Chitooligosaccharide Biguanide Repairs Islet β‐Cell Dysfunction by Activating the IRS‐2/PI3K/Akt Signaling Pathway in Type 2 Diabetic Rats

2019 ◽  
Vol 2 (5) ◽  
pp. 1800136 ◽  
Author(s):  
Yalu Zou ◽  
Yuanyuan Wang ◽  
Shengsheng Zhang ◽  
Yuntang Wu ◽  
Xiaofei Liu
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Diabetic Rats ◽  
Akt Signaling Pathway ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Type 2 Diabetic

scholarly journals Body temperature elevation during exercise is essential for activating the Akt signaling pathway in the skeletal muscle of type 2 diabetic rats

PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0205456 ◽  
Author(s):  
Takamasa Tsuzuki ◽  
Toshinori Yoshihara ◽  
Noriko Ichinoseki-Sekine ◽  
Ryo Kakigi ◽  
Yuri Takamine ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Temperature ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Diabetic Rats ◽  
Temperature Elevation ◽  
Akt Signaling Pathway ◽  
Type 2 Diabetic

Upregulation of PPARγ by Aegle marmelos Ameliorates Insulin Resistance and β-cell Dysfunction in High Fat Diet Fed-Streptozotocin Induced Type 2 Diabetic Rats

2011 ◽  
Vol 25 (10) ◽  
pp. 1457-1465 ◽  
Author(s):  
Ashok Kumar Sharma ◽  
Saurabh Bharti ◽  
Sameer Goyal ◽  
Sachin Arora ◽  
Saroj Nepal ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
High Fat ◽  
Aegle Marmelos ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Type 2 Diabetic

scholarly journals Up-regulation of PPARγ, heat shock protein-27 and -72 by naringin attenuates insulin resistance, β-cell dysfunction, hepatic steatosis and kidney damage in a rat model of type 2 diabetes

2011 ◽  
Vol 106 (11) ◽  
pp. 1713-1723 ◽  
Author(s):  
Ashok Kumar Sharma ◽  
Saurabh Bharti ◽  
Shreesh Ojha ◽  
Jagriti Bhatia ◽  
Narender Kumar ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Diabetic Rats ◽  
Kidney Damage ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Hsp 27 ◽  
Liver And Kidney ◽  
Type 2 Diabetic

Naringin, a bioflavonoid isolated from grapefruit, is well known to possess lipid-lowering and insulin-like properties. Therefore, we assessed whether naringin treatment ameliorates insulin resistance (IR), β-cell dysfunction, hepatic steatosis and kidney damage in high-fat diet (HFD)–streptozotocin (STZ)-induced type 2 diabetic rats. Wistar albino male rats were fed a HFD (55 % energy from fat and 2 % cholesterol) to develop IR and on the 10th day injected with a low dose of streptozotocin (40 mg/kg, intraperitoneal (ip)) to induce type 2 diabetes. After confirmation of hyperglycaemia (>13·89 mmol/l) on the 14th day, different doses of naringin (25, 50 and 100 mg/kg per d) and rosiglitazone (5 mg/kg per d) were administered orally for the next 28 d while being maintained on the HFD. Naringin significantly decreased IR, hyperinsulinaemia, hyperglycaemia, dyslipidaemia, TNF-α, IL-6, C-reactive protein and concomitantly increased adiponectin and β-cell function in a dose-dependent manner. Increased thiobarbituric acid-reactive substances and decreased antioxidant enzyme activities in the serum and tissues of diabetic rats were also normalised. Moreover, naringin robustly increased PPARγ expression in liver and kidney; phosphorylated tyrosine insulin receptor substrate 1 in liver; and stress proteins heat shock protein (HSP)-27 and HSP-72 in pancreas, liver and kidney. In contrast, NF-κB expression in these tissues along with sterol regulatory element binding protein-1c and liver X receptor- expressions in liver were significantly diminished. In addition, microscopic observations validated that naringin effectively rescues β-cells, hepatocytes and kidney from HFD-STZ-mediated oxidative damage and pathological alterations. Thus, this seminal study provides cogent evidence that naringin ameliorates IR, dyslipidaemia, β-cell dysfunction, hepatic steatosis and kidney damage in type 2 diabetic rats by partly regulating oxidative stress, inflammation and dysregulated adipocytokines production through up-regulation of PPARγ, HSP-27 and HSP-72.

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