  
Maddalena Trombetta ◽  
Silvia Sordelli ◽  
Monica Storti ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Body Fat ◽  
Fat Distribution ◽  
Fat Content ◽  
Liver Fat ◽  
P Value ◽  
Inflammation Markers ◽  
Liver Fat Content ◽  
Prepubertal Children

Abstract Aim: Our aim was to explore the relationship between insulin sensitivity, body fat distribution, ectopic (liver and skeletal muscle) fat deposition, adipokines (leptin and adiponectin), and inflammation markers (highly sensitive C-reactive protein, IL-6, IL-10, and TNF-α) in prepubertal children. Subjects and Methods: Thirty overweight and obese children (16 males and 14 females with body mass index z-score range of 1.1–3.2) were recruited. Body fat distribution and fat accumulation in liver and skeletal muscle were measured using magnetic resonance imaging. Insulin sensitivity was assessed by iv glucose tolerance test. Results: Insulin sensitivity was associated with sc abdominal adipose tissue (SAT) (r = −0.52; P &lt; 0.01) and liver fat content (r = −0.44; P &lt; 0.02) but not with visceral abdominal adipose tissue (VAT) (r = −0.193; P value not significant) and fat accumulation in skeletal muscle (r = −0.210; P value not significant). Adipokines, but not inflammation markers, were significantly correlated to insulin sensitivity. VAT correlated with C-reactive protein (r = 0.55; P &lt; 0.01) as well as adiponectin (r = −0.53; P &lt;0.01). Multiple regression analysis showed that only SAT and liver fat content were independently correlated to insulin sensitivity (P &lt; 0.01; 20 and 16% of explained variance, respectively). Conclusions: In overweight and moderately obese prepubertal children, insulin sensitivity was negatively correlated with SAT and liver fat content. Furthermore, contrary to adults, VAT and inflammation markers were not correlated with insulin sensitivity in children.

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