Abstract
Obesity and its associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are a particular worldwide health problem at present. Momordica cochinchinensis (MC) is consumed widely in Southeast Asia. However, whether it has functional effects on fat-induced metabolic syndrome remains unclear. This study was conducted to examine the prevention effect of Momordica cochinchinensis aril (MCA) on obesity, non-alcoholic fatty liver and insulin resistance in mice. MCA protected the mice against high-fat diet (HFD)-induced body weight gain, hyperlipidemia and hyperglycemia, compared with mice that were not treated. MCA inhibited the expansion of adipose tissue and adipocyte hypertrophy. In addition, the insulin sensitivity-associated index that evaluates insulin function was also significantly restored. MCA also regulated the secretion of adipokines in HFD-induced obese mice. Moreover, hepatic fat accumulation and liver damage were reduced, which suggested that fatty liver was prevented by MCA. Furthermore, MCA supplementation suppressed hepatic lipid accumulation by activation of the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) signaling pathway in the human fatty liver HuS-E/2 cell model. Our data indicate that MCA altered the microbial contents of the gut and modulated microbial dysbiosis in the host, and consequently is involved in the prevention of HFD-induced adiposity, insulin resistance and non-alcoholic fatty liver disease.
Highlights
As a leading public health issue, obesity has been shown to be associated with various chronic diseases and metabolic disorder, such as cardiovascular diseases, hypertension, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and various cancers [1,2].Studies have shown that a high fat diet may be a risk factor for the development of obesity and metabolic diseases [3]
The food efficiency ratios (FER) of the high-fat diet (HFD)-Momordica cochinchinensis aril (MCA) groups were significantly lower than the HFD group (Figure 1C)
We found the levels of plasma glutamic oxaloacetic transaminase (GOT) and plasma glutamic pyruvic transaminase (GPT) were upregulated in HFD mice and this increase was prevented significantly by treatment with 3% MCA (Figure 4E,F)
Summary
As a leading public health issue, obesity has been shown to be associated with various chronic diseases and metabolic disorder, such as cardiovascular diseases, hypertension, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and various cancers [1,2]. Studies have shown that a high fat diet may be a risk factor for the development of obesity and metabolic diseases [3]. The liver is one of the major organs involved in fat metabolism. NAFLD is a form of chronic fatty liver disease that is linked to diet and obesity. NAFLD may cause hepatic damage and progression to other chronic conditions, in which steatosis progresses to non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and hepatocellular carcinoma [4,5]
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