Chinese Synonyms: 3α-Hydroxy-7-oxo-5β-cholanic acid
CAS No.: 4651-67-6
EINECS No.: 225-083-2
Molecular Formula: C24H38O4
Boiling Point: 545.9°C at 760 mmHg
Flash Point: 298°C
Density: 1.124 g/cm³
Safety Statements: 22-24/25
7-Ketolithocholic acid (7-keto-LCA) is an endogenous secondary bile acid, primarily generated through microbial metabolism in the liver and intestines. It exerts multifaceted effects, including the regulation of bile metabolism, intestinal protection, and the modulation of metabolism and inflammation.
I. Core Physiological Functions
1. Regulation of Bile Acid Metabolism (A Core Hepatic Function)
• **Inhibition of Cholesterol and Bile Acid Synthesis:** Upon intestinal absorption, it significantly suppresses the hepatic production of endogenous bile acids and reduces both the concentration and secretion of cholesterol in bile.
• **Reduction of the Lithogenic Index:** It mitigates cholesterol supersaturation in bile, thereby lowering the risk of gallstone formation; studies suggest its potential utility in the dissolution therapy for cholesterol gallstones.
• **Precursor to Ursodeoxycholic Acid (UDCA):** It serves as a crucial biosynthetic intermediate for the synthesis of UDCA—a key therapeutic agent for cholestatic liver diseases.
• **Linking Glucocorticoid and Bile Acid Metabolism:** Acting as a substrate for 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), it is converted in the liver into chenodeoxycholic acid (CDCA), thereby bridging endocrine and metabolic pathways.
2. Intestinal Protection and Mucosal Repair (A Current Research Hotspot)
• **Antagonism of FXR Receptors to Promote Intestinal Repair:** As a natural inhibitor of intestinal FXR receptors, it relieves the receptor's inhibitory effect on the Wnt signaling pathway, thereby activating intestinal stem cells and accelerating the healing of intestinal mucosal injuries.
• **Alleviation of Drug-Induced Intestinal Injury:** It effectively counteracts intestinal dysbiosis, disruption of the intestinal barrier, and mucosal inflammation induced by non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin.
• **Maintenance of Intestinal Barrier Integrity:** It reinforces intestinal tight junctions, reduces "leaky gut" (increased intestinal permeability), and lowers the risk of endotoxin translocation into the bloodstream.
3. Regulation of Metabolism and Inflammation
• **Amelioration of Metabolic Disorders:** It modulates lipid and glucose metabolism, offering potential benefits in the management of obesity, fatty liver disease, and insulin resistance. • Anti-inflammatory and Antioxidant Effects: Inhibits inflammatory pathways—such as NF-κB—to alleviate systemic chronic low-grade inflammation, offering potential benefits for Inflammatory Bowel Disease (IBD).
• Gut Microbiota Modulation: Functions as a microbiota-host co-metabolite, helping to maintain the balance of the intestinal microecosystem.
II. Key Applications and Research Value
1. Drug Development
o A key raw material for the synthesis of Ursodeoxycholic Acid (UDCA).
o Intestinal Protection: Developed as a protective agent to prevent or alleviate NSAID-induced intestinal injury.
o Metabolic Diseases: A candidate drug or adjunctive therapeutic agent for conditions such as gallstones, fatty liver disease, and Type 2 diabetes.
2. Biomarkers
o Levels of 7-ketolithocholic acid in serum or stool can serve as indicators of liver function, gut microbiota health, and disturbances in bile acid metabolism.
III. Summary
7-ketolithocholic acid is a pivotal molecule linking hepatic metabolism, gut health, and immune-inflammatory processes. Its most promising applications lie in protecting the intestinal mucosa and combating drug-induced intestinal injury, while it also holds significant research value in the fields of gallstones and metabolic syndrome.
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