Why Do BAs Promote Fat Digestion, Regulate Metabolism, and Protect the Liver
Bile acids are steroid compounds synthesized by the liver from cholesterol and serve as key active components of bile. Initially recognized for their critical role in promoting the digestion and absorption of dietary fats, recent studies have unveiled their complex functions as metabolic regulatory hormones. They play multiple essential roles in animals, primarily including the following aspects:
1. Promoting the Digestion and Absorption of Lipids
Bile acids are amphipathic molecules with both hydrophilic and hydrophobic domains, endowing them with potent emulsifying capabilities. In the small intestine of animals, bile acids emulsify large fat particles (such as triglycerides) from the diet into tiny fat droplets, significantly increasing the surface area for lipase action. Subsequently, bile acids further encapsulate the breakdown products of fats (such as fatty acids and monoglycerides) to form "mixed micelles," enabling efficient passage through the aqueous layer on the surface of intestinal villi for absorption by epithelial cells. After completing their absorption tasks, approximately 95% of bile acids are actively reabsorbed at the terminal ileum, returning to the liver via the portal vein to enter the "enterohepatic circulation" for efficient reuse.
In this way, bile acids facilitate the absorption of these fat-soluble substances through the intestinal mucosa, a function crucial for the effective utilization of fats and fat-soluble vitamins (A, D, E, K), particularly in high-energy, high-fat diets.
2. Acting as Signaling Molecules to Regulate Metabolism and Immunity
Beyond their digestive role, bile acids are now widely recognized as important signaling molecules that regulate systemic metabolic networks by activating specific intracellular receptors.
- Farnesoid X Receptor (FXR)
FXR is the primary nuclear receptor for bile acids and is highly expressed in the liver and intestines. Upon activation by bile acids, FXR initiates a series of gene transcription programs that not only suppress bile acid synthesis to maintain homeostasis but also regulate glucose and lipid metabolism. For instance, FXR activation can inhibit fatty acid synthesis, promote β-oxidation, and influence gluconeogenesis and insulin sensitivity.
- G Protein-Coupled Bile Acid Receptor (TGR5)
TGR5 is a cell membrane receptor widely distributed in intestinal L-cells, immune cells, and brown adipose tissue. Activation of TGR5 by bile acids stimulates intestinal L-cells to secrete glucagon-like peptide-1 (GLP-1). GLP-1 is an important incretin that promotes insulin secretion, suppresses appetite, and delays gastric emptying, thereby exerting profound effects on blood glucose homeostasis and energy balance.
- Modulating the Gut Microbiota
Bile acids and gut microbiota engage in bidirectional interactions. On one hand, gut microbes (e.g., Clostridium species) can metabolize primary bile acids synthesized by the liver into secondary bile acids, altering the composition and signaling activity of the bile acid pool. On the other hand, the antimicrobial properties and signaling functions of bile acids reciprocally shape the structure and abundance of the gut microbiota. Studies have shown that bile acid supplementation can increase the abundance of bacteria beneficial for bile acid metabolism, such as Romboutsia and Clostridium sensu stricto.
3. Liver Protection and Antioxidant Effects
Bile acids possess hepatoprotective and antioxidant capabilities. Research indicates that bile acids supplementation can significantly elevate levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in dairy cow serum while reducing markers of oxidative damage such as malondialdehyde (MDA). This antioxidant effect helps protect vital organs like the liver from oxidative stress, which is particularly important for dairy cows under high metabolic demands.
Special Note: This article aims to provide an objective review and academic discussion of relevant research progress. The content is based on published scientific research literature and is not intended for product promotion or usage recommendations.
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