Abstract
Obesity is one of the major risk factors for nonalcoholic fatty liver disease (NAFLD), and NAFLD is highly associated with an increased risk of cardiovascular disease (CVD). Scholars have suggested that certain probiotics may significantly impact cardiovascular health, particularly certain Lactobacillus species, such as Lactobacillus reuteri GMNL-263 (Lr263) probiotics, which have been shown to reduce obesity and arteriosclerosis in vivo. In the present study, we examined the potential of heat-killed bacteria to attenuate high fat diet (HFD)-induced hepatic and cardiac damages and the possible underlying mechanism of the positive effects of heat-killed Lr263 oral supplements. Heat-killed Lr263 treatments (625 and 3125 mg/kg-hamster/day) were provided as a daily supplement by oral gavage to HFD-fed hamsters for eight weeks. The results show that heat-killed Lr263 treatments reduce fatty liver syndrome. Moreover, heat-killed Lactobacillus reuteri GMNL-263 supplementation in HFD hamsters also reduced fibrosis in the liver and heart by reducing transforming growth factor β (TGF-β) expression levels. In conclusion, heat-killed Lr263 can reduce lipid metabolic stress in HFD hamsters and decrease the risk of fatty liver and cardiovascular disease.
Highlights
Metabolic syndrome comprises of hypertension, dyslipidemia, obesity, glucose intolerance, and cardiovascular disease (CVD) [1,2,3,4,5]
HMG-CoA reductase increased in the high fat diet (HFD) group rats and decreased only slightly in the heat-killed Lactobacillus reuteri GMNL-263 (Lr263) treatment groups, which was not significant (Figure 1C)
The liver section results show higher transforming growth factor β (TGF-β) expression in the HFD hamster fatty liver (Figure 3), whereas the HFD hamster fatty liver only exhibits slight fibrosis (Figure 2). Another in vitro study evaluated probiotic cholesterol assimilation in culture media and under simulated intestinal conditions; the results show that most Lactobacillus strains exhibit strong cholesterol assimilation and that Lactobacillus reuteri NCIMB 701089 assimilated over 67% of the cholesterol [39]
Summary
Metabolic syndrome comprises of hypertension, dyslipidemia, obesity, glucose intolerance, and cardiovascular disease (CVD) [1,2,3,4,5]. Carbon tetrachloride-induced liver injury in animal experiments showed that liver damage-induced abnormal lipid metabolism increased both cholesterol and transforming growth factor β (TGF-β) levels in blood [9,10]. The most accepted mechanism underlying these effects is that Lactobacillus features bile salt hydrolase (BSH) activity, which suggests that probiotics may cause deconjugation effects in primary bile acids and promote the secondary bile salts by amino acid conjugations in the gut [23]. These effects will break down the cholesterol-bile salt reabsorption and lower the cholesterol levels of the hosts [24,25,26]. A high-fat diet was employed to induce obesity and cardiac fibrosis in hamsters; the protective effects exerted by different doses of heat-killed Lr263 on the heart and liver were investigated in hamsters with high-fat diet-induced obesity
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