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Publication
Postprandial activation of leukocyte-endothelium interaction by fatty acids in
the visceral adipose tissue microcirculation.
Authors Preston KJ, Rom I, Vrakas C, Landesberg G, Etwebi Z, Muraoka S, Autieri M,
Eguchi S, Scalia R
Submitted By Submitted Externally on 2/12/2020
Status Published
Journal FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Year 2019
Date Published 11/1/2019
Volume : Pages 33 : 11993 - 12007
PubMed Reference 31393790
Abstract High-fat diet (HFD)-induced obesity is associated with accumulation of
inflammatory cells predominantly in visceral adipose depots [visceral adipose
tissue (VAT)] rather than in subcutaneous ones [subcutaneous adipose tissue
(SAT)]. The cellular and molecular mechanisms responsible for this phenotypic
difference remain poorly understood. Controversy also exists on the overall
impact that adipose tissue inflammation has on metabolic health in diet-induced
obesity. The endothelium of the microcirculation regulates both the transport of
lipids and the trafficking of leukocytes into organ tissue. We hypothesized that
the VAT and SAT microcirculations respond differently to postprandial processing
of dietary fat. We also tested whether inhibition of endothelial postprandial
responses to high-fat meals (HFMs) preserves metabolic health in chronic
obesity. We demonstrate that administration of a single HFM or ad libitum access
to a HFD for 24 h quickly induces a transient P-selectin-dependent inflammatory
phenotype in the VAT but not the SAT microcirculation of lean wild-type mice.
Studies in P-selectin-deficient mice confirmed a mechanistic role for P-selectin
in the initiation of leukocyte trafficking, myeloperoxidase accumulation, and
acute reduction in adiponectin mRNA expression by HFMs. Despite reduced VAT
inflammation in response to HFMs, P-selectin-deficient mice still developed
glucose intolerance and insulin resistance when chronically fed an HFD. Our data
uncover a novel nutrient-sensing role of the vascular endothelium that
instigates postprandial VAT inflammation. They also demonstrate that inhibition
of this transient postprandial inflammatory response fails to correct metabolic
dysfunction in diet-induced obesity.-Preston, K. J., Rom, I., Vrakas, C.,
Landesberg, G., Etwebe, Z., Muraoka, S., Autieri, M., Eguchi, S., Scalia, R.
Postprandial activation of leukocyte-endothelium interaction by fatty acids in
the visceral adipose tissue microcirculation.




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