scholarly journals β-Sitosterol Circumvents Obesity Induced Inflammation and Insulin Resistance by down-Regulating IKKβ/NF-κB and JNK Signaling Pathway in Adipocytes of Type 2 Diabetic Rats

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 2101
Author(s):  
Selvaraj Jayaraman ◽  
Nalini Devarajan ◽  
Ponnulakshmi Rajagopal ◽  
Shyamaladevi Babu ◽  
Senthil Kumar Ganesan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Signaling Pathway ◽  
Nuclear Factor Kappa B ◽  
Diabetic Rats ◽  
Nuclear Factor ◽  
Antidiabetic Drug ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway ◽  
Type 2 Diabetic

β-sitosterol (SIT), the most abundant bioactive component of vegetable oil and other plants, is a highly potent antidiabetic drug. Our previous studies show that SIT controls hyperglycemia and insulin resistance by activating insulin receptor and glucose transporter 4 (GLUT-4) in the adipocytes of obesity induced type 2 diabetic rats. The current research was undertaken to investigate if SIT could also exert its antidiabetic effects by circumventing adipocyte induced inflammation, a key driving factor for insulin resistance in obese individuals. Effective dose of SIT (20 mg/kg b.wt) was administered orally for 30 days to high fat diet and sucrose induced type-2 diabetic rats. Metformin, the conventionally used antidiabetic drug was used as a positive control. Interestingly, SIT treatment restores the elevated serum levels of proinflammatory cytokines including leptin, resistin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) to normalcy and increases anti-inflammatory adipocytokines including adiponectin in type 2 diabetic rats. Furthermore, SIT decreases sterol regulatory element binding protein-1c (SREBP-1c) and enhances Peroxisome Proliferator–activated receptor-γ (PPAR-γ) gene expression in adipocytes of diabetic rats. The gene and protein expression of c-Jun-N-terminal kinase-1 (JNK1), inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ) and nuclear factor kappa B (NF-κB) were also significantly attenuated in SIT treated groups. More importantly, SIT acts very effectively as metformin to circumvent inflammation and insulin resistance in diabetic rats. Our results clearly show that SIT inhibits obesity induced insulin resistance by ameliorating the inflammatory events in the adipose tissue through the downregulation of IKKβ/NF-κB and c-Jun-N-terminal kinase (JNK) signaling pathway.

Duodenal-jejunal exclusion improves insulin resistance in type 2 diabetic rats by upregulating the hepatic insulin signaling pathway

Nutrition ◽  
2015 ◽  
Vol 31 (5) ◽  
pp. 733-739 ◽  
Author(s):  
Ze-Qiang Ren ◽  
Peng-Bo Zhang ◽  
Xiu-Zhong Zhang ◽  
Shou-Kun Chen ◽  
Hong Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Diabetic Rats ◽  
Insulin Signaling Pathway ◽  
Hepatic Insulin Signaling ◽  
Type 2 Diabetic

Effects of Diet on Bile Acid Metabolism and Insulin Resistance in Type 2 Diabetic Rats after Roux-en-Y Gastric Bypass

2018 ◽  
Vol 28 (10) ◽  
pp. 3044-3053 ◽  
Author(s):  
Cheng-Xiang Shan ◽  
Nian-Cun Qiu ◽  
Miao-E Liu ◽  
Si-Luo Zha ◽  
Xin Song ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Bile Acid ◽  
Acid Metabolism ◽  
Diabetic Rats ◽  
Bile Acid Metabolism ◽  
Type 2 Diabetic

Lycopsamine Attenuates Diabetes Mellitus via The Nuclear Factor Kappa B-Induced 5′ Adenosine Monophosphate-Activated Protein Kinase Signal Pathway

2021 ◽  
Vol 20 (1) ◽  
pp. 169-176
Author(s):  
Jingfang Hu ◽  
Jie Jin ◽  
Yan Chen ◽  
Jinyi Wei ◽  
Hanbei Chen
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Protein Kinase ◽  
Nuclear Factor Kappa B ◽  
Adenosine Monophosphate ◽  
Interleukin 10 ◽  
Diabetic Rats ◽  
Nuclear Factor ◽  
Nonesterified Fatty Acids ◽  
Nuclear Factor Kappa

Diabetes mellitus is a metabolic disorder characterized by inflammation, abnormal glycolipid metabolism, insulin resistance, and mitochondrial dysfunction leading to hyperglycemia. The aim of the present investigation was to determine the efficacy of lycopsamine in a rat model of diabetes mellitus to understand its mechanism. Lycopsamine treatment markedly lowered the level of total cholesterol, triglyceride, nonesterified fatty acids, and low-density lipoprotein in diabetic rats. There was also a reduction in interleukin-6, interleukin-10, C-reactive protein, and tumor necrosis factor-α levels. Lycopsamine treatment normalized the metabolism of lipid and glucose, insulin resistance, and body weight of diabetic rats. Findings of immunohistochemical analyses exhibited rise in precipitation of immunocytes in renal cells. Results potentially demonstrated that lycopsamine treatment remarkably reduced the nuclear factor-kappa B level and enhanced the 5′ adenosine monophosphate-activated protein kinase expression. Altogether, administration of lycopsamine suppressed the expression of inflammatory cytokines and attenuated the metabolic symptoms in diabetes mellitus experimental rats.

scholarly journals SUN-656 Hypoglycemic Effect of Oral Administered Superoxide Dismutase

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shutao Liu ◽  
Hangqi Liu
Keyword(s):  
Insulin Resistance ◽  
Superoxide Dismutase ◽  
Resistance Index ◽  
Diabetic Rats ◽  
Hypoglycemic Effect ◽  
Model Group ◽  
Curative Effect ◽  
Insulin Resistance Index ◽  
Type 2 Diabetic

Abstract Hypoglycemic Effect of Oral Administered Superoxide Dismutase on Type 2 Diabetes via reduction of glucogan and insulin resistance Background & Objective: Superoxide dismutase (SOD) is carefully used in food industry for the concern of its easy degradation and difficult adsorption in digestive tract, although it plays central role in antioxidant system. It is previous reported that orally administered SOD was effective in alleviating hyperglycemia, cerebral ischemia-reperfusion and chronic hepatitis. This work aimed to investigate in-depth the hypoglycaemic effect and possible mechanism of orally administered SOD in the model of type 2 diabetic rats. Methods:The model of type 2 diabetic rats were divided into 6 groups and orally administered with different Cu/Zn-SOD (abbreviated as SOD) samples and negative or positive controls. The 6 groups included SOD, SOD hydrolysate (pepsin-treated SOD), L-SOD (liposome-embedded SOD), model group and metformin positive groups, as well as normal group. Results of the body weight, serum indexes (including blood glucose, glycated albumin, insulin, glucagon, AMPK, MDA), SOD enzymatic activity in organs (liver, heart, kidney, skeletal muscle, spleen, and pancreas) as well as intestinal density and HE staining were measured to evaluate the hypoglycemic effect and possible mechanism. Results: SOD showed substantial hypoglycemic effect and improved serum indicators. Moreover, L-SOD group exhibited better effect than SOD group, though the effect of SOD hydrolysate was not obvious. Colon density and HE staining showed obvious intestinal injury in the model group, and SOD was beneficial to repair intestinal structural integrity. Furthermore, the reparative effect of SOD was much better than that of the SOD hydrolysate, but not as good as that of the L-SOD. The SOD enzymatic activity of tissues was positively correlated with the curative effect of three kinds of SOD samples. The contents of serum MDA were negatively correlated with the curative effect. Compared with the model group, the insulin resistance index of SOD group, L-SOD group and positive group were significantly reduced; and glucagon significantly decreased by 68.38, 77.50 and 65.01%, respectively. Conclusion: Oral SOD showed obvious hypoglycemic effect on type 2 diabetic rats, and liposome could improve this effect. The mechanism may be that SOD effectively reduces intestinal injury, so as to reduce glucongen and insulin resistance index.

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