scholarly journals A Regenerative Antioxidant Protocol of Vitamin E andα-Lipoic Acid Ameliorates Cardiovascular and Metabolic Changes in Fructose-Fed Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jatin Patel ◽  
Nur Azim Matnor ◽  
Abishek Iyer ◽  
Lindsay Brown
Keyword(s):  
Type 2 Diabetes ◽  
Vitamin E ◽  
Lipoic Acid ◽  
Fixed Combination ◽  
Natural Antioxidants ◽  
Collagen Deposition ◽  
Cardiovascular Damage ◽  
Male Wistar Rats ◽  
Tocotrienol Rich Fraction

Type 2 diabetes is a major cause of cardiovascular disease. We have determined whether the metabolic and cardiovascular changes induced by a diet high in fructose in young adult male Wistar rats could be prevented or reversed by chronic intervention with natural antioxidants. We administered a regenerative antioxidant protocol using two natural compounds:α-lipoic acid together with vitamin E (α-tocopherol alone or a tocotrienol-rich fraction), given as either a prevention or reversal protocol in the food. These rats developed glucose intolerance, hypertension, and increased collagen deposition in the heart together with an increased ventricular stiffness. Treatment with a fixed combination of vitamin E (eitherα-tocopherol or tocotrienol-rich fraction, 0.84 g/kg food) andα-lipoic acid (1.6 g/kg food) normalized glucose tolerance, blood pressure, cardiac collagen deposition, and ventricular stiffness in both prevention and reversal protocols in these fructose-fed rats. These results suggest that adequate antioxidant therapy can both prevent and reverse the metabolic and cardiovascular damage in type 2 diabetes.

Mutation of the 5' untranslated region stem-loop mRNA structure reduces type I collagen deposition and arterial stiffness in male obese mice

2021 ◽  
Author(s):  
Francisco I. Ramirez-Perez ◽  
Makenzie L. Woodford ◽  
Mariana Morales-Quinones ◽  
Zachary I. Grunewald ◽  
Francisco J Cabral-Amador ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Arterial Stiffness ◽  
Type I Collagen ◽  
Type I ◽  
Collagen Deposition ◽  
Wild Type ◽  
Stem Loop ◽  
Arterial Stiffening

Arterial stiffening, a characteristic feature of obesity and type 2 diabetes, contributes to the development and progression of cardiovascular diseases (CVD). Currently, no effective prophylaxis or therapeutics is available to prevent or treat arterial stiffening. A better understanding of the molecular mechanisms underlying arterial stiffening is vital to identify newer targets and strategies to reduce CVD burden. A major contributor to arterial stiffening is increased collagen deposition. In the 5' untranslated regions of mRNAs encoding for type I collagen, an evolutionally conserved stem-loop (SL) structure plays an essential role in its stability and post-transcriptional regulation. Here, we show that feeding a high fat/high sucrose (HFHS) diet for 28 weeks increases adiposity, insulin resistance, and blood pressure in male wild-type littermates. Moreover, arterial stiffness, assessed in vivo via aortic pulse wave velocity, and ex vivo using atomic force microscopy in aortic explants or pressure myography in isolated femoral and mesenteric arteries, was also increased in those mice. Notably, all these indices of arterial stiffness, along with collagen type I levels in the vasculature, were reduced in HFHS-fed mice harboring a mutation in the 5'SL structure, relative to wild-type littermates. This protective vascular phenotype in 5'SL-mutant mice did not associate with a reduction in insulin resistance or blood pressure. These findings implicate the 5'SL structure as a putative therapeutic target to prevent or reverse arterial stiffening and CVD associated with obesity and type 2 diabetes.

scholarly journals Effect of metformin on the expression of SNAER proteins in the skeletal muscle of rats with type 2 diabetes

2021 ◽  
pp. 270-278
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Snare Complex ◽  
Snare Proteins ◽  
Glucose Levels ◽  
Male Wistar Rats

Background and Aims: SNARE proteins are composed of a combination of SNAP-23, Stx-4, and VAMP-2 isoforms that are significantly expressed in skeletal muscle. These proteins control the transport of GLUT4 to the cell membranes. The modifications in the expression of SNARE proteins can cause Type 2 diabetes. The present study aimed to assess the effect of metformin on the expression of these proteins in rats. Materials and Methods: For the purpose of the study, 40 male Wistar rats were randomly selected. Streptozotocin and Nicotinamide were used for the induction of type 2 diabetes. The animals were assigned to five groups (n=8), including healthy and diabetic groups as control, as well as three experimental groups which were treated with different doses of metformin (100, 150, and 200 mg/kg body weight) for 30 days. The quantitative reverse transcription PCR (RT-qPCR) method was applied to evaluate the expression of SNARE complex proteins.. Results: Based on the results, metformin (100, 150, and 200 mg/kg body weight) decreased serum glucose levels and increased serum insulin levels. This difference in dose of 200 mg/kg body weight was statistically significant (P<0.05). Moreover, all three doses of metformin increased the expression of SNAP- 23, syntaxin-4, and VAMP-2 proteins in skeletal muscle tissue. Metformin at a dose of 200 mg/kg body weight demonstrated the most significant effects (P<0.05). Conclusion: As evidenced by the results of the current study, another anti-diabetic mechanism of metformin is to increase the expression of SNARE proteins, which effectively improves insulin resistance and lowers blood glucose.

scholarly journals Antioxidant status and hepato-protective role of Anchomanes difformis in streptozotocin-induced diabetes in male Wistar rats

2020 ◽  
Vol 66 (1) ◽  
pp. 18-36
Author(s):  
Toyin D. Alabi ◽  
Nicole L. Brooks ◽  
Oluwafemi O. Oguntibeju
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Aqueous Extract ◽  
Liver Dysfunction ◽  
Antioxidant Status ◽  
Wistar Rats ◽  
Serum Levels ◽  
Male Wistar Rats ◽  
Hepatic Injuries

SummaryIntroduction: The liver is involved in the metabolism of xenobiotics and their metabolites and it is vulnerable to oxidative damage. Hyperglycaemia is highly implicated in the progression of diabetes mellitus, and adversely affects the liver. Though, conventional hypoglycaemic drugs may be effective in reducing blood glucose, they do not appear to be effective in attenuating the progression of diabetes and its complications.Objective: This study evaluated the ameliorative effects of Anchomanes difformis on hyperglycaemia and hepatic injuries in type 2 diabetes.Methods: Type 2 diabetes was induced in male Wistar rats with a single intraperitoneal injection of streptozotocin (40 mg/kg BW) after two weeks of fructose (10%) administration. Aqueous extract of A. difformis (200 and 400 mg/kg BW) and glibenclamide (5 mg/kg BW) were administered orally for six weeks. Blood glucose concentrations were measured. Serum levels of liver dysfunction markers (ALT, AST, and ALP), total cholesterol, triglycerides, HDL- and LDL-cholesterol were investigated. Total protein, albumin, and globulin were also assessed. Antioxidant parameters: ORAC, GSH, GSSG, SOD, CAT and FRAP were evaluated in the liver while ORAC, FRAP and lipid peroxidation were determined in the serum. Histological examination of the liver tissue was carried out.Results: Treatment with aqueous extract of A. difformis significantly (p<0.05) reduced blood glucose and reversed steatosis in the diabetic-treated rats. The antioxidant status of diabetic-treated rats was significantly (p<0.05) improved. Serum levels of liver dysfunction markers were significantly (p<0.05) reduced in diabetic-treated rats.Conclusion: The findings in this study revealed that 400 mg/kgBW Anchomanes difformis was more effective than 200 mg/kg BW in ameliorating diabetes-induced hepatopathy, however, both doses of Anchomanes difformis demonstrated more antidiabetic ability than glibenclamide. Anchomanes difformis may be a novel and potential therapeutic agent in the management of diabetes and resulted hepatic injuries.

Sign in / Sign up

Export Citation Format

Share Document