Propionate Effects refer to the systemic physiological impacts of propionate, a three-carbon short-chain fatty acid (SCFA) predominantly produced by the fermentation of dietary fiber by the gut microbiota. Its primary clinical significance lies in its role as a precursor for gluconeogenesis in the liver, contributing to host glucose homeostasis, and its ability to modulate satiety and energy intake through signaling pathways in the gut. Propionate also exhibits anti-inflammatory properties, influencing overall gut and metabolic health.
Origin
Propionate is derived from the Greek protos meaning first, and pion meaning fat, reflecting its status as one of the first recognized fatty acids. The understanding of its “effects” has expanded significantly with the realization that it is a critical signaling molecule linking the gut microbiome’s activity directly to host endocrine and metabolic control. This highlights its central role in the entero-endocrine system.
Mechanism
Propionate is absorbed into the bloodstream and travels to the liver, where it is efficiently converted into glucose via the propionyl-CoA pathway, thereby contributing to stable blood sugar levels. In the gut, it binds to specific G-protein coupled receptors (GPCRs), particularly free fatty acid receptor 2 (FFAR2), stimulating the release of appetite-regulating hormones such as peptide YY (PYY) and glucagon-like peptide-1 (GLP-1). This dual action on hepatic metabolism and gut hormone release defines its systemic effects.
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