Propionate Induces Energy Expenditure via Browning in Mesenteric Adipose Tissue.

Background: Short-chain fatty acids, such as propionate, are produced from the fermentation of dietary fibre by gut microbiota and modulate adipose tissue metabolism to influence whole-body metabolic processes. Abdominal adipose tissue, critical in glucose and lipid homeostasis, is categorised into mesenteric, omental, and subcutaneous types based on its location. Adipose tissues display different metabolic phenotypes due to their distinct adipocyte lineages-white, brown, and beige. Recent evidence points to a significant impact of propionate on abdominal adipose tissue. Our study investigated the actions of propionate on the three types of human abdominal adipose tissue.

Methods: Adipose tissue from distinct depots (mesenteric, omental and subcutaneous) were collected from 40 patients who underwent open abdominal surgery for cholecystectomy or explorative laparotomy. Tissue explants and isolated adipocytes were treated with 1 mM propionate to assess adipose tissue browning and metabolic homeostatis.

Results: Propionate upregulated brown fat markers UCP1 and PGC1α in adipose tissue and mature adipocytes, particularly of mesenteric origin.Propionate exposure led to increased mitochondrial respiration and ATP production, primarily in mesenteric adipocytes, along with improved glucose uptake and reduced lipolysis and inflammation. In addition, propionate increased thermogenesis, glycolysis, and lipogenesis.

Conclusions: The pronounced response of mesenteric adipose tissue to propionate underscores its potential as a therapeutic target for managing abdominal obesity and metabolic disorders.