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 Changes in adipose tissue lipolysis gene expression and insulin sensitivity after weight loss

2020 ◽  
Vol 9 (2) ◽  
pp. 90-100 ◽  
Author(s):  
Monika Karczewska-Kupczewska ◽  
Agnieszka Nikołajuk ◽  
Radosław Majewski ◽  
Remigiusz Filarski ◽  
Magdalena Stefanowicz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Intervention Program ◽  
Dietary Intervention ◽  
Normal Weight ◽  
Control Group ◽  
Metabolic Complications ◽  
Obese Subjects

Objective Insulin resistance is a major pathophysiological link between obesity and its metabolic complications. Weight loss (WL) is an effective tool to prevent obesity-related diseases; however, the mechanisms of an improvement in insulin sensitivity (IS) after weight-reducing interventions are not completely understood. The aim of the present study was to analyze the relationships between IS and adipose tissue (AT) expression of the genes involved in the regulation of lipolysis in obese subjects after WL. Methods Fifty-two obese subjects underwent weight-reducing dietary intervention program. The control group comprised 20 normal-weight subjects, examined at baseline only. Hyperinsulinemic-euglycemic clamp and s.c. AT biopsy with subsequent gene expression analysis were performed before and after the program. Results AT expression of genes encoding lipases (PNPLA2, LIPE and MGLL) and lipid-droplet proteins enhancing (ABHD5) and inhibiting lipolysis (PLIN1 and CIDEA) were decreased in obese individuals in comparison with normal-weight individuals. The group of 38 obese participants completed dietary intervention program and clamp studies, which resulted in a significant WL and an improvement in mean IS. However, in nine subjects from this group IS did not improve in response to WL. AT expression of PNPLA2, LIPE and PLIN1 increased only in the group without IS improvement. Conclusions Excessive lipolysis may prevent an improvement in IS during WL. The change in AT PNPLA2 and LIPE expression was a negative predictor of the change in IS after WL.

scholarly journals Increased adiponectin receptor-1 expression in adipose tissue of impaired glucose-tolerant obese subjects during weight loss

2006 ◽  
Vol 155 (1) ◽  
pp. 161-165 ◽  
Author(s):  
M J Kim ◽  
M Maachi ◽  
C Debard ◽  
E Loizon ◽  
K Clément ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Metabolic Parameters ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Very Low Calorie Diet ◽  
Peroxisome Proliferator Activated Receptor ◽  
Before And After ◽  
Obese Subjects

Objective: To investigate the mRNA expression of adiponectin, AdipoR1 and AdipoR2, the two recently cloned adiponectin receptors and peroxisome proliferator activated receptor (PPAR)γ2 in adipose tissue of obese individuals before and during a very low calorie diet (VLCD) inducing weight loss. Methods: Twenty-three non-diabetic obese subjects with normal (NGT, n=11) or impaired glucose tolerance (IGT, n=12) (age, 47±3 years; body mass index, 39.3±1.3 kg/m2) were studied before and after a 3-week 3.9 MJ diet daily without exercise. mRNA levels of nine IGT and six NGT subjects were measured by real-time PCR in s.c. abdominal adipose tissue. Results: Metabolic parameters and insulin sensitivity were improved by VLCD in the IGT group, but minimally affected in the NGT group. VLCD increased expression of AdipoR1 in the IGT (P=0.02), but not in the NGT group. Adiponectin, AdipoR2 and PPARγ2 mRNA levels did not change during VLCD in any group. In the IGT, but not in the NGT group, AdipoR1 and AdipoR2 expressions were positively related to that of PPARγ2 and, after VLCD, AdipoR1 and AdipoR2 expressions were positively related to each other and to that of adiponectin. Conclusion: In the NGT group, the 3-week VLCD inducing weight loss did not modify metabolic parameters, insulin sensitivity and the expression of the adiponectin system in adipose tissue. By contrast, in the IGT group, AdipoR1 expression increased and we found a coordinate regulation of the expression of adiponectin and its receptors. These modifications could participate, through adiponectin action on adipocytes, to the improved metabolic parameters observed in IGT subjects.

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 ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Serum Levels ◽  
Tissue Expression ◽  
The Metabolic Syndrome ◽  
Obese Subjects

scholarly journals Serum concentrations and expressions of serum amyloid A and leptin in adipose tissue are interrelated: the Genobin Study

2008 ◽  
Vol 158 (3) ◽  
pp. 333-341 ◽  
Author(s):  
T Lappalainen ◽  
M Kolehmainen ◽  
U Schwab ◽  
L Pulkkinen ◽  
D E Laaksonen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Weight Reduction ◽  
Serum Amyloid A ◽  
Normal Weight ◽  
Serum Amyloid ◽  
Serum Concentrations ◽  
Amyloid A ◽  
Obese Subjects

ObjectiveSerum amyloid A (SAA) is a novel link between increased adipose tissue mass and low-grade inflammation in obesity. Little is known about the factors regulating its serum concentration and mRNA levels. We investigated the association between SAA and leptin in obese and normal weight subjects and analyzed the effect of weight reduction on serum SAA concentration and gene expression in adipose tissue of the obese subjects.MethodsSeventy-five obese subjects (60±7 years, body mass index (BMI) 32.9±2.8 kg/m2, mean±s.d.) with impaired fasting plasma glucose or impaired glucose tolerance and other features of metabolic syndrome, and 11 normal weight control subjects (48±9 years, BMI 23.7±1.9 kg/m2) were studied at the baseline. Twenty-eight obese subjects underwent a 12-week intensive weight reduction program followed by 5 months of weight maintenance. Blood samples and abdominal s.c. adipose tissue biopsies were taken at the baseline and after the follow-up. Gene expression was studied using real-time quantitative PCR.ResultsThe gene expressions in women and serum concentrations of leptin and SAA were interrelated independently of body fat mass in the obese subjects (r=0.54, P=0.001; r=0.24, P=0.039 respectively). In multiple linear regression analyses, leptin mRNA explained 38% of the variance in SAA mRNA (P=0.002) in the obese women. Weight loss of at least 5% increased SAA mRNA expression by 48 and 36% in men and women, but serum SAA concentrations did not change.ConclusionsThe association between SAA and leptin suggests an interaction between these two adipokines, which may have implications in inflammatory processes related to obesity and the metabolic syndrome.

Adipokines oversecreted by omental adipose tissue in human obesity

2007 ◽  
Vol 293 (3) ◽  
pp. E656-E665 ◽  
Author(s):  
E. Maury ◽  
K. Ehala-Aleksejev ◽  
Y. Guiot ◽  
R. Detry ◽  
A. Vandenhooft ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Causative Role ◽  
Mrna Levels ◽  
Human Obesity ◽  
Omental Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Enhanced Production ◽  
Inflammatory Protein ◽  
Secretory Products

Central-omental obesity plays a causative role in the pathogenesis of the metabolic syndrome. Adipokines are involved in the pathogenesis of this syndrome. However, adipokines secreted by omental adipose tissue (OAT) are still poorly characterized in human obesity. Therefore, we searched for novel adipokines abnormally secreted by OAT in obesity and examined their relationships with some features of metabolic syndrome and the respective contribution of adipocytes vs. stromal-vascular cells. OAT from obese and nonobese men was fractionated into adipocytes and SV cells, which were then cultured. Medium was screened by medium-scale protein arrays and ELISAs. Adipokine mRNA levels were measured by real-time RT-qPCR. We detected 16 cytokines secreted by each cellular fraction of lean and obese subjects. Of the 16 cytokines, six adipokines were newly identified as secretory products of OAT, which were dysregulated in obesity: three chemokines (growth-related oncogen factor, RANTES, macrophage inflammatory protein-1β), one interleukin (IL-7), one tissue inhibitor of metalloproteinases (TIMP-1), and one growth factor (thrombopoietin). Their secretion and expression were enhanced in obesity, with a relatively similar contribution of the two fractions. The higher proportion of macrophages and endothelial cells in obesity may contribute to this enhanced production as well as changes in intrinsic properties of hypertrophied adipocytes. Accordingly, mRNA concentrations of most of these adipokines increased during adipocyte differentiation. Eventually, expression of the investigated adipokines did correlate with several features of the metabolic syndrome. In conclusion, six adipokines were newly identified as oversecreted by OAT in obesity. These adipokines may link obesity to its cardiovascular or metabolic comorbidities.

scholarly journals Adiponectin Gene Expression and Plasma Values in Obese Women during Very-Low-Calorie Diet. Relationship with Cardiovascular Risk Factors and Insulin Resistance

2004 ◽  
Vol 89 (2) ◽  
pp. 756-760 ◽  
Author(s):  
Marta Garaulet ◽  
Nathalie Viguerie ◽  
Stefan Porubsky ◽  
Eva Klimcakova ◽  
Karine Clement ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Obese Women ◽  
Adiponectin Gene ◽  
Very Low Calorie Diet ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Low Calorie Diet ◽  
Calorie Diet

Adiponectin, a newly discovered adipose-tissue-specific protein, is thought to be involved in the regulation of insulin action. The aim of the present study was to determine whether adiponectin contributes to the improvement in insulin sensitivity during very-low-calorie diet (VLCD). Biopsies of sc abdominal adipose tissue and blood sampling for analysis of plasma adiponectin and related hormones and metabolites were performed before and at the end of a 4-wk VLCD in 33 nonmorbidly obese women (body mass index, 34.4 ± 4.1 kg/m2). VLCD produced a decrease in weight (7.1 ± 0.4 kg) and in insulin and leptin levels and led to an improvement in insulin sensitivity. Adiponectin gene expression and plasma levels were not modified during calorie restriction. Before VLCD, we found negative correlations between plasma adiponectin and variables related to the metabolic syndrome. Adiponectin mRNA levels showed a negative correlation with lipoprotein a plasma values. The correlations observed before VLCD were not found after VLCD. The data suggest that adiponectin is related to the protection against the metabolic syndrome but is not involved in the regulation of VLCD-induced improvement of insulin sensitivity.

Enhanced fatty acid uptake in visceral adipose tissue is not reversed by weight loss in obese individuals with the metabolic syndrome

Diabetologia ◽  
2014 ◽  
Vol 58 (1) ◽  
pp. 158-164 ◽  
Author(s):  
Marco Bucci ◽  
Anna C. Karmi ◽  
Patricia Iozzo ◽  
Barbara A. Fielding ◽  
Antti Viljanen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Visceral Adipose Tissue ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
The Metabolic Syndrome ◽  
Visceral Adipose

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.

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