Insulin-sensitive obesity

2010 ◽  
Vol 299 (3) ◽  
pp. E506-E515 ◽  
Author(s):  
Nora Klöting ◽  
Mathias Fasshauer ◽  
Arne Dietrich ◽  
Peter Kovacs ◽  
Michael R. Schön ◽  
...  

The association between obesity and impaired insulin sensitivity has long been recognized, although a subgroup of obese individuals seems to be protected from insulin resistance. In this study, we systematically studied differences in adipose tissue biology between insulin-sensitive (IS) and insulin-resistant (IR) individuals with morbid obesity. On the basis of glucose infusion rate during euglycemic hyperinsulinemic clamps, 60 individuals with a BMI of 45 ± 1.3 kg/m2 were divided into an IS and IR group matched for age, sex, and body fat prior to elective surgery. We measured fat distribution, circulating adipokines, and parameters of inflammation, glucose, and lipid metabolism and characterized adipose tissue morphology, function, and mRNA expression in abdominal subcutaneous (sc) and omental fat. IS compared with IR obese individuals have significantly lower visceral fat area (138 ± 27 vs. 316 ± 91 cm2), number of macrophages in omental adipose tissue (4.9 ± 0.8 vs. 13.2 ± 1.4%), mean omental adipocyte size (528 ± 76 vs. 715 ± 81 pl), circulating C-reactive protein, progranulin, chemerin, and retinol-binding protein-4 (all P values <0.05), and higher serum adiponectin (6.9 ± 3.4 vs. 3.4 ± 1.7 ng/ml) and omental adipocyte insulin sensitivity (all P values <0.01). The strongest predictors of insulin sensitivity by far were macrophage infiltration together with circulating adiponectin ( r2 = 0.98, P < 0.0001). In conclusion, independently of total body fat mass, increased visceral fat accumulation and adipose tissue dysfunction are associated with IR obesity. This suggests that mechanisms beyond a positive caloric balance such as inflammation and adipokine release determine the pathological metabolic consequences in patients with obesity.

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

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Kristoffer Jensen Kolnes ◽  
Maria Houborg Petersen ◽  
Teodor Lien-Iversen ◽  
Kurt Højlund ◽  
Jørgen Jensen

In obesity, excessive abdominal fat, especially the accumulation of visceral adipose tissue (VAT), increases the risk of metabolic disorders, such as type 2 diabetes mellitus (T2DM), cardiovascular disease, and non-alcoholic fatty liver disease. Excessive abdominal fat is associated with adipose tissue dysfunction, leading to systemic low-grade inflammation, fat overflow, ectopic lipid deposition, and reduced insulin sensitivity. Physical activity is recommended for primary prevention and treatment of obesity, T2DM, and related disorders. Achieving a stable reduction in body weight with exercise training alone has not shown promising effects on a population level. Because fat has a high energy content, a large amount of exercise training is required to achieve weight loss. However, even when there is no weight loss, exercise training is an effective method of improving body composition (increased muscle mass and reduced fat) as well as increasing insulin sensitivity and cardiorespiratory fitness. Compared with traditional low-to-moderate-intensity continuous endurance training, high-intensity interval training (HIIT) and sprint interval training (SIT) are more time-efficient as exercise regimens and produce comparable results in reducing total fat mass, as well as improving cardiorespiratory fitness and insulin sensitivity. During high-intensity exercise, carbohydrates are the main source of energy, whereas, with low-intensity exercise, fat becomes the predominant energy source. These observations imply that HIIT and SIT can reduce fat mass during bouts of exercise despite being associated with lower levels of fat oxidation. In this review, we explore the effects of different types of exercise training on energy expenditure and substrate oxidation during physical activity, and discuss the potential effects of exercise training on adipose tissue function and body fat distribution.


2005 ◽  
Vol 58 (5-6) ◽  
pp. 258-264 ◽  
Author(s):  
Biljana Srdic ◽  
Edita Stokic ◽  
Agneza Polzovic ◽  
Sinisa Babovic

Introduction. The presence of excess fat in the abdomen, out of proportion to total body fat, is associated with increased risk for cardiovascular and metabolic diseases and other complications of obesity. Histoanatomical characteristics of the abdominal adipose tissue In regard to subcutaneous fat, accumulation of visceral abdominal adipose tissue is more associated with increased metabolic risk. However, mean have more visceral fat than pre-menopausal women. Compared with pre-menopausal women, postmenopausal women have 49% more intraabdominal fat, regardless of age and total fat mass. Measurement of abdominal fat depots Various anthropometric indicators have been suggested for measuring body fat distribution. All of them have advantages and disadvantages, in relation to their interpretation and use. Many are specified as ratios and are difficult to interpret biologically, whereas a change in body fat distribution may exhibit little or no change in the ratios. Waist circumference and sagittal abdominal diameter are good predictors of visceral fat. But, extreme individual variations in visceral to subcutaneous ratio demonstrate the limitations of external anthropometry. The best methods to estimate the amount of visceral fat are imaging techniques like computed tomography or magnetic resonance, but they are expensive and inconvinient in routine practice. Conclusion. Further investigations should provide a simple and optimal indicator of abdominal obesity which should correlate with the amount of viscelar fat and the risk. .


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Henzel ◽  
M Makarewicz-Wujec ◽  
L Wardziak ◽  
P Trochimiuk ◽  
C Kepka ◽  
...  

Abstract Introduction Contradictory reports are available on the role of adipose tissue in the pathophysiology and progression of coronary artery disease (CAD). It seems accepted that local fat distribution is more relevant than the general amount of body fat. As in the case of visceral fat, pericardial adipose tissue (PEAT) has been postulated an important mediator of metabolic risk, with a special role attributed to epicardial adipose tissue (EAT). Purpose To study the effect of intensive dietary and lifestyle modification on the distribution of body fat in patients diagnosed with stable CAD qualified to conservative treatment. Methods Total body fat mass (TBF), visceral fat area (VFA), PEAT volume, and EAT volume were measured in 67 participants (43% women) of the DISCO-CT trial (Dietary Intervention to Stop COronary Atherosclerosis in Computed Tomography, NCT02571803) who completed the study by the end of 2018. All patients, randomly assigned to either experimental or control arm in a 1:1 fashion, were regularly followed-up at our site, with those in the experimental arm being strictly supervised by a dietitian to stick to Dietary Approaches to Stop Hypertension (DASH) diet and encouraged to lifestyle changes atop optimal medical therapy. Contrast-enhanced coronary computed tomography was performed at baseline and after the median time of 59 weeks (2x192-multislice scanner, temporal resolution 66 ms, Somatom Force, Siemens). PEAT and EAT volumes, expressed in mm3, were measured with a dedicated offline workstation (syngo.via Frontier, Siemens Healthcare) using a semiautomatic segmentation technique (window width range −195 to −45 Hounsfield units). TBF, expressed in kg, and VFA, expressed in cm2, were measured using the InBody S10 Body Water Analyser at baseline and completion of the study. 57% of subjects included into the analysis represented the experimental arm. Results There were no significant between-arm differences in baseline TBF, VFA, PEAT, and EAT volumes. A significant reduction by 3.7±5.0 kg in TBF (p<0.001; 95% CI 2.1, 5.3) and by 19.7±30.1 cm2 in VFA (p<0.001; 95% CI 9.8, 29.6) was observed in the experimental arm, while in the control group both TBF and VFA irrelevantly increased, by 0.6±4.7 kg (p=0.53; 95% CI −2.4, 1.3) and 2.2±27.0 cm2 (p=0.67; 95% CI −12.7, 8.2), respectively. A significant decrease in PEAT volume, by 19.9±43.0 mm3 (p=0.007; 95% CI 5.8, 34.1), was observed in the experimental group, compared to a non-significant PEAT volume reduction by 5.8±3.5.0 mm3 (p=0.38, 95% CI −7.5; 19.2) in the control group. Contrarily, no significant changes in EAT volumes were observed in either experimental (reduction by 3.8±15.2 mm3; p=0.13, 95% CI −1.2, 8.8) or control arm (reduction by 5.1±17.2 mm3; p=0.13, 95% CI −1.5, 11.6). Conclusion Intensive dietary intervention in patients with stable CAD can lead to a significant reduction in total body fat, visceral fat and pericardial fat, this effect, however, may not apply to epicardial fat. Acknowledgement/Funding This study was founded by a grant (2.15/III/15) from the Institute of Cardiology in Warsaw, Poland


2015 ◽  
Vol 112 (14) ◽  
pp. 4363-4368 ◽  
Author(s):  
James E. N. Minchin ◽  
Ingrid Dahlman ◽  
Christopher J. Harvey ◽  
Niklas Mejhert ◽  
Manvendra K. Singh ◽  
...  

Genome-wide association studies have implicated PLEXIN D1 (PLXND1) in body fat distribution and type 2 diabetes. However, a role for PLXND1 in regional adiposity and insulin resistance is unknown. Here we use in vivo imaging and genetic analysis in zebrafish to show that Plxnd1 regulates body fat distribution and insulin sensitivity. Plxnd1 deficiency in zebrafish induced hyperplastic morphology in visceral adipose tissue (VAT) and reduced lipid storage. In contrast, subcutaneous adipose tissue (SAT) growth and morphology were unaffected, resulting in altered body fat distribution and a reduced VAT:SAT ratio in zebrafish. A VAT-specific role for Plxnd1 appeared conserved in humans, as PLXND1 mRNA was positively associated with hypertrophic morphology in VAT, but not SAT. In zebrafish plxnd1 mutants, the effect on VAT morphology and body fat distribution was dependent on induction of the extracellular matrix protein collagen type V alpha 1 (col5a1). Furthermore, after high-fat feeding, zebrafish plxnd1 mutant VAT was resistant to expansion, and excess lipid was disproportionately deposited in SAT, leading to an even greater exacerbation of altered body fat distribution. Plxnd1-deficient zebrafish were protected from high-fat-diet-induced insulin resistance, and human VAT PLXND1 mRNA was positively associated with type 2 diabetes, suggesting a conserved role for PLXND1 in insulin sensitivity. Together, our findings identify Plxnd1 as a novel regulator of VAT growth, body fat distribution, and insulin sensitivity in both zebrafish and humans.


2019 ◽  
Vol 3 (7) ◽  
pp. 1409-1416 ◽  
Author(s):  
Satoshi Kadowaki ◽  
Yoshifumi Tamura ◽  
Yuki Someya ◽  
Kageumi Takeno ◽  
Hideyoshi Kaga ◽  
...  

Abstract Context Asians have a high prevalence of insulin resistance, even in the nonobese state. Whereas both visceral fat accumulation (VFA) and fatty liver (FL) have been shown to be associated with insulin resistance, it is still unclear which is a better marker to predict insulin resistance in nonobese Asians. Objective The aim of this study was to investigate the relation between VFA or FL and insulin resistance in nondiabetic nonobese Japanese men who do not have diabetes. Design and Participants We studied 87 nonobese (body mass index <25 kg/m2) Japanese men without diabetes. Using a two-step hyperinsulinemic euglycemic clamp, we evaluated insulin sensitivity in adipose tissue, muscle, and liver. Intrahepatic lipid and abdominal visceral fat area were measured by 1H-magnetic resonance spectroscopy and MRI, respectively. Subjects were divided into four groups based on the presence or absence of VFA (visceral fat area ≥100 cm2) and FL (intrahepatic lipid ≥ 5%): control (non-VFA, non-FL; n = 54), VFA only (n = 18), FL only (n = 7), and VFA plus FL (n = 8). Results Subjects in the FL only and VFA plus FL groups had insulin resistance in adipose tissue and muscle, as well as relatively lower hepatic insulin sensitivity. The specific insulin sensitivities in these organs were comparable in the VFA only and control groups. Conclusions In nonobese Japanese men without diabetes, subjects with FL only or VFA plus FL but not VFA only had insulin resistance, suggesting that FL may be a more useful clinical marker than VFA to predict insulin resistance in nonobese Japanese men without diabetes.


2004 ◽  
Vol 89 (11) ◽  
pp. 5517-5522 ◽  
Author(s):  
Tongjian You ◽  
Alice S. Ryan ◽  
Barbara J. Nicklas

Abstract The purpose of this study was to investigate whether aerobic fitness, body composition, body fat distribution, and inflammation are different in obese postmenopausal women with and without the metabolic syndrome (MS), and whether the severity of MS is associated with these characteristics. Fifty-eight women (age, 59 ± 1 yr; body mass index, 33.0 ± 0.6 kg/m2) completed testing of maximal aerobic capacity, body composition (fat mass, lean mass, and percent body fat), body fat distribution (sc and visceral fat areas, and regional adipocyte sizes), and inflammation (C-reactive protein, IL-6, and TNF-α, and their soluble receptors). Lean mass (44.4 ± 0.9 vs. 41.2 ± 0.9 kg; P &lt; 0.05), visceral fat area (180 ± 10 vs. 135 ± 7 cm2; P &lt; 0.001), and plasma soluble TNF receptor 1 (sTNFR1; 860 ± 25 vs. 765 ± 42 pg/ml; P &lt; 0.05) were higher in women with the MS (n = 27) than in those without the MS (n = 31). The number of MS components was directly related to weight, body mass index, fat mass, lean mass, visceral fat area, and plasma sTNFR1. We conclude that obese older women with the MS are characterized by high lean mass, high visceral fat, and elevated sTNFR1, and the severity of the MS is associated with body composition, visceral adiposity, and inflammation.


Author(s):  
Giada Ostinelli ◽  
Jinchu Vijay ◽  
Marie-Claude Vohl ◽  
Elin Grundberg ◽  
Andre Tchernof

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Sabet ◽  
S Elkaffas ◽  
S.W.G Bakhoum ◽  
H Kandil

Abstract Introduction Smoking and obesity are recognized as important modifiable risk factors for coronary artery disease (CAD). However, the general perception that smoking protects against obesity is a common reason for starting, and/or not quitting smoking. Purpose To detect the quantity, quality and relative distribution of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) estimated by abdominal computed tomography in smokers versus non- smokers. Methods The abdominal muscular wall was traced manually to calculate SAT and VAT areas (cm2) (outside and inside abdominal muscular wall respectively) as well as SAT density [Hounsfield units (HU)] at L4-L5 in 409 consecutive patients referred for evaluation of chest pain by multi-slice computed tomography coronary angiography (MSCT-CA). Results 26% of the studied patients (n=107) were current smokers, while the remaining 74% (n=302) never smoked. Coronary artery atherosclerosis was more prevalent in smokers compared to non-smokers (64.5% vs 55.0%; p=0.09). Smokers had statistically significantly lower body mass index (BMI) (31.2±4.3 vs. 32.5±4.7 kg/m2; p=0.015), hip circumference (HC) (98.6±22.5 vs. 103.9±20.9 cm; p=0.031), total fat area (441.62±166.34 vs. 517.95±169.51cm2; p&lt;0.001), and SAT area (313.07±125.54 vs. 390.93±143.28 cm2; p&lt;0.001) as compared to non-smokers. However, smokers had statistically significantly greater waist-to-hip ratio (0.98±0.08 vs. 0.96±0.08; p=0.010), VAT/SAT area ratio (0.41±0.23 vs. 0.35±0.20; p=0.013), and denser SAT depot (−98.91±7.71 vs. −102.08±6.44 HU; p&lt;0.001). Conclusion Smoking contributes to CAD and to the pathogenic redistribution of body fat towards VAT, through limiting SAT potential to expand. Funding Acknowledgement Type of funding source: None


Sign in / Sign up

Export Citation Format

Share Document