Allyl methyl sulfide, a garlic active component mitigates hyperglycemia by restoration of circulatory antioxidant status and attenuating glycoprotein components in streptozotocin-induced experimental rats.

Diabetes is a major noncommunicable life-threatening chronic and pervasive condition that is consuming the world health in a petrifying rate. The circulatory system is one of the major sources of hyperglycemia-induced ROS generation. Historically, garlic has been revered as part of a healthful diet. Organosulfur compounds have been attributed to the medicinal properties and health benefits of garlic. The present study focuses on the ameliorative role of allyl methyl sulfide (AMS) in combating diabetic complications in diabetic rats. Male Wistar rats were randomly divided into four groups. Experimental diabetes was induced by a single intraperitoneal injection (i.p), of streptozotocin (STZ) (40 mg/kg b.w). STZ treated diabetic rats showed significant augment in plasma glucose level, lipidperoxidative (LPO) markers, glycoprotein components (hexose, hexosamine, sialic acid, and fucose), and significant decline in plasma insulin level, nonenzymatic antioxidants and activities of antioxidant enzymes in the circulatory system and tissues. Further, periodic acid-Schiff (PAS) staining of hepatic and renal tissues revealed positive stain accumulation and Western blot investigation of glucose transporter 2 (GLUT 2) in pancreas of STZ-induced hyperglycemic rats. Dietary intervention with AMS (100 mg/kg b.w) for 30 days demonstrated significant protective effects on all the biochemical parameters studied. Besides, biochemical findings were corroborated by histological exertion and Western blot study. The findings of current investigations recommended that AMS can ameliorate the consequences of diabetes due to their antioxidant efficacy and can be used as a potential therapeutic approach. Further studies are warranted to explore the clinical application of AMS.

Allyl methyl sulfide, an organosulfur compound alleviates hyperglycemia mediated hepatic oxidative stress and inflammation in streptozotocin - induced experimental rats.

Therapeutic approaches based on dietary compounds obtained from food products to handle diabetes involving oxidative stress and inflammation. Garlic is a common spice and has a long history as a folk remedy. Allyl methyl sulfide (AMS) is a potential garlic-derived organosulfur compound displaying a substantial range of optimistic actions in various diseases. Herein, we investigated the potential role of AMS in ameliorating the effects of oxidative stress and inflammation in the liver of streptozotocin (STZ)-induced experimental rats. Diabetes was induced by single intraperitoneal (i.p.) injection of STZ (40 mg/kg/b.w). STZ-induced hyperglycemic rats received daily intragastric doses of 50, 100 and 200 mg/kg/b.w of the AMS for 30 days. Dietary intervention of AMS (100 mg/kg b.w) resulted in significant attenuation in blood glucose and expression of pro-inflammatory markers TNF-α, IL-6, NF-κB p65 unit and significant elevation in the plasma insulin level. Moreover, AMS instigated a marked enhance in the levels of hepatic tissue non enzymatic antioxidants and the activities enzymatic antioxidants of diabetic rats with significant decline in lipid peroxides and hydroperoxides formation, serum biomarkers of liver damage, thus representing the protecting efficacy of AMS in hyperglycemic state. The pathological abnormalities in hepatic tissues of diabetic rats were significantly ameliorated by AMS supplementation and offered great support to the biochemical findings. These conclusions explicate the prospective use of AMS as a promising compound against glucotoxicity mediated hepatic oxidative dysfunction in rats. Clinical trials in validating this benefit for optimizing the AMS nutrition are however warranted.

Betanin exhibits significant potential as an antihyperglycemic and attenuating the glycoprotein components in streptozotocin-nicotinamide-induced experimental rats.

This study hypothesized to evaluate the effect of betanin, a chromoalkaloid on plasma and altered tissues glycoprotein components in streptozotocin-nicotinamide-induced diabetic rats. Diabetes was induced by a single intraperitoneal (i.p.) injection of streptozotocin (45 mg/kg b.w.) dissolved in 0.1 M citrate buffer (pH 4.5) 15 min after the i.p. administration of nicotinamide (110 mg/kg b.w.). Experimental rats were administered betanin at the dose of 20 mg/kg b.w. and glibenclamide (600 µg/kg b.w.) once a day for 30 days. Diabetic rats revealed significant (p < 0.05) increase in the levels of glucose, HbA1C, hexose, hexosamine, sialic acid and fucose in the plasma; decrease in the levels of plasma insulin, Hb and sialic acid in the liver and kidney; significant (p < 0.05) increase in hexose, hexosamine and fucose in the liver and kidney. Moreover, periodic acid-Schiff staining of tissues revealed positive-stain accumulation in diabetic rats. On co-supplementation of betanin and glibenclamide to diabetic rats for the period of 30 days brought back the levels of plasma and tissues glycoprotein components. Based on the present study, we propose that betanin possesses significant protective effect on glycoprotein components in plasma and tissue of diabetic rats.

Antidiabetic and antihyperlipidemic activity of p-coumaric acid in diabetic rats, role of pancreatic GLUT 2: In vivo approach.

P-coumaric acid (p-CA, 3-[4-hydroxyphenyl]-2-propenoic acid), the major component widely found in nutritious plant foods, has various antioxidant, antiinflammatory and anticancer property. To evaluate the antidiabetic and antihyperlipidemic mechanisms, via the effects on carbohydrate, lipids and lipoproteins responses in adult male albino Wistar rats were examined by treated with p-CA. Rats were injected with streptozotocin (STZ, 40mg/kg b.w.) by intraperitonially (i.p.) 30days for the induction of experimental diabetes mellitus. Diabetic rats were treated with p-CA orally at a dose of 100mg/kg b.w. The potential defending character of p-CA against diabetic rats was evaluated by performing the various biochemical parameters and glucose transporter such as GLUT2 mRNA expression of pancreas. Administration of p-CA significantly lowers the blood glucose level, gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-bisphosphatase whereas increases the activities of hexokinase, glucose-6 phosphatase dehydrogenase and GSH via by increasing level of insulin. p-CA reduces the total cholesterol and triglycerides in both plasma and tissues i.e. liver and kidney. p-CA also decreases the LDL-C, VLDL-C and it considerably increase the level of HDL-C. A significant decreased expression of GLUT 2 mRNA in the pancreas was recorded in the supplementation of p-CA treated groups. Taken together, these results suggest that p-CA modulates glucose and lipid metabolism via GLUT 2 activation in the pancreatic and has potentially beneficial effects in improving or treating metabolic disorders.

Evaluation of antioxidant and stabilizing lipid peroxidation nature of Solanum xanthocarpum leaves in experimentally diethylnitrosamine induced hepatocellular carcinogenesis.

Solanum xanthocarpum Schrad. & Wendl, is a traditional edible leaves as a form of decoction, extracts used as a herbal medicine, and consumed for health promoting profiles. The present investigation was carried out to evaluate antioxidant status and lipid peroxidation level of anticancer activity of Solanum xanthocarpum (SXC) on Diethylnitrosamine (DEN) induced hepato carcinogenesis in male Wistar albino rats. Hepatic cancer was developed on the liver of Wistar rats treated by DEN or vehicle three times a week for 16 weeks. Tumour incidence, tumour volume, tumour burden, lipid peroxidation, antioxidant, liver marker enzymes and histopathological changes were assessed in DEN alone and in DEN+SXC leaves extract treated rats. Hundred percent tumour incidences with an imbalance in carcinogen metabolizing enzymes and cellular redox status were observed in rats treated with DEN alone. Oral administration of SXC aqueous leaves extract treatment at a dose of 150mg/kg b.w. to DEN treated rats were prevented tumour incidence and restored the elevated activities of liver marker enzymes and antioxidant status to near normal with decreased lipid peroxide levels. The biochemical consistent with histopathological observations suggesting marked hepatoprotective effect of the leaves extract in a dose dependent manner. These results clearly suggest that SXC aqueous leaves extract treatment prevents liver damage, lipid peroxidation, protects the antioxidant defense system and anti-carcinogenic potential in DEN induced hepatic carcinogenesis.

Effect of Bisphenol-A on insulin signal transduction and glucose oxidation in liver of adult male albino rat.

Bisphenol-A (BPA) has been classified as an endocrine disruptor which disrupts normal cell function by acting as an estrogen agonist. Environmentally relevant doses of the Bisphenol-A have profound effects on rat endocrine pancreas, an essential organ involved in glucose homeostasis. Bisphenol-A acts on insulin releasing ß-cells whereby it increases the pancreatic insulin content and secretion and also favours post prandial hyperinsulinemia and insulin resistance in male mice. Liver plays a central role in the control of glucose production and regulation of insulin secretion. It is one of the primary organs that are initially confronted by damage from toxic substances, xenobiotics and environmental hormones. The present study was designed to assess the effect of Bisphenol-A on insulin signal transduction and glucose oxidation in liver of adult male albino rat. Wistar strain albino rats were selected and divided into three groups, Group-I: Control, Group-II: 20 mg BPA treated, Group-III: 200 mg BPA treated. The IR (insulin receptor) and Akt (PKB: protein kinase B) mRNA and protein showed a decreased expression pattern in the high dose group. Eventhough there was an increase in serum insulin and a decrease in serum testosterone levels in the high dose group, the fasting blood glucose level remained unaltered. Glucose oxidation and glycogen content were found to be decreased in both high and low dose treated groups. Results of this study suggest that Bisphenol-A treatment impairs hepatic glucose oxidation and glycogen content through defective insulin signal transduction.