Probiotic Yogurt Alleviates High-Fat Diet-Induced Lipid Accumulation and Insulin Resistance in Mice via the Adiponectin Pathway

A high-fat diet (HFD) easily contributes to the pathogenesis of obesity and insulin resistance. Obesity and insulin resistance have been clinical and public health challenges all over the world. Probiotic-fermented yogurt is one type of popular and functional beverage in people's daily lives. This study mainly explored the lipid-and glucose-lowering effects of Lactobacillus acidophilus NX2-6-fermented yogurt (LA-Y) in HFD-fed mice. The results showed that LA-Y administration improved the lipid profile in the serum and liver, reduced fasting blood glucose levels, and enhanced insulin sensitivity. Protein analysis showed that LAY treatment promoted fatty acid oxidation and suppressed de novo lipogenesis in the adipose tissue and liver. LA-Y effectively alleviated glucose metabolism disorders by activating the insulin signaling pathway, suppressing gluconeogenesis in the liver and muscle, reducing the concentration of pro-inflammatory cytokines in the serum, and promoting glycolysis and gluconeogenesis in the small intestine. LA-Y supplementation also promoted fat browning via the adiponectin/AMPK alpha/PGC-1 alpha/UCP1 pathway and enhanced mitochondrial biogenesis in the liver and muscle by activating the adiponectin/AdipoR1/APPL1/AMPK alpha/PGC-1 alpha pathway, leading to increased energy expenditure. Therefore, LA-Y may be a functional dairy food for preventing and alleviating diet induced metabolic disorders.

Automated summary

This study investigated the effects of Lactobacillus acidophilus NX2-6-fermented yogurt (LA-Y) on lipid and glucose levels in high-fat diet-fed mice. The results showed that LA-Y improved lipid profile, reduced fasting blood glucose levels, and enhanced insulin sensitivity. LA-Y also alleviated glucose metabolism disorders by activating the insulin signaling pathway, reducing inflammation, and promoting glycolysis and gluconeogenesis in the small intestine. Additionally, LA-Y promoted fat browning and increased energy expenditure through adiponectin/AMPK alpha/PGC-1 alpha/UCP1 pathway and mitochondrial biogenesis via adiponectin/AdipoR1/APPL1/AMPK alpha/PGC-1 alpha pathway.