JNK and IKKβ phosphorylation is reduced by glucocorticoids in adipose tissue from insulin-resistant rats

2015 ◽  
Vol 145 ◽  
pp. 1-12 ◽  
Author(s):  
Katia Motta ◽  
Amanda Marreiro Barbosa ◽  
Franciane Bobinski ◽  
Antonio Carlos Boschero ◽  
Alex Rafacho
Keyword(s):  
Adipose Tissue ◽  
Insulin Resistant

Does intra-abdominal adipose tissue in black men determine whether NIDDM is insulin-resistant or insulin-sensitive?

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 141-146 ◽  
Author(s):  
M. A. Banerji ◽  
R. L. Chaiken ◽  
D. Gordon ◽  
J. G. Kral ◽  
H. E. Lebovitz
Keyword(s):  
Adipose Tissue ◽  
Black Men ◽  
Abdominal Adipose Tissue ◽  
Insulin Resistant

scholarly journals Exercise training enhances white adipose tissue metabolism in rats selectively bred for low- or high-endurance running capacity

2013 ◽  
Vol 305 (3) ◽  
pp. E429-E438 ◽  
Author(s):  
Erin J. Stephenson ◽  
Sarah J. Lessard ◽  
Donato A. Rivas ◽  
Matthew J. Watt ◽  
Ben B. Yaspelkis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Citrate Synthase ◽  
Mitochondrial Protein ◽  
Treadmill Running ◽  
Endurance Running ◽  
Insulin Resistant ◽  
Disease States ◽  
Hcr Model

Impaired visceral white adipose tissue (WAT) metabolism has been implicated in the pathogenesis of several lifestyle-related disease states, with diminished expression of several WAT mitochondrial genes reported in both insulin-resistant humans and rodents. We have used rat models selectively bred for low- (LCR) or high-intrinsic running capacity (HCR) that present simultaneously with divergent metabolic phenotypes to test the hypothesis that oxidative enzyme expression is reduced in epididymal WAT from LCR animals. Based on this assumption, we further hypothesized that short-term exercise training (6 wk of treadmill running) would ameliorate this deficit. Approximately 22-wk-old rats (generation 22) were studied. In untrained rats, the abundance of mitochondrial respiratory complexes I–V, citrate synthase (CS), and PGC-1 was similar for both phenotypes, although CS activity was greater than 50% in HCR ( P = 0.09). Exercise training increased CS activity in both phenotypes but did not alter mitochondrial protein content. Training increased the expression and phosphorylation of proteins with roles in β-adrenergic signaling, including β3-adrenergic receptor (16% increase in LCR; P < 0.05), NOR1 (24% decrease in LCR, 21% decrease in HCR; P < 0.05), phospho-ATGL (25% increase in HCR; P < 0.05), perilipin (25% increase in HCR; P < 0.05), CGI-58 (15% increase in LCR; P < 0.05), and GLUT4 (16% increase in HCR; P < 0.0001). A training effect was also observed for phospho-p38 MAPK (12% decrease in LCR, 20% decrease in HCR; P < 0.05) and phospho-JNK (29% increase in LCR, 20% increase in HCR; P < 0.05). We conclude that in the LCR-HCR model system, mitochondrial protein expression in WAT is not affected by intrinsic running capacity or exercise training. However, training does induce alterations in the activity and expression of several proteins that are essential to the intracellular regulation of WAT metabolism.

Cell Non-Autonomous Regulation of Aging and Mitochondrial Uncoupling by Insulin-Resistant Adipose Tissue

2011 ◽  
pp. P3-388-P3-388
Author(s):  
Steven J Russell ◽  
Carly Cederquist ◽  
Ji Sun Park ◽  
Marcelo A Mori ◽  
C Ronald Kahn
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Uncoupling ◽  
Insulin Resistant ◽  
Autonomous Regulation

scholarly journals Specific Preservation of Biosynthetic Responses to Insulin in Adipose Tissue May Contribute to Hyperleptinemia in Insulin-Resistant Obese Mice

2004 ◽  
Vol 134 (5) ◽  
pp. 1045-1050 ◽  
Author(s):  
Tooru M. Mizuno ◽  
Toshiya Funabashi ◽  
Steven P. Kleopoulos ◽  
Charles V. Mobbs
Keyword(s):  
Adipose Tissue ◽  
Obese Mice ◽  
Insulin Resistant

Alterations of the classic pathway of complement in adipose tissue of obesity and insulin resistance

2007 ◽  
Vol 292 (5) ◽  
pp. E1433-E1440 ◽  
Author(s):  
Jinhui Zhang ◽  
Wendy Wright ◽  
David A. Bernlohr ◽  
Samuel W. Cushman ◽  
Xiaoli Chen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Epididymal Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Insulin Resistant ◽  
Obese Rats ◽  
Initial Activation ◽  
Adipose Cells ◽  
Classic Pathway

Adipose tissue inflammation has recently been linked to the pathogenesis of obesity and insulin resistance. C1 complex comprising three distinct proteins, C1q, C1r, and C1s, involves the key initial activation of the classic pathway of complement and plays an important role in the initiation of inflammatory process. In this study, we investigated adipose expression and regulation of C1 complement subcomponents and C1 activation regulator decorin in obesity and insulin resistance. Expression of C1q in epididymal adipose tissue was increased consistently in ob/ob mice, Zucker obese rats, and high fat-diet-induced obese (HF-DIO) mice. Decorin was found to increase in expression in Zucker obese rats and HF-DIO mice but decrease in ob/ob mice. After TZD administration, C1q and decorin expression was reversed in Zucker obese rats and HF-DIO mice. Increased expression of C1 complement and decorin was observed in both primary adipose and stromal vascular cells isolated from Zucker obese rats. Upregulation of C1r and C1s expression was also perceived in adipose cells from insulin-resistant humans. Furthermore, expression of C1 complement and decorin is dysregulated in TNF-α-induced insulin resistance in 3T3-L1 adipocytes and cultured rat adipose cells as they become insulin resistant after 24-h culture. These data suggests that both adipose and immune cells are the sources for abnormal adipose tissue production of C1 complement and decorin in obesity. Our findings also demonstrate that excessive activation of the classic pathway of complement commonly occurs in obesity, suggesting its possible role in adipose tissue inflammation and insulin resistance.

scholarly journals Donor metabolic characteristics drive effects of faecal microbiota transplantation on recipient insulin sensitivity, energy expenditure and intestinal transit time

Gut ◽  
2019 ◽  
Vol 69 (3) ◽  
pp. 502-512 ◽  
Author(s):  
Pieter de Groot ◽  
Torsten Scheithauer ◽  
Guido J Bakker ◽  
Andrei Prodan ◽  
Evgeni Levin ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Bile Acids ◽  
Transit Time ◽  
Intestinal Transit ◽  
Faecal Microbiota ◽  
Intestinal Transit Time ◽  
Insulin Resistant

ObjectiveBariatric surgery improves glucose metabolism. Recent data suggest that faecal microbiota transplantation (FMT) using faeces from postbariatric surgery diet-induced obese mice in germ-free mice improves glucose metabolism and intestinal homeostasis. We here investigated whether allogenic FMT using faeces from post-Roux-en-Y gastric bypass donors (RYGB-D) compared with using faeces from metabolic syndrome donors (METS-D) has short-term effects on glucose metabolism, intestinal transit time and adipose tissue inflammation in treatment-naïve, obese, insulin-resistant male subjects.DesignSubjects with metabolic syndrome (n=22) received allogenic FMT either from RYGB-D or METS-D. Hepatic and peripheral insulin sensitivity as well as lipolysis were measured at baseline and 2 weeks after FMT by hyperinsulinaemic euglycaemic stable isotope (2H2-glucose and 2H5-glycerol) clamp. Secondary outcome parameters were changes in resting energy expenditure, intestinal transit time, faecal short-chain fatty acids (SCFA) and bile acids, and inflammatory markers in subcutaneous adipose tissue related to intestinal microbiota composition. Faecal SCFA, bile acids, glycaemic control and inflammatory parameters were also evaluated at 8 weeks.ResultsWe observed a significant decrease in insulin sensitivity 2 weeks after allogenic METS-D FMT (median rate of glucose disappearance: from 40.6 to 34.0 µmol/kg/min; p<0.01). Moreover, a trend (p=0.052) towards faster intestinal transit time following RYGB-D FMT was seen. Finally, we observed changes in faecal bile acids (increased lithocholic, deoxycholic and (iso)lithocholic acid after METS-D FMT), inflammatory markers (decreased adipose tissue chemokine ligand 2 (CCL2) gene expression and plasma CCL2 after RYGB-D FMT) and changes in several intestinal microbiota taxa.ConclusionAllogenic FMT using METS-D decreases insulin sensitivity in metabolic syndrome recipients when compared with using post-RYGB-D. Further research is needed to delineate the role of donor characteristics in FMT efficacy in human insulin-resistant subjects.Trial registration numberNTR4327.

scholarly journals Visfatin levels in non-obese, obese, and insulin resistant adolescents

2017 ◽  
Vol 56 (5) ◽  
pp. 291
Author(s):  
Indra Ihsan ◽  
Eka Agustia Rini ◽  
Rismawati Yaswir
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Serum Insulin ◽  
Enzyme Linked Immunosorbent Assay ◽  
Model Assessment ◽  
Fasting Serum ◽  
Obese Adolescents ◽  
Insulin Resistant ◽  
Resistant Group ◽  
Visfatin Level

Background Adipose tissue is not merely a site for energy storage, but is also the largest endocrine organ, secreting various adipocytokines. Plasma visfatin, an adipocytokine predominantly secreted from visceral adipose tissue, has insulin-mimetic effects, and has been closely linked to insulin resistance.Objective To compare plasma visfatin levels between obese and non-obese adolescents, as well as between obese adolecents with and without insulin resistance.Methods This cross-sectional study was conducted in students who attended three senior high schools in Padang. Subjects comprised 28 obese and 28 non-obese adolescents. The age of the subjects ranged from 14-18 years. Obesity criteria were based on body mass index (BMI) measurements. Fasting serum glucose level was measured by glucose hexokinase photometry and serum insulin was measured by chemiluminesence immunoassay. Plasma visfatin was measured by enzyme-linked immunosorbent assay (ELISA). The insulin resistance index was estimated from fasting serum insulin and glucose levels using the homeostatic model assessment for insulin resistance (HOMA-IR). Differences in the variables were tested using independent T-test and Mann-Whitney test, depending on the distribution of the variables.Results The mean plasma visfatin level was significantly higher in the obese than in the control group [2.55 (SD 1.54) vs. 1.61 (SD 0.64) ng/mL, respectively; (P=0.005)]. The insulin resistant group had significantly higher mean plasma visfatin level than the non-resistant group [3.61 (SD 1.59) vs. 1.96 (SD 1.18) ng/mL, respectively; (P=0.004)].Conclusion Obese adolescents with insulin resistance have signifcantly higher plasma visfatin levels compared to those without insulin resistance.

Oral L-glutamine restores adenosine and glutathione content in the skeletal muscle and adipose tissue of insulin-resistant pregnant rats

Nutrition ◽  
2020 ◽  
Vol 77 ◽  
pp. 110789 ◽  
Author(s):  
Kehinde Samuel Olaniyi ◽  
Isaiah Woru Sabinari ◽  
Lawrence Aderemi Olatunji
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Pregnant Rats ◽  
Insulin Resistant
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