Dissociation between adipose tissue expression and serum levels of adiponectin during and after diet-induced weight loss in obese subjects with and without the metabolic syndrome

Metabolism ◽  
2007 ◽  
Vol 56 (8) ◽  
pp. 1022-1028 ◽  
Author(s):  
Carl Johan Behre ◽  
Anders Gummesson ◽  
Margareta Jernås ◽  
Theodore C. Lystig ◽  
Björn Fagerberg ◽  
...  
Author(s):  
Per-arne Svensson ◽  
Britt Gabrielsson ◽  
Margareta Jernås ◽  
Anders Gummesson ◽  
Kajsa Sjöholm

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.


Diabetologia ◽  
2014 ◽  
Vol 58 (1) ◽  
pp. 158-164 ◽  
Author(s):  
Marco Bucci ◽  
Anna C. Karmi ◽  
Patricia Iozzo ◽  
Barbara A. Fielding ◽  
Antti Viljanen ◽  
...  

2012 ◽  
pp. 469-480 ◽  
Author(s):  
M. BRÚSIK ◽  
J. UKROPEC ◽  
P. JOPPA ◽  
B. UKROPCOVÁ ◽  
P. SKYBA ◽  
...  

Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3±7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using real-time PCR. From underweight [n=9; body mass index (BMI) <20.0 kg.m−2], to normal weight-overweight (n=24, BMI=20.0-29.9 kg.m−2) and obese patients (n=11; BMI≥30 kg.m−2), REE adjusted for body weight decreased (32.9±6.1 vs. 26.2±5.8 vs. 23.9±6.6 kcal.kg−1.24 h−1, p=0.006), serum levels and adipose tissue expression of leptin increased (p<0.001 for both), and serum and adipose tissue adiponectin decreased (p<0.001; p=0.004, respectively). REE was inversely related to serum and adipose tissue leptin (R=−0.547, p<0.001; R=−0.458, p=0.002), and directly to serum adiponectin (R=0.316, p=0.039). Underweight patients had increased REE compared to normal weight-overweight patients, in association with reductions in serum and adipose tissue leptin, and increased serum adiponectin, suggesting a role of adipokines in energy imbalance in COPD-related cachexia.


2011 ◽  
Vol 9 (3) ◽  
pp. 189-195 ◽  
Author(s):  
Gael Bories ◽  
Robert Caiazzo ◽  
Bruno Derudas ◽  
Corinne Copin ◽  
Violeta Raverdy ◽  
...  

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.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Eva Tumova ◽  
Wensheng Sun ◽  
Peter H. Jones ◽  
Michal Vrablik ◽  
Christie M. Ballantyne ◽  
...  

Objective. Obesity is linked with a state of increased oxidative stress, which plays an important role in the etiology of atherosclerosis and type 2 diabetes mellitus. The aim of our study was to evaluate the effect of rapid weight loss on oxidative stress markers in obese individuals with metabolic syndrome (MetS).Design and Methods. We measured oxidative stress markers in 40 obese subjects with metabolic syndrome (MetS+), 40 obese subjects without metabolic syndrome (MetS−), and 20 lean controls (LC) at baseline and after three months of very low caloric diet.Results. Oxidized low density lipoprotein (ox-LDL) levels decreased by 12% in MetS+ subjects, associated with a reduction in total cholesterol (TC), even after adjustment for age and sex. Lipoprotein associated phospholipase A2(Lp-PLA2) activity decreased by 4.7% in MetS+ subjects, associated with a drop in LDL-cholesterol (LDL-C), TC, and insulin levels. Multivariate logistic regression analysis showed that a model including ox-LDL, LpPLA2activity, and myeloperoxidase (MPO) improved prediction of MetS status among obese individuals compared to each oxidative stress marker alone.Conclusions. Oxidative stress markers were predictive of MetS in obese subjects, suggesting a higher oxidative stress. Rapid weight loss resulted in a decline in oxidative stress markers, especially in MetS+ patients.


2006 ◽  
Vol 20 (5) ◽  
Author(s):  
Carrie Christine Coughlin ◽  
Jennifer McCrea ◽  
J. Christopher Eagon ◽  
Valerie Halpin ◽  
Brian Finck ◽  
...  

Open Medicine ◽  
2006 ◽  
Vol 1 (2) ◽  
pp. 136-147 ◽  
Author(s):  
Joanna Jankiewicz-Wika ◽  
Krzysztof Kołomecki ◽  
Jacek Cywiński ◽  
Katarzyna Piestrzeniewicz ◽  
Henryk Stępień ◽  
...  

AbstractBariatric surgery is the most effective method to achieve weight loss in obese subjects.The aim of this study was to evaluate some adipocytokines and insulin, as well as parameters of metabolic syndrome of the obese patients, for three and six months after vertical banded gastroplasty, in the time of dynamic weight loss.Seven males and two females aged 28 to 49 years, with long lasting simple obesity and the presence of metabolic syndrome, were studied. After surgical treatment the values of the body mass index, waist circumference, systolic and diastolic blood pressure, total cholesterol, LDL cholesterol, triglycerides, and blood concentrations of leptin decreased significantly.Before surgical operation of all obese patients no statistically significant correlations between studied parameters were noted. Three and six months later a lot of correlations between studied parameters appeared.In conclusion, (a) vertical-banded gastroplasty is a valuable method in treatment of obese subjects, leading to a significant decrease in body weight and improvement in some parameters of metabolic syndrome in a few months after surgery, (b) adipocytokines, together with an unknown gastric factor, may be key factors in the control of some features of the metabolic syndrome.


2007 ◽  
Vol 157 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Mònica Bulló ◽  
Muhammad R Peeraully ◽  
Paul Trayhurn ◽  
J Folch ◽  
Jordi Salas-Salvadó

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.


2013 ◽  
Vol 305 (8) ◽  
pp. E999-E1006 ◽  
Author(s):  
Demidmaa Tuvdendorj ◽  
Manisha Chandalia ◽  
Tumurbaatar Batbayar ◽  
Manish Saraf ◽  
Carine Beysen ◽  
...  

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.


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