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Intestinal luminal fat refers to dietary triglycerides and other lipids present in the lumen of the small intestine, primarily the jejunum, where they undergo digestion and absorption rather than functioning as a discrete molecular entity or receptor. Digestion begins with emulsification by bile salts, enabling pancreatic lipase to hydrolyze triglycerides into free fatty acids and 2-monoacylglycerols, which form micelles for diffusion across the enterocyte brush border. Inside enterocytes, these components are re-esterified into triglycerides, packaged with apolipoprotein B48 into chylomicrons by microsomal triglyceride transfer protein (MTP), and secreted into lymphatics for systemic delivery, supporting energy homeostasis, membrane synthesis, and hormone production. This process is not mediated by a specific receptor but involves facilitators like fatty acid translocase (CD36/FAT), fatty acid transport protein 4 (FATP4), and NPC1L1 for cholesterol subsets. Dysregulation leads to fat malabsorption, as seen in bile salt deficiency or colipase absence, causing steatorrhea, but it is not a therapeutic target itself—rather, associated proteins like NPC1L1 are drugged to modulate absorption in hyperlipidemia. No direct drugs target "fat in the intestinal lumen"; efforts focus on enzymes, transporters, or bile acid pathways to influence its handling.
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