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 Secretion of adiponectin multimeric complexes from adipose tissue explants is not modified by very low calorie diet

2009 ◽  
Vol 160 (4) ◽  
pp. 585-592 ◽  
Author(s):  
Zuzana Kovacova ◽  
Michaela Vitkova ◽  
Michaela Kovacikova ◽  
Eva Klimcakova ◽  
Magda Bajzova ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Dietary Intervention ◽  
Culture Media ◽  
Very Low Calorie Diet ◽  
Low Calorie Diet ◽  
Total Adiponectin ◽  
Calorie Diet ◽  
Obese Subjects

ObjectiveAdiponectin is a protein abundantly secreted by the adipose tissue (AT). Plasma adiponectin levels are decreased in obese, insulin-resistant, and type 2 diabetic patients. Various multimeric complexes, i.e. high-, middle-, and low-molecular weight isoforms (HMW, MMW and LMW), are present in plasma. Here, we investigated the effect of weight reducing diet on the distribution of adiponectin isoforms in plasma and on their secretion in AT explants from obese subjects.DesignA total of 20 obese subjects (age 37.8±7.3 years, body mass index 33.9±5.0 kg/m2) underwent eight weeks of very low-calorie diet (VLCD). A needle biopsy of subcutaneous abdominal AT and blood samples were taken before and after dietary intervention. AT explants were incubated in culture medium for 4 h. ELISA assay and western blot analyses were used to identify adiponectin complexes in culture media and in plasma.ResultsThe distribution of adiponectin polymers in plasma was different from that secreted in human AT explants. Before VLCD, the relative amount of HMW isoform was 75.5±9.1% of total adiponectin in culture media and 52.2±11.2% in plasma. Despite the diet-induced weight loss and improvement of insulin sensitivity, VLCD neither induced change in total adiponectin level nor in the ratio of HMW to total adiponectin in plasma and in culture media of AT explants.ConclusionsThe profile of adiponectin polymeric isoforms secreted by AT explants into culture media differs from the plasma profile. A dietary intervention leading to weight loss and improvement of insulin sensitivity was not associated with modifications of AT secretion of total or HMW adiponectin.

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 Profiling Cellular Processes in Adipose Tissue during Weight Loss Using Time Series Gene Expression

Genes ◽  
2018 ◽  
Vol 9 (11) ◽  
pp. 525 ◽  
Author(s):  
Samar Tareen ◽  
Michiel Adriaens ◽  
Ilja Arts ◽  
Theo de Kok ◽  
Roel Vink ◽  
...  
Keyword(s):  
Gene Expression ◽  
Time Series ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Dietary Intervention ◽  
Network Biology ◽  
Analysis Tool ◽  
Cellular Processes ◽  
Time Series Gene Expression

Obesity is a global epidemic identified as a major risk factor for multiple chronic diseases and, consequently, diet-induced weight loss is used to counter obesity. The adipose tissue is the primary tissue affected in diet-induced weight loss, yet the underlying molecular mechanisms and changes are not completely deciphered. In this study, we present a network biology analysis workflow which enables the profiling of the cellular processes affected by weight loss in the subcutaneous adipose tissue. Time series gene expression data from a dietary intervention dataset with two diets was analysed. Differentially expressed genes were used to generate co-expression networks using a method that capitalises on the repeat measurements in the data and finds correlations between gene expression changes over time. Using the network analysis tool Cytoscape, an overlap network of conserved components in the co-expression networks was constructed, clustered on topology to find densely correlated genes, and analysed using Gene Ontology enrichment analysis. We found five clusters involved in key metabolic processes, but also adipose tissue development and tissue remodelling processes were enriched. In conclusion, we present a flexible network biology workflow for finding important processes and relevant genes associated with weight loss, using a time series co-expression network approach that is robust towards the high inter-individual variation in humans.

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.

scholarly journals Interleukin-18 in plasma and adipose tissue: effects of obesity, insulin resistance, and weight loss

2007 ◽  
Vol 157 (4) ◽  
pp. 465-471 ◽  
Author(s):  
Jens M Bruun ◽  
Bente Stallknecht ◽  
Jørn W Helge ◽  
Bjørn Richelsen
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Rt Pcr ◽  
Reduced Body ◽  
Daily Exercise ◽  
Life Style Intervention ◽  
Obese Subjects ◽  
Isolated Adipocytes

Objective: Interleukin (IL)-18 is associated with obesity, insulin resistance, and cardiovascular disease. The present study compared 1) IL-18 in adipocytes versus stromal vascular (SV) cells, 2) IL-18 in plasma and adipose tissue (AT) in obese versus lean subjects, and 3) IL-18 in plasma, AT, and skeletal muscle (SM) in obese subjects after weight loss. Subjects and methods: At baseline, plasma and AT IL-18 in 23 obese subjects were compared with that in 12 lean subjects. The obese subjects were submitted to a 15-week life-style intervention (hypocaloric diet and daily exercise) after which plasma samples, AT, and SM biopsies were obtained. Analyses were performed by ELISA and RT-PCR respectively. Results: IL-18 expression in isolated adipocytes was ~2% of that in SV cells. Plasma IL-18 was higher in obese subjects (P < 0.001) and associated with insulin resistance (HOMA; P < 0.001). AT expression of IL-18, CD14, and CD68 was higher in obese (P < 0.01). The intervention reduced body weight (P < 0.001), plasma IL-18 (P < 0.001), and increased insulin sensitivity (HOMA; P < 0.05). AT and SM expression of IL-18 remained unchanged after the intervention. Changes in plasma IL-18 were associated with changes in insulin sensitivity (P < 0.05) but not with BMI or AT expression of IL-18. Conclusion: Plasma IL-18 is associated with changes in insulin resistance and reduced after weight loss. AT expression of IL-18 is increased in obesity but not affected by weight loss, indicating that changes in plasma IL-18 are related to insulin resistance rather than changes in obesity per se.

scholarly journals Markers of Adipogenesis, but Not Inflammation, in Adipose Tissue Are Independently Related to Insulin Sensitivity

2017 ◽  
Vol 102 (8) ◽  
pp. 3040-3049 ◽  
Author(s):  
Natalia Matulewicz ◽  
Magdalena Stefanowicz ◽  
Agnieszka Nikołajuk ◽  
Monika Karczewska-Kupczewska
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Immune Cells ◽  
Insulin Signaling ◽  
Transcriptional Level ◽  
Altered Expression ◽  
Ecm Remodeling ◽  
Expression Of Genes ◽  
Obese Subjects

Abstract Context In obesity, adipose tissue (AT) undergoes dynamic remodeling, including an alternation in adipogenesis, AT-resident cell content, angiogenesis, and turnover of extracellular matrix (ECM) components. Studies of AT in humans have been carried out mostly in people with severe metabolic abnormalities, like type 2 diabetes or morbid obesity. Objective The purpose of this study was to investigate subcutaneous AT gene expression of markers of adipogenesis, ECM remodeling, and inflammation in young, healthy, overweight or obese subjects. Design The study group comprised 83 normal-weight, 48 overweight, and 19 obese subjects. Euglycemic hyperinsulinemic clamp, biopsy of subcutaneous AT, and isolation of peripheral blood mononuclear cells (PBMCs) were performed. Gene expression was measured with real-time polymerase chain reaction. Results Overweight/obese subjects had lower AT expression of markers of adipogenesis, insulin signaling, and angiogenesis; higher expression of markers of ECM remodeling; altered expression of genes of the nuclear factor-κ-B (NFκB), but not c-Jun NH2-terminal kinase, pathway; and higher expression of macrophage markers but not markers of other immune cells. In multiple regression analysis, the expression of CEBPA, ADIPOQ, IRS1, IRS2, SLC2A4, and MMP9 was associated with insulin sensitivity independently of body mass index. No differences were found in inflammatory-gene PBMC expression. Conclusion Overweight/obesity is associated with altered expression of genes of adipogenesis, insulin signaling, ECM remodeling, and inflammation. NFκB seems to be the earliest inflammatory pathway altered at the transcriptional level in AT. Macrophages seem to be the first immune cells to infiltrate AT. Adipogenesis and ECM remodeling are the initial processes in AT that are independently associated with insulin sensitivity.

scholarly journals Adipose Tissue Inflammation is Not Related to Adipose Insulin Resistance in Humans

2021 ◽  
Author(s):  
Ana Elena Espinosa De Ycaza ◽  
Esben Søndergaard ◽  
Maria Morgan-Bathke ◽  
Kelli Lytle ◽  
Danae A. Delivanis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Strong Predictor ◽  
Normal Weight ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Fat Cell ◽  
Before And After

The role of adipose tissue (AT) inflammation on AT function in humans is unclear. We tested whether AT macrophage (ATM) content, cytokine gene expression and senescent cell burden (markers of AT inflammation) predict AT insulin resistance measured as the insulin concentration that suppresses lipolysis by 50% (IC<sub>50</sub>). We studied 86 volunteers with normal weight or obesity at baseline, and a subgroup of 25 volunteers with obesity before and after weight loss. There was a strong, positive relationship between IC<sub>50 </sub>and abdominal subcutaneous and femoral fat cell size (FCS). The positive, univariate relationships between IC<sub>50 </sub>and abdominal AT inflammatory markers: CD68, CD14, CD206 ATM/100 adipocytes, senescent cells, IL-6 and TNF-α mRNA were not significant after adjustment for FCS. A 10% weight loss significantly reduced IC<sub>50</sub>, however, there was no reduction in adipose ATM content, senescent cells or cytokine gene expression. Our study suggests that commonly used markers of AT inflammation are not causally linked to AT insulin resistance, whereas FCS is a strong predictor of AT insulin resistance with respect to lipolysis.

Network analyses reveal negative link between changes in adipose tissue GDF15 and BMI during dietary induced weight loss

2021 ◽  
Author(s):  
Alyssa Imbert ◽  
Nathalie Vialaneix ◽  
Julien Marquis ◽  
Julie Vion ◽  
Aline Charpagne ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Dietary Intervention ◽  
Mrna Level ◽  
Clinical Variable ◽  
Isolated Cells ◽  
Two Phase ◽  
Network Analyses ◽  
Anti Inflammatory

Abstract Context Adipose tissue (AT) transcriptome studies provide holistic pictures of adaptation to weight and related bioclinical settings changes. Objective To implement AT gene expression profiling and investigate the link between changes in bioclinical parameters and AT gene expression during three steps of a two-phase dietary intervention (DI). Design AT transcriptome profiling was obtained from sequencing 1051 samples, corresponding to 556 distinct individuals enrolled in a weight loss intervention (8-week low calorie diet (LCD) at 800 kcal/d) followed with a 6-month ad libitum randomized DI. Methods Transcriptome profiles obtained with QuantSeq sequencing were benchmarked against Illumina RNAseq. RT-qPCR was used to further confirm associations. Cell specificity was assessed using freshly isolated cells and THP-1 cell line. Results During LCD, five modules were found, of which three included at least one bio-clinical variable. Change in BMI connected with changes in mRNA level of genes with inflammatory response signature. In this module, change in BMI was negatively associated to changes in expression of genes encoding secreted protein (GDF15, CCL3 and SPP1). Through all phases of the DI, change in GDF15 was connected to changes in SPP1, CCL3, LIPA and CD68. Further characterization showed that these genes were specific to macrophages (with LIPA, CD68 and GDF15 expressed in anti-inflammatory macrophages) and GDF15 also expressed in preadipocytes. Conclusion Network analyses identified a novel AT feature with GDF15 upregulated with calorie restriction induced weight loss, concomitantly to macrophage markers. In AT, GDF15 was expressed in preadipocytes and macrophages where it was a hallmark of anti-inflammatory cells.

scholarly journals Dynamic Strength Training Improves Insulin Sensitivity without Altering Plasma Levels and Gene Expression of Adipokines in Subcutaneous Adipose Tissue in Obese Men

2006 ◽  
Vol 91 (12) ◽  
pp. 5107-5112 ◽  
Author(s):  
E. Klimcakova ◽  
J. Polak ◽  
C. Moro ◽  
J. Hejnova ◽  
M. Majercik ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Strength Training ◽  
Plasma Levels ◽  
Dynamic Strength ◽  
Whole Body ◽  
Obese Subjects ◽  
Dynamic Strength Training

Abstract Context: Obesity is characterized by a low-grade inflammatory state, which could play a role in insulin resistance. Dynamic strength training improves insulin sensitivity. Objective: The objective of this study was to investigate, in obese subjects, whether the insulin sensitizing effect of dynamic strength training is associated with changes in plasma levels and gene expression of adipokines potentially involved in the development of insulin resistance. Design: Twelve obese male subjects were investigated before and at the end of 3 months of dynamic strength training. Insulin sensitivity was evaluated using euglycemic-hyperinsulinemic clamp. Blood samples and needle biopsy samples of sc abdominal adipose tissue were obtained. The plasma levels and adipose tissue mRNA levels of adiponectin, leptin, IL-1β, IL-6, and TNF-α were determined. Results: The training induced an increase in the whole-body glucose disposal rate by 24% (P = 0.04). The body weight was not altered during the training. Plasma levels of leptin decreased during the training (16.6 ± 6.3 vs. 13.1 ± 5.7 ng/ml) by 21% (P &lt; 0.02), whereas no change in plasma levels of other adipokines and C-reactive protein was observed. Gene expression of the investigated adipokines was not changed in sc adipose tissue during the training. Conclusions: In obese subjects, the dynamic strength training resulted in an improvement of whole-body insulin sensitivity. The increase in insulin sensitivity was not associated with training-induced modifications of plasma levels or adipose tissue gene expression of adipokines supposedly involved in the development of insulin resistance.

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