• J. Nutr. Biochem. · Dec 2011

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

    • Tim Lubbers, Jacco J de Haan, M'hamed Hadfoune, Lennart Zabeau, Jan Tavernier, Yiren Zhang, David Grundy, Jan Willem M Greve, and Wim A Buurman.
    • Department of Surgery, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, 6200 MD Maastricht, The Netherlands.
    • J. Nutr. Biochem. 2011 Dec 1; 22 (12): 1105-11.

    AbstractEnteral 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<.05). L-81 blunted the beneficial effects of lipid-enriched nutrition on systemic inflammation and intestinal integrity in both species (all parameters, P<.01). Ob/Ob mice required a higher dose of nutrition compared with wild-type mice to attenuate plasma levels of TNF-α and ileum-lipid binding protein, a marker for enterocyte damage (both P<.01), suggesting a higher stimulation threshold in leptin-deficient mice. Administration of a glucagon-like peptide 1-receptor antagonist, but not leptin or peptide YY antagonists, suppressed the effects of lipid-enriched nutrition. These data indicate that chylomicron formation is essential and activation of the glucagon-like peptide 1-receptor is involved in activation of the nutritional anti-inflammatory pathway by lipid-enriched nutrition.Copyright © 2011 Elsevier Inc. All rights reserved.

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