Abstract
Obesity is closely associated with various metabolic disorders, including leptin resistance, which is characterized by high circulating leptin levels. Probiotics can decrease circulating leptin levels by alteration of the gut microbiota. Thus, they may have anti-obesogenic effects. In this study, the effects of administration of a probiotic bacterium, Lactobacillus rhamnosus GG (LGG), on gut microbiota and modulation of leptin resistance were evaluated in mice. Male Balb/C mice aged 7 weeks were fed either a normal diet (ND), high-fat diet (HFD), HFD supplemented with low-dose LGG (108 CFU/mouse/day), or HFD supplemented with high-dose LGG (1010 CFU/mouse/day) for 10 weeks. Significantly increased body weight, epididymal fat weight, and decreased leptin responsiveness to exogenous leptin treatment and ratio of villus height to crypt depth were observed in the HFD-fed mice compared to the ND-fed mice. Moreover, a remarkable increase in the proportion of Proteobacteria and ratio of Firmicutes/Bacteroidetes in the fecal microbiota were also observed in the HFD-fed mice. Supplementation of HFD with high-dose LGG restored exogenous leptin responsiveness, increased the ratio of villus height to crypt depth, and decreased the proportion of Proteobacteria in fecal microbiota. These findings suggest that LGG supplementation might alleviate leptin resistance caused by an HFD through the improvement of the digestive health of the host.
Highlights
Obesity is defined by the World Health Organization (WHO) as a body mass index (BMI) of 30 or more
Supplementation of high-fat diet (HFD) with high-dose Lactobacillus rhamnosus GG (LGG) restored exogenous leptin responsiveness, increased the ratio of villus height to crypt depth, and decreased the proportion of Proteobacteria in fecal microbiota. These findings suggest that LGG supplementation might alleviate leptin resistance caused by an HFD through the improvement of the digestive health of the host
We found that the fecal microbiota compositions of the mice fed a normal diet and those fed a high-fat diet differed (Figure 5D)
Summary
Obesity is defined by the World Health Organization (WHO) as a body mass index (BMI) of 30 or more. It is a chronic disease that has reached epidemic proportions globally. According to the data released by the WHO, in 2016, more than 1.9 billion adults (18 years and older) were overweight, and, of these, over 650 million were obese [1]. Obesity is closely associated with various metabolic disorders, including hypertension, type 2 diabetes mellitus, cardiovascular disease, and nonalcoholic fatty liver, which are highly associated with mortality. The fundamental cause of obesity is an imbalance between energy intake and energy expenditure. Energy homeostasis is controlled by the hypothalamus in the central nervous system, which receives signals from the adipose tissue, digestive system, and endocrine system and manages appetite via the nervous system [2]
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