Hypolipidemic effect of Salicornia herbacea in animal model of type 2 diabetes mellitus

Abstract

To control blood glucose level as close to normal is a major goal of treatment of diabetes mellitus. Hyperglycemia and hyperlipidemia are the major risk factors for cardiovascular complications, the major cause of immature death among the patients with type 2 diabetes. The purpose of this study is to determine the hypoglycemic and hypolipidemic effects of Salicornia herbacea in animal model of type 2 diabetes and to investigate the possible mechanisms for the beneficial effects of S. herbacea. S. herbacea was extracted with 70% ethanol and desalted with 100% ethanol. Three week-old db/db mice (C57BL/KsJ, n=16) were fed AIN-93G semipurified diet or diet containing 1% desalted ethanol extract of S. herbacea for 6 weeks after 1 week of adaptation. Fasting plasma glucose, triglyceride, and total cholesterol were measured by enzymatic methods and blood glycated hemoglobin (HbA1C) by the chromatographic method. Body weight and food intake of S. herbacea group were not significantly different from those of the control group. Fasting plasma glucose and blood glycated hemoglobin levels tended to be lowered by S. herbacea treatment. Consumption of S. herbacea extract significantly decreased plasma triglyceride and cholesterol levels (p<0.05). The inhibition of S. herbacea extract against yeast α-glucosidase was 31.9% of that of acarbose at the concentration of 0.5 mg/mL in vitro. The inhibitory activity of ethanol extract of S. herbacea against porcine pancreatic lipase was 59.0% of that of orlistat at the concentration of 0.25 mg/mL in vitro. Thus, these results suggest that S. herbacea could be effective in controlling hyperlipidemia by inhibition of pancreatic lipase in animal model of type 2 diabetes.

3‐Caffeoyl, 4‐dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose‐induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK‐dependent pathway

“…Thus, the novel finding of the present study is that CDCQ beneficially regulates hepatic fatty acid metabolism through a SIRT and LKB1/AMPK-SREBP-1c pathway. Previous studies reported that S. herbacea exerted several pharmacological effects, including lowering blood glucose levels, inhibiting lipogenesis-related genes (SREBP-1a, FAS, GAPT), and PEPCK and glucose 6-phosphatase gene expression in the liver [27,28]. The present study demonstrated for the first time that CDCQ inhibited lipid accumulation in human hepatocytes through inhibition of SREBP-1c and FAS expression, with a detailed molecular mechanism, supporting previous reports of its therapeutic potential in lipogenesis.…”

Microbial biocatalysis of quercetin-3-glucoside and isorhamnetin-3-glucoside inSalicornia herbaceaand their contribution to improved anti-inflammatory activity

“…2,3,6 Multiple scholars have reported that S. herbacea exhibits multiple bioactive functionalities, including antioxidant, anticancer, anti-inammatory, osteoblastogenesis, antihyperglycemic, and anti-hyperlipidemic effects. [5][6][7][8][9][10][11][12][13][14] Recently, S. herbacea has been widely cultivated and processed in various forms as commercially available functional cosmetics, dietary supplements and medicines due to its proven health benets and marketing strengths. 1,3 Previous phytochemical studies revealed that S. herbacea contains bioactive molecules such as avonoids, minerals, and polysaccharides.…”

Production of novel vinegar having antioxidant and anti‐fatigue activities from Salicornia herbacea L.

“…Recently, many studies have focused on the health benefits of glasswort with respect to numerous diseases. For example, administration of glasswort extract has been shown to have hypolipidemic effects in an animal model of type 2 diabetes mellitus, along with hypocholesterolemic effects in rats fed a high‐cholesterol diet . Studies have also reported that intake of glasswort powder can reduce blood glucose and triglyceride levels in streptozotocin‐induced diabetic rats .…”