Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/107936
Title: Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients.
Author: Clemente Postigo, M.
Queipo-Ortuño, María Isabel
Murri, M.
Boto Ordóñez, María
Perez Martinez, P.
Andrés Lacueva, Ma. Cristina
Cardona, F.
Tinahones, Francisco J.
Keywords: Obesitat mòrbida
Resistència a la insulina
Nutrició
Triglicèrids
Metabolisme
Morbid obesity
Insulin resistance
Nutrition
Triglycerides
Metabolism
Issue Date: 5-Mar-2012
Publisher: American Society for Biochemistry and Molecular Biology
Abstract: The low-grade inflammation observed in obesity has been associated with a high-fat diet, though this relation is not fully understood. Bacterial endotoxin, produced by gut microbiota, may be the linking factor. However, this has not been confirmed in obese patients. To study the relationship between a high-fat diet and bacterial endotoxin, we analyzed postprandial endotoxemia in morbidly obese patients after a fat overload. The endotoxin levels were determined in serum and the chylomicron fraction at baseline and 3 h after a fat overload in 40 morbidly obese patients and their levels related with the degree of insulin resistance and postprandial hypertriglyceridemia. The morbidly obese patients with the highest postprandial hypertriglyceridemia showed a significant increase in lipopolysaccharide (LPS) levels in serum and the chylomicron fraction after the fat overload. Postprandial chylomicron LPS levels correlated positively with the difference between postprandial triglycerides and baseline triglycerides. There were no significant correlations between C-reactive protein (CRP) and LPS levels. The main variables contributing to serum LPS levels after fat overload were baseline and postprandial triglyceride levels but not glucose or insulin resistance. Additionally, superoxide dismutase activity decreased significantly after the fat overload. Postprandial LPS increase after a fat overload is related to postprandial hypertriglyceridemia but not to degree of insulin resistance in morbidly obese patients.
Note: Reproducció del document publicat a: https://doi.org/10.1194/jlr.P020909
It is part of: Journal of Lipid Research, 2012, vol. 53, num. 5, p. 973-978
Related resource: https://doi.org/10.1194/jlr.P020909
URI: http://hdl.handle.net/2445/107936
ISSN: 0022-2275
Appears in Collections:Articles publicats en revistes (Nutrició, Ciències de l'Alimentació i Gastronomia)

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