Abstract
Obesity is one of the major worldwide epidemics and has became a public health problem of the 21st century because of its association with metabolic syndrome, which increases the risks of developing type 2 diabetes and hepatic steatosis. The expansive prevalence of obesity is caused by the dramatic changes of lifestyle. Western diet, made up of high-fat and high-sugars, is the major dietary concern for obesity prevalence. Albusin B is a 32-kDa bacteriocin from the ruminal bacterium Ruminococcus albus 7 and mass-produced by Saccharomyces cerevisiae expression system. In the previous study, administration of albusin B caused a decrease in body weight (BW) and plasma triglycerides (TG) levels, and improved lipid metabolism of healthy BALB/C mice. However, the effect of albusin B on energy homeostasis of obese mice has not been elucidated. In this study, 7-week-old C57BL/6 male mice were fed with Western diet for 20 weeks to induce obesity. Then the obese mice (W) were randomly assigned to 3 groups: saline (WS), WLA [0.125 μg albusin B /g body weight (BW)], and WHA (0.625 μg albusin B /g BW). Saline / albusin B was orally administrated for extra 4 weeks then sacrificed. Results showed that Western diet induced morbid obesity in mice, including hyperglycemia, dyslipidemia, fatty liver, and hypertrophy of adipocytes. Oral administration of 0.125 μg albusin B/g BW significantly reduced BW, plasma levels of total cholesterol (TC) and low density lipoprotein (LDL), hepatic lipid accumulation, and adipocyte size. High concentration of albusin B did not change BW and lipid profiles in plasma, but reduced adipocyte size. Administration of albusin B decreased fatty acid absorption in the ileum, liver, and muscle. Compared with WS group, WLA group had higher lipid oxidation rate in the liver and white adipose tissue (WAT) and lower lipid synthesis in the WAT and muscle. WHA group had a decrease of lipogenic gene expressions in the WAT as compared to WS group. Moreover, albusin B treatment suppressed hepatic fructose uptake and WLA mice had higher glycolytic gene expressions in the liver and muscle. Administration of albusin B increased the respiratory quotient of obese mice, demonstrated that a higher efficiency of carbohydrate utilization for energy expenditure. Albusin B treatments also promoted systemic antioxidant defense and increased caecal counts of Bifidobacterium. Taken together, oral administration of 0.125 μg albusin B/g BW albusin B resulted in body weight loss and promoted lipid metabolism, carbohydrate utilization, and antioxidant capacity, and elevated caecal population of Bifidobacterium in diet-induced obese mice. These results therefore partially improve the health of obese mice.
Published Version
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