scholarly journals Altered subcutaneous abdominal adipose tissue lipid synthesis in obese, insulin-resistant humans

2013 ◽  
Vol 305 (8) ◽  
pp. E999-E1006 ◽  
Author(s):  
Demidmaa Tuvdendorj ◽  
Manisha Chandalia ◽  
Tumurbaatar Batbayar ◽  
Manish Saraf ◽  
Carine Beysen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Nonesterified Fatty Acid ◽  
Oral Glucose ◽  
Large Variability ◽  
Abdominal Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Wide Range ◽  
Obese Subjects ◽  
Subcutaneous Abdominal Adipose Tissue

The purpose of this study was to evaluate the variability of subcutaneous abdominal adipose tissue (AT) dynamics in obese subjects with a wide range of insulin sensitivity (IS) and the correlation between these two metabolic measures. Ten obese (BMI 30–40 kg/m2) nondiabetic subjects with ( n = 6) and without ( n = 4) the metabolic syndrome were studied following a 12-wk 2H2O labeling period. Subcutaneous abdominal AT biopsies were collected. Deuterium incorporation into triglyceride (TG)-glycerol and TG-palmitate were measured by gas chromatography-mass spectrometry for the calculation of fractional TG synthesis ( fTG) and fractional de novo lipogenesis ( fDNL). Muscle IS and insulin-mediated nonesterified fatty acid (NEFA) suppression (a measure for adipose IS) indexes were derived from the oral glucose tolerance test (OGTT). The ability of subcutaneous abdominal AT to synthesize lipids varied significantly in obese subjects ( fTG range 7–28%, fDNL range 1.1–4.6%) with significantly lower values (>35% reduction) for both parameters in obese with the metabolic syndrome. fTG correlated positively with muscle IS ( r = 0.64, P = 0.04) and inversely with NEFA suppression during the OGTT ( r = −0.69, P = 0.03). These results demonstrate a large variability in subcutaneous abdominal AT lipid turnover in obesity. Moreover, a reduced capacity for subcutaneous abdominal AT fat storage is associated with muscle and adipose tissue insulin resistance as well as with the metabolic syndrome, thus identifying a form of obesity at heightened risk for type 2 diabetes and cardiovascular disease.

scholarly journals Impaired alternative macrophage differentiation of peripheral blood mononuclear cells from obese subjects

2011 ◽  
Vol 9 (3) ◽  
pp. 189-195 ◽  
Author(s):  
Gael Bories ◽  
Robert Caiazzo ◽  
Bruno Derudas ◽  
Corinne Copin ◽  
Violeta Raverdy ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
The Metabolic Syndrome ◽  
Blood Mononuclear Cells ◽  
Obese Subjects ◽  
Anti Inflammatory

Visceral obesity is a chronic, low-grade inflammatory disease that predisposes people to the metabolic syndrome, type 2 diabetes and its cardiovascular complications. Adipose tissue is not a passive storehouse for fat, but an endocrine organ synthesizing and releasing a variety of bioactive molecules, some of which are produced by infiltrated immune-inflammatory cells including macrophages. Two different subpopulations of macrophages have been identified in adipose tissue: pro-inflammatory ‘classical’ M1 and anti-inflammatory ‘alternative’ M2 macrophages, and their ratio is suggested to influence the metabolic complications of obesity. These macrophages derive primarily from peripheral blood mononuclear cells (PBMCs). We hypothesised that obesity and the metabolic syndrome modulate PBMC functions. Therefore, alteration of the monocyte response, and more specifically their ability to differentiate toward alternative anti-inflammatory macrophages, was assessed in PBMCs isolated from lean and obese subjects with or without alterations in glucose homeostasis. Our results indicate that PBMCs from obese subjects have an altered expression of M2 markers and that their monocytes are less susceptible to differentiate toward an alternative phenotype. Thus PBMCs in obesity are programmed, which may contribute to the inflammatory dysregulation and increased susceptibility to inflammatory diseases in these patients.

Abstract 040: Comparison of Effects of Reux en Y Gastric Bypass and Intra-abdominal Lipectomy on Cardiovascular Function in the Metabolic Syndrome

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Amanda Soler ◽  
Brenda Hutcheson ◽  
Jenny Yang ◽  
Chastity Bradford ◽  
Frank Zhang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Gastric Bypass ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Carotid Artery ◽  
Abdominal Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Artery Stiffness ◽  
Abdominal Lipectomy

Central (visceral) obesity is a key feature of the metabolic syndrome and an independent predictor of cardiovascular disease. Reux en Y gastric bypass (RnY) has been shown to offer protection against cardiovascular disease, but residual risk remains. It is also unknown whether the cardiovascular benefit is a consequence of a decrease in visceral (intra-abdominal) adipose tissue or of other factors. In this study, we compared the effects of RnY vs. removal of 90% of visceral adipose tissue (=5% body weight) by intra-abdominal lipectomy on cardiac function (echocardiography), macrovascular function (carotid artery stiffness) and microvascular function (coronary artery endothelium-dependent vasorelaxation) in a metabolic syndrome rat model (JCR:LA-cp, JCR). Cardiac output (CO) and ejection fraction (EF) were significantly decreased in JCR vs. normal (Sprague-Dawley, SD) rats (CO=50±5%, EF=45±2% of normal), and were significantly improved by both RnY and intra-abdominal lipectomy (CO=75±6%, EF=82±2% and CO=80±3%, EF=90±2% of normal, respectively). Likewise, acetylcholine-dependent coronary artery vasorelaxation was impaired in JCR rats (50±1% of normal), and was significantly improved by both RnY and intra-abdominal lipectomy (98±2% and 98±3% of normal, respectively). Carotid artery stiffness was significantly increased in JCR rats (~2 fold vs. SD), and was normalized by intra-abdominal lipectomy (to equal SD), but not by RnY (~2 fold vs. SD). Intra-abdominal lipectomy but not RnY also decreased cardiac and vascular elastin degradation in JCR rats (Lipectomy: ~50% (heart), ~75% (carotid); RnY: ~15% (heart), ~5% (carotid) vs. untreated JCR, respectively), concomitant with a decrease in matrix metalloproteinase 12 (MMP12), a major elastase, activation (~50% (heart), ~75% (carotid), ~87% (visceral fat), ~75% (circulating) vs. untreated JCR) and in 20-hydroxyeicosatetraeonic acid (20-HETE) levels (~4 (heart), ~7 (carotid), ~4 (visceral fat), ~4 (circulating) fold vs. untreated JCR). Thus, our data indicate that intra-abdominal adipose tissue itself is a source of factors that may be important negative regulators of micro- and macrovascular and cardiac function, but are not eliminated by RnY.

scholarly journals Insulin Gene Variable Number of Tandem Repeats (INS VNTR) Genotype and Metabolic Syndrome in Childhood Obesity

2006 ◽  
Vol 91 (11) ◽  
pp. 4641-4644 ◽  
Author(s):  
Nicola Santoro ◽  
Grazia Cirillo ◽  
Alessandra Amato ◽  
Caterina Luongo ◽  
Paolo Raimondo ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Tandem Repeats ◽  
Whole Body ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
Obese Children ◽  
Insulin Levels ◽  
Ins Vntr ◽  
The Metabolic Syndrome ◽  
Obese Subjects

Abstract Objective: The insulin variable number of tandem repeats (VNTR) polymorphism located in the insulin gene promoter (INS VNTR) has been associated with insulin levels in obese children. Hyperinsulinemia is a pivotal factor in the development of metabolic syndrome, an emerging complication in childhood obesity. With the present study, we aimed to test the associations between INS VNTR and the metabolic syndrome in juvenile-onset obesity. Subjects and Methods: We screened for the INS VNTR in 320 obese children (152 girls; mean age, 11.2 ± 2.3 yr; mean z-score body mass index, 3.6 ± 1.1). All of them underwent a standard oral glucose tolerance test; baseline measurements included blood pressure and plasma lipid and fasting insulin levels. By using the data derived from the oral glucose tolerance test, the whole-body insulin sensitivity and the insulinogenic index were calculated. Results: The prevalence of metabolic syndrome reached 39%. No differences in INS VNTR genotype distribution were observed between obese subjects and 200 lean, age- and sex-matched children (P = 0.7). Among obese subjects, the prevalence of the metabolic syndrome was significantly higher in subjects with the I/I genotype (P = 0.006); the risk for developing the metabolic syndrome was significantly higher in subjects carrying the I/I genotype (odds ratio, 2.5; 95% confidence interval, 1.5–3.9). Obese subjects homozygous for the class I allele showed higher insulin levels and insulinogenic index but lower whole-body insulin sensitivity. Conclusions: We conclude that the I variant of the insulin promoter, when expressed in homozygotes, can predispose obese children to develop the metabolic syndrome.

scholarly journals Regulation of human aldoketoreductase 1C3 (AKR1C3) gene expression in the adipose tissue

2008 ◽  
Vol 13 (4) ◽  
Author(s):  
Per-arne Svensson ◽  
Britt Gabrielsson ◽  
Margareta Jernås ◽  
Anders Gummesson ◽  
Kajsa Sjöholm
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Mrna Levels ◽  
Very Low Calorie Diet ◽  
Metabolic Complications ◽  
Realtime Pcr ◽  
The Metabolic Syndrome ◽  
Obese Subjects

AbstractAldoketoreductase 1C3 (AKR1C3) is a functional prostaglandin F synthase and a negative modulator of the availability of ligands for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARγ). AKR1C3 expression is known to be associated with adiposity, one of the components of the metabolic syndrome. The aim of this study was to characterize the expression of AKR1C3 in the adipose tissue and adipocytes and to investigate its potential role in the metabolic syndrome. Using microarray analysis and realtime PCR, we studied the expression of AKR1C3 in adipose tissue samples from obese subjects with or without metabolic complications, during very low calorie diet-induced weight loss, and its expression in isolated human adipocytes of different sizes. The adipose tissue AKR1C3 expression levels were marginally lower in obese subjects with the metabolic syndrome compared with the levels in healthy obese subjects when analyzed using microarray (p = 0.078) and realtime PCR (p < 0.05), suggesting a secondary or compensatory effect. The adipose tissue mRNA levels of AKR1C3 were reduced during and after dietinduced weight-loss compared to the levels before the start of the diet (p < 0.001 at all time-points). The gene expression of AKR1C3 correlated with both adipose tissue mRNA levels and serum levels of leptin before the start of the diet (p < 0.05 and p < 0.01, respectively). Furthermore, large adipocytes displayed a higher expression of AKR1C3 than small adipocytes (1.5-fold, p < 0.01). In conclusion, adipose tissue AKR1C3 expression may be affected by metabolic disease, and its levels are significantly reduced in response to dietinduced weight loss and correlate with leptin levels.

scholarly journals Circulating nerve growth factor levels in relation to obesity and the metabolic syndrome in women

2007 ◽  
Vol 157 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Mònica Bulló ◽  
Muhammad R Peeraully ◽  
Paul Trayhurn ◽  
J Folch ◽  
Jordi Salas-Salvadó
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Nerve Growth Factor ◽  
Inflammatory Markers ◽  
Normal Weight ◽  
Morbidly Obese ◽  
The Metabolic Syndrome ◽  
Obese Subjects

Objective: Neurotrophins (NTs) could be involved in the development and progression of inflammatory and immune diseases. Because obesity and the metabolic syndrome (MetSyn) are related to a low-grade systemic inflammation, plasma NT levels (neurotrophinemia) could play an important role in the ethiopathogenic mechanisms underlying these metabolic derangements. This is the first study evaluating the plasma NT levels in a group of women with obesity and MetSyn, and also the adipose tissue nerve growth factor (NGF) expression in a small group of them. Methods: Included were 146 adult women with different degrees of adiposity, with or without MetSyn. Plasma NT levels were measured. NGF expression was analyzed in s.c. adipose tissue of a subgroup of morbidly obese and normal-weight females. Results: NGF plasma levels were 1.4-fold higher in overweight and obese subjects. Plasma NGF was, however, lower in a group of morbidly obese subjects than in overweight or obesity, but it remained elevated relative to the normal-weight group. Plasma NGF was significantly correlated with body mass index (BMI), percentage body fat, and waist circumference in non-morbidly obese subjects. NGF was positively related to inflammatory markers. NT3 and brain-derived neurotrophin factor seem to be more related to lipid profile than to BMI, adipose tissue distribution, or peripheral inflammatory markers. Subjects with type 2 diabetes, abdominal fat distribution, or the MetSyn showed significantly higher levels of NGF. The MetSyn was the only independent predictor of the variability observed in the NGF plasma values. Conclusion: NGF is upregulated in obesity, type 2 diabetes, and the MetSyn. Whether this NT may contribute to inflammation and the metabolic derangements associated with body weight gain remains to be elucidated.

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