Oral Administration ofHoodia parvifloraAlleviates Insulin Resistance and Nonalcoholic Steatohepatitis

Abstract

Metabolic syndrome is recognized as a proinflammatory condition leading to hepatic steatosis and nonalcoholic steatohepatitis (NASH). We tested the effects of a succulent species Hoodia parviflora N.E. Br., of the genus Hoodia sweetex Dence, on animal models of NASH and insulin resistance (ob/ob mouse and the sand rat Psammomys obesus). IL6 secretion was evaluated by ELISA and hepatic signal transducer and activator of transcription 3 by Western blot. We followed liver enzymes, weight, glucose, hepatic histology, hepatic triglycerides (TGs), and total fat and serum insulin. Oral administration of extracts derived from H. parviflora alleviated the insulin resistance manifested by improved glucose tolerance tests. Treatment alleviated the liver injury noted by a decrease in liver enzyme levels, improved intrahepatic TG content, total hepatic fat, and improved hepatic histology. Similarly, treatment with H. parviflora reduced hepatic inflammation in mice with Concanavalin A-induced hepatitis. These effects were independent of food consumption and weight. H. parviflora was associated with alleviated insulin resistance, hepatic steatosis, and liver injury. The data support its use as a liver protector.

Increased hepatic Akt phosphorylation alleviated glucose intolerance and improved liver function in leptin-deficient mice

“…These effects were attributed to the potential immunomodulatory effect of GSLs [19,37]. They also support a potential oralimmunotherapy-based mechanism of action recently described for several compounds [21,25,29,[37][38][39][40][41][42][43][44][45][46][47][48].…”

Therapeutic effects of myocardin-related transcription factor A (MRTF-A) knockout on experimental mice with nonalcoholic steatohepatitis induced by high-fat diet

“…22 Because of insulin resistance, the body would present lipid metabolism disorder with significantly increased lipolysis of fat tissues, thus a lot of free fatty acids would be released into the blood to promote liver intake of free fatty acids from the blood, thereby eventually inducing lipid accumulation in liver cells, especially TG accumulation, which is directly related to the development and progression of NASH. 23,24 From this study, MRTF-A knockout can reduce the blood glucose, plasma insulin and hepatic TG of NASH mice. In the similar vein, another study also reported that MRTF-A deficiency can effectively ameliorate HFD-induced obesity, inflammatory responses, insulin resistance and hepatic steatosis.…”

Natural Products: New Hope for Nonalcoholic Steatohepatitis?

“…However, latestage programs have thus far shown marginal efficacy and have troubling safety signals, suggesting the need for alternative approaches. In this issue of the journal, Mizrahi et al 12 provide promising data demonstrating antiinflammatory effects of Hoodia extracts (Hesperaloe parviflora), which result in marked improvements in chemically induced immune hepatitis. They further show that H. parviflora improves glucose tolerance as well as hepatic triglycerides and liver histology in both genetic (ob/ob mice) and nutritionally induced (high-energy diets) models of NAFLD/NASH.…”