Antiobesity efficacy of asiatic acid: down-regulation of adipogenic and inflammatory processes in high fat diet induced obese rats.

In the current study, we evaluated the effects of Asiatic acid (AA) on lipid metabolic markers in HFD-induced obese Sprague-Dawley rat model. AA (20 mg/kg BW) was administered orally to HFD-fed rats for 42 days. Changes in body composition, glucose, insulin resistance (IR) and lipid profiles of tissues, plasma and the pattern of gene expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) and its target genes fatty-acid synthase (FAS), adipocyte protein-2 (aP2) and uncoupling protein-2 (UCP-2) and pro-inflammatory factor tumor necrosis factor (TNF)-α were observed in experimental rats. Oral administration of AA exerts therapeutic effects similar to orlistat in attenuating body weight gain, glucose, IR, plasma and tissue lipids and mRNA levels of PPAR-γ, FAS, aP2 and inflammatory factor TNF-α and increasing UCP-2 expression in HFD-fed rats. Hence, these findings concluded that AA attenuate HFD-induced obesity by modulating PPAR-γ and its target genes and regulate lipid metabolism, suggesting their possible antiobesity effects.

Obesity-alleviating potential of asiatic acid and its effects on ACC1, UCP2, and CPT1 mRNA expression in high fat diet-induced obese Sprague-Dawley rats.

The present study evaluated the effects of asiatic acid (AA), a pentacyclic triterpenoid from Centella asiatica on lipid metabolism parameters in a rat model of obesity induced using a high fat diet (HFD) for 42 days. AA (20 mg/kg body weight [BW]) was administered orally once daily for 42 days, and an orlistat-treated group of rats (10 mg/kg BW) was included for comparison. Changes in BW, blood glucose levels, insulin resistance and leptin, adiponectin, amylase, and lipase levels in the blood; lipid profiles of plasma; liver antioxidants levels; and acetyl CoA carboxylase(ACC), uncoupling protein-2 (UCP2), and carnitine palmitoyltransferase-1 (CPT1) mRNA expression were observed in the experimental rats. Our results revealed that AA (20 mg/kg BW), similar to orlistat, reduced the increase in BW; increased bone mineral contents and bone mineral densities; reduced blood glucose levels, insulin resistance, leptin, plasma lipid levels; increased adiponectin, amylase, lipase levels in the blood; showed antioxidant activity; and altered mRNA expression of lipid metabolism-related genes, including ACC, UCP 2, and CPT 1, in the HFD-fed rats. From these results, we concluded that AA possesses significant anti-obesity potential through the suppression of BW gain, lipid lowering action, development of insulin and leptin sensitivity, antioxidant activity, and increased mRNA expression of lipid metabolism-related genes.

Reversal of endothelial dysfunction in aorta of streptozotocin-nicotinamide-induced type-2 diabetic rats by S-Allylcysteine.

Dietary measures and plant-based therapies as prescribed by native systems of medicine have gained attraction among diabetics with claims of efficacy. The present study investigated the effects of S-Allylcysteine (SAC) on body weight gain, glucose, insulin, insulin resistance, and nitric oxide synthase in plasma and argininosuccinate synthase (AS) and argininosuccinate lyase (ASL), lipid peroxides and antioxidant enzymes in aorta of control and streptozotocin-nicotinamide (STZ-NA)-induced diabetic rats. Changes in body weight, glucose, insulin, insulin resistance, and antioxidant profiles of aorta and mRNA expressions of nitric oxide synthase, AS, and ASL were observed in experimental rats. SAC (150 mg/kg b.w) showed its therapeutic effects similar to gliclazide in decreasing glucose, insulin resistance, lipid peroxidation, and increasing body weight; insulin, antioxidant enzymes, and mRNA levels of nitric oxide synthase, argininosuccinate synthase, and argininosuccinate lyase genes in STZ-NA rats. Histopathologic studies also revealed the protective nature of SAC on aorta. In conclusion, garlic and its constituents mediate the anti-diabetic potential through mitigating hyperglycemic status, changing insulin resistance by alleviating endothelial dysregulation in both plasma and tissues.