# Administration of heat killed Fructobacillus fructosus OS-1010 attenuates metabolic disease induced by high fat diet in mice

## TL;DR

Heat-killed Fructobacillus fructosus OS-1010 reduces obesity and related health issues in mice on a high-fat diet.

## Contribution

First in vivo evidence that heat-killed F. fructosus OS-1010 improves obesity and metabolic disease in mice.

## Key findings

- Heat-killed F. fructosus OS-1010 reduced body weight gain in mice on a high-fat diet.
- The treatment improved liver health and reduced non-alcoholic fatty liver disease progression.
- Muscle weakness was mitigated, with increased mitochondrial density and reduced fat accumulation in muscle.

## Abstract

Heat-killed Fructobacillus fructosus OS-1010 reportedly enhance the number and membrane potential of mitochondria in muscle cell C2C12 in vitro. However, there are no reports on the effects of this strain on mitochondria or the resulting effects on the body in animal models. In this study, we investigated the effects of heat-killed F. fructosus OS-1010 on obesity and other metabolic abnormalities and muscle weakness in mice with high-fat diet (HFD)-induced sarcopenic obesity. C57BL/6 mice were fed HFD supplemented with heat-killed F. fructosus OS-1010 for 13 weeks. The HFD-induced body weight gain was significantly reduced. Additionally, there was a significant decrease in alanine aminotransferase levels, improvement in serum lipid profiles, and a reduction in non-alcoholic fatty liver disease (NAFLD) progression. Skeletal muscle weakness was also mitigated, with changes in gene expression in the quadriceps indicating suppression of intramuscular fat accumulation, and enhancement of mitochondrial density. The findings of this study suggest that heat-killed F. fructosus OS-1010 functions as an anti-obesity postbiotic, potentially benefiting both NAFLD and muscle weakness associated with obesity.