An optimized dose of raspberry ketones controls hyperlipidemia and insulin resistance in male obese rats: Effect on adipose tissue expression of adipocytokines and Aquaporin 7

2018 ◽  
Vol 832 ◽  
pp. 81-89 ◽  
Author(s):  
Eman T. Mehanna ◽  
Bassant M. Barakat ◽  
Mohamed H. ElSayed ◽  
Mona K. Tawfik
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expression ◽  
Obese Rats ◽  
Aquaporin 7

scholarly journals Adipose tissue expression of CCL19 chemokine is positively associated with insulin resistance

2018 ◽  
Vol 35 (2) ◽  
pp. e3087 ◽  
Author(s):  
Shihab Kochumon ◽  
Fatema Al-Rashed ◽  
Mohamed Abu-Farha ◽  
Sriraman Devarajan ◽  
Jaakko Tuomilehto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expression

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 RBP4: A Culprit for Insulin Resistance in End Stage Renal Disease That Can Be Cleared by Hemodiafiltration

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Fabrizio Grosjean ◽  
Pasquale Esposito ◽  
Rosario Maccarrone ◽  
Carmelo Libetta ◽  
Antonio Dal Canton ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Kidney Transplant ◽  
Glucose Transporter ◽  
Serum Levels ◽  
Tissue Expression ◽  
Serum Glucose ◽  
Retinol Binding Protein ◽  
Retinol Binding Protein 4 ◽  
Glut4 Expression

Introduction. Retinol Binding Protein 4 (RBP4) is mainly excreted by the kidney and plays a pivotal role in insulin resistance (IR). In our study, we evaluated the association between RBP4 and IR in hemodialysis subjects (HD). We also assessed how circulating RBP4 could be influenced by kidney transplant or different dialytic techniques.Methods. RBP4 serum levels were evaluated in HD (n=16) and matched healthy controls (C;n=16). RBP4 and glucose transporter type 4 (GLUT4) mRNA expressions were also determined in adipose tissue. Circulating RBP4 was evaluated after kidney transplant (n=7) and in hemodialysis patients (n=10) enrolled in a cross-over study treated with standard bicarbonate dialysis (BD) or hemodiafiltration (HDF).Results. HOMA index (P<0.05) and serum RBP4 (P<0.005) were higher in HD compared to C. RBP4 levels positively correlated with fasting serum glucose (P<0.05). RBP4 mRNA was lower in HD compared to C (P<0.05) and positively correlated with kidney function (P<0.05) and GLUT4 mRNA (P<0.001). Transplant or HDF reduced circulating RBP4 (P<0.01andP<0.05, resp.). Our results demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are effective in lowering serum RBP4 levels.

Modifications of glucose and lipid metabolism in cold-acclimated lean and genetically obese rats

1994 ◽  
Vol 76 (3) ◽  
pp. 1106-1112 ◽  
Author(s):  
E. Bobbioni-Harsch ◽  
F. Assimacopoulos-Jeannet ◽  
B. Jeanrenaud
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Turnover Rate ◽  
Glucose Utilization ◽  
Liver Lipid ◽  
Lipid Synthesis ◽  
Glucose Turnover ◽  
Muscle Insulin Resistance ◽  
Brown Adipose ◽  
Obese Rats

Glucose turnover rate, 2-deoxy-D-[3H]glucose (2-DG) uptake, lipid synthesis in liver, white adipose tissue, and brown adipose tissue (BAT) were measured in lean FA/FA and genetically obese fa/fa rats either kept at 21 degrees C or acclimated to a cold environment (4 degrees C). After 10 days at 4 degrees C, lean rats increased their glucose turnover rate; 2-DG uptake as well as lipid synthesis in BAT were markedly stimulated. After cold acclimation, obese rats also increased glucose turnover; however, BAT glucose utilization was only slightly stimulated. Basal hyperinsulinemia and muscle insulin resistance of the obese group (as assessed by reduced 2-DG uptake in the soleus muscle) were present at room temperature and persisted at 4 degrees C. Total BAT lipid synthesis was increased to the same extent as in lean rats. Obese rat liver lipid synthesis, already much higher than normal at 21 degrees C, was further increased by cold exposure. We conclude that obese cold-acclimated fa/fa rats do not improve their muscle insulin resistance and barely improve BAT glucose utilization. We further suggest that an additional activation of hepatic lipid synthesis and oxidation thereof could participate in the heat production needed by the cold-acclimated obese rats.

Insulin sensitizer YM268 ameliorates insulin resistance by normalizing the decreased content of GLUT4 in adipose tissue of obese Zucker rats

1997 ◽  
pp. 693-700 ◽  
Author(s):  
A Shimaya ◽  
O Noshiro ◽  
R Hirayama ◽  
T Yoneta ◽  
K Niigata ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Transporter ◽  
Zucker Rats ◽  
Epididymal Adipose Tissue ◽  
Maximum Effect ◽  
Insulin Sensitizer ◽  
Peripheral Insulin Resistance ◽  
Obese Rats ◽  
Obese Zucker Rats

Genetically obese Zucker rats exhibit mild hyperglycaemia and hyperinsulinaemia suggesting the existence of peripheral insulin resistance. We have examined the effects of YM268, an analogue of thiazolidinedione, on the content and translocation of a glucose transporter (GLUT4) in epididymal adipose tissue in 11-week-old obese and lean Zucker rats. The administration of YM268 at a dose of 10 mg/kg for 2 weeks ameliorated hyperglycaemia, hyperinsulinaemia, and impaired glucose tolerance after glucose load in obese rats. The GLUT4 content per fat pad in obese rats was reduced to 36% of that in lean littermates. Obese rats treated with YM268 increased GLUT4 concentrations in their fat pads from a basal value of 36% up to 191% of the level in lean rats. Furthermore, in adipocytes prepared from obese rats, an increase in the ratio of GLUT4 in plasma membrane to the total amount of GLUT4 (PM-GLUT4 ratio) induced by the submaximal concentration of insulin (0.3 nmol/l) was significantly attenuated compared with that in lean rats. But the maximum effect of insulin (3 nmol/l) was not attenuated. Meanwhile, YM268 had no significant effect on the attenuated PM-GLUT4 ratio in response to insulin in obese rats. These data suggested that one of the mechanisms by which YM268 improved insulin resistance in obese Zucker rats was to normalize the decreased GLUT4 content in the adipose tissue.

Increased adipose tissue expression of Grb14 in several models of insulin resistance

2004 ◽  
Vol 18 (9) ◽  
pp. 965-967 ◽  
Author(s):  
Bertrand Cariou ◽  
Nadège Capitaine ◽  
Véronique Le Marcis ◽  
Nathalie Vega ◽  
Véronique Béréziat ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expression

scholarly journals Adipose Tissue Expression of the Glycerol Channel Aquaporin-7 Gene Is Altered in Severe Obesity But Not in Type 2 Diabetes

2007 ◽  
Vol 92 (9) ◽  
pp. 3640-3645 ◽  
Author(s):  
V. Ceperuelo-Mallafré ◽  
M. Miranda ◽  
M. R. Chacón ◽  
N. Vilarrasa ◽  
A. Megia ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Severe Obesity ◽  
Tissue Expression ◽  
Aquaporin 7

scholarly journals Increased adipose tissue expression of IL-18R and its ligand IL-18 associates with inflammation and insulin resistance in obesity

2017 ◽  
Vol 5 (3) ◽  
pp. 318-335 ◽  
Author(s):  
Rasheed Ahmad ◽  
Reeby Thomas ◽  
Shihab Kochumon ◽  
Sardar Sindhu
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Expression

scholarly journals Improvement of Insulin Sensitivity after Peroxisome Proliferator-Activated Receptor-α Agonist Treatment Is Accompanied by Paradoxical Increase of Circulating Resistin Levels

Endocrinology ◽  
2006 ◽  
Vol 147 (9) ◽  
pp. 4517-4524 ◽  
Author(s):  
M. M. Haluzik ◽  
Z. Lacinova ◽  
M. Dolinkova ◽  
D. Haluzikova ◽  
D. Housa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Liver Steatosis ◽  
Tissue Expression ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Insulin Levels ◽  
Fenofibrate Treatment ◽  
Adiponectin Mrna

We studied the effect of peroxisome proliferator-activated receptor-α (PPAR-α) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-α agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-α activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.

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