Improvement Effects of Trehangelin A on High-Fat Diet Causing Metabolic Clinical Conditions

Abstract

The purpose of this study is to determine whether or not trehangelin A (THG-A) is effective in treating the metabolic clinical condition caused by a high-fat diet. The body weight, epididymal adipose volume, alanine transaminase (ALT), total-cholesterol (T-CHO), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) and glucose concentrations in serum increased in mice fed a high-fat diet compared to mice fed a control diet. On the other hand, adiponectin level in serum of mice fed a high-fat diet decreased compared to that of control mice. When mice fed a high-fat diet were intraperitoneally administered THG-A of 20 mg/kg three times per week, the levels of TG and glucose in serum were significantly reduced compared to those fed high-fat without THG-A. Interestingly, the levels of high-density lipoprotein cholesterol (HDL-C) in serum were increased by THG-A administration in both mice fed a control diet and those fed high-fat diet. The decreased level of adiponectin by a high-fat diet was also recovered by THG-A treatment. The liver expression of mRNA from pro-inflammatory cytokines, including interleukin (IL)-6 and tumor necrosis factor (TNF)-α, were significantly increased in mice fed a high-fat diet compared to those fed a control diet. However, the increased IL-6 levels in mice fed a high-fat diet were significantly suppressed by THG-A treatment. Furthermore, the increased expression of TNF-α mRNA or COL1A2 mRNA by a high-fat diets tended to be decreased in mice treated with THG-A. These results show that THG-A treatment attenuates the progression of metabolic clinical conditions, suggesting its potential efficacy against obesity-related metabolic disorders.

Tilianin Protects against Nonalcoholic Fatty Liver Disease in Early Obesity Mice

“…6) Moreover, Oxidative stress is considered to be a pathway of hepatocyte injury and is closely related to inflammation and NASH onset. 7) NOD-like receptor protein 3 (NLRP3) inflammasome is widely reported as a factor that induces inflammation in NAFLD. 8,9) The sensor molecule NLRP3, aptamer protein ASC and effector molecule pro-caspase-1 constitute NLRP3 inflammasome, a cytoplasmic multiprotein scaffold.…”