Chylomicron formation and glucagon-like peptide 1 receptor are involved in activation of the nutritional anti-inflammatory pathway

• Published in: The Journal of nutritional biochemistry 2011-12, Vol.22 (12), p.1105-1111
• Main Authors: Lubbers, Tim, de Haan, Jacco J, Hadfoune, M'hamed, Zabeau, Lennart, Tavernier, Jan, Zhang, Yiren, Grundy, David, Greve, Jan Willem M, Buurman, Wim A
• Format: Article
• Language: English
• Subjects: Animals; antagonists; Anti-Inflammatory Agents; binding proteins; Biological and medical sciences; cholecystokinin; Chylomicrons - biosynthesis; digestive system; endotoxemia; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; glucagon-like peptide 1; Glucagon-Like Peptide-1 Receptor; inflammation; Inflammation - metabolism; Intestines - metabolism; leptin; Lipids - pharmacology; Male; Mesenteric afferents; Mesenteric Arteries - metabolism; Mice; nutrition; Nutritional anti-inflammatory pathway; Peptide YY; Pluronic L-81; Poloxamer - metabolism; Rats; Rats, Sprague-Dawley; Receptors, Glucagon - metabolism; Receptors, Leptin - metabolism; Signal Transduction; tumor necrosis factor-alpha; Tumor Necrosis Factor-alpha - metabolism; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/j.jnutbio.2010.09.006

Enteral administration of lipid-enriched nutrition effectively attenuates inflammation via a cholecystokinin (CCK)-mediated vagovagal anti-inflammatory reflex. Cholecystokinin release and subsequent activation of the vagus are dependent on chylomicron formation and associated with release of additional gut peptides. The current study investigates the intestinal processes underlying activation of the CCK-mediated vagal anti-inflammatory pathway by lipid-enriched nutrition. Rats and mice were subjected to hemorrhagic shock (HS) or endotoxemia, respectively. Prior to the experimental procedures, animals were fasted or fed lipid-enriched nutrition. Pluronic L-81 (L-81) was added to the feeding to investigate involvement of chylomicron formation in activation of mesenteric afferent fibers and the immune-modulating potential of lipid-enriched nutrition. Ob/Ob mice and selective receptor antagonists were used to study the role of leptin, glucagon-like peptide 1 and peptide YY in activation of the nutritional reflex. Electrophysiological analysis of mesenteric afferents in mice revealed that lipid-enriched nutrition-mediated neural activation was abrogated by L-81 (P