Abstract
The activation of peroxisome proliferator-activated rece ptor gamma (PPAR-γ) is known to induce the differentiation of adipocytes. This study aimed to investigate the probiotic effect of Leuconostoc mesenteroides (L. mesenteroides) on high-fat diet (HFD)-induced PPAR-γ activation and abdominal fat depots. Incubation of differentiated 3T3-L1 adipocytes with media of L. mesenteroides EH-1, a butyric acid-producing strain, significantly reduced the amounts of lipid droplets. The oral administration of L. mesenteroides EH-1 produced large amounts (>1 mM) of butyric acid in cecum and attenuated the HFD-induced upregulation of PPAR-γ and accumulation of abdominal fats in mice. The combination of 2% glucose with L. mesenteroides EH-1 increased the production of butyric acid and potentiated the probiotic activity of L. mesenteroides EH-1 against the formation of lipid droplets in 3T3-L1 adipocytes as well as abdominal fats in HFD-fed mice. The inhibition of free fatty acid receptor 2 (Ffar2) by its antagonist, GLPG-0974, markedly diminished the probiotic effects of L. mesenteroides EH-1 plus glucose on the suppression of HFD-induced PPAR-γ and abdominal fats. Besides demonstrating the probiotic value of L. mesenteroides EH-1, our results highlight the possible therapy targeting the butyric acid-activated Ffar2 pathway to reduce abdominal fats.
Highlights
The accumulation of fat in abdominal adipose depot is related to the development of obesity-related cardiometabolic risk, referring to the chances of having type 2 diabetes, heart disease or stroke [1]
Our previous studies revealed that L. mesenteroides EH-1 is a butyric acid-producing bacterial strain when cultured in the presence of glucose in vitro [16]
We previously demonstrated that butyric acid was detectable in the culture media of L. mesenteroides EH-1 [16]
Summary
The accumulation of fat in abdominal adipose depot is related to the development of obesity-related cardiometabolic risk, referring to the chances of having type 2 diabetes, heart disease or stroke [1]. Genomic insights into the multiple factors that control the abdominal fat deposition have been proposed [3]. Adipocytes require several transcription factors, such as peroxisome proliferator-activated receptor gamma (PPAR-γ), CCAAT/enhancer-binding proteins (C/EBPs), signal transducers and activators of transcription (STATs) and Krüppel-like factor (KLF) proteins to facilitate the differentiation of adipocyte precursor cells into mature adipocytes [4]. PPAR-γ is a transcriptional factor belonging to the ligand-activated nuclear receptor superfamily, which directly regulates the expression of genes involved in adipocyte differentiation, lipid and carbohydrate metabolism and adipokine synthesis. Adipokine released by adipose tissues is a key factor linking obesity-induced inflammation. PPAR-γ activation induces the preadipocyte differentiation to adipocytes and stimulates triglyceride storage [5]
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