Published January 1, 2009 | Version v1
Journal article

Elevated Expression of Osteopontin May Be Related to Adipose Tissue Macrophage Accumulation and Liver Steatosis in Morbid Obesity

Others:
Centre méditérannéen de médecine moléculaire (C3M) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Digestive Center ; Centre Hospitalier Universitaire de Nice (CHU Nice)
Institut Mondor de Recherche Biomédicale (IMRB) ; Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)
Pôle Digestif ; Centre Hospitalier Universitaire de Nice (CHU Nice)-Hôpital l'Archet
Centre méditerranéen de médecine moléculaire (C3M) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UniCA)
Centre Hospitalier Universitaire de Nice (CHU Nice)
Hôpital Archet 2 [Nice] (CHU)
Génétique et pathologies moléculaires (GPM) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UniCA)
Nutrition et obésités: approches systémiques (UMR-S 1269) (Nutriomics) ; Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)
Génétique des maladies multifactorielles (GMM) ; Université de Lille, Droit et Santé-Centre National de la Recherche Scientifique (CNRS)
Déterminants Biologiques et Comportementaux des Obésités ; Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôtel-Dieu-EA3502
Service de nutrition ; Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital de l'Hôtel-Dieu
Nutrition et obésité : approches génétique et transcriptomique ; Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR58-Institut National de la Santé et de la Recherche Médicale (INSERM)
Département de nutrition ; Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôtel-Dieu
Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM) ; University of Oxford
Hépato-Gastroentérologie ; Centre Hospitalier Universitaire de Nice (CHU Nice)
Univ Paris Est Créteil, INSERM, IMRB, F-94010 Créteil, France

Description

OBJECTIVE—Osteopontin (OPN) plays an important role in the development of insulin resistance and liver complications in dietary murine models. We aimed to determine the expression pattern of OPN and its receptor CD44 in obese patients and mice according to insulin resistance and liver steatosis. RESEARCH DESIGN AND METHODS—OPN and CD44 expressions were studied in 52 morbidly obese patients and in mice. Cellular studies were performed in HepG2 cells. RESULTS—Hepatic OPN and CD44 expressions were strongly correlated with liver steatosis and insulin resistance in obese patients and mice. This increased OPN expression could be due to the accumulation of triglycerides, since fat loading in HepG2 promotes OPN expression. In contrast, OPN expression in adipose tissue (AT) was enhanced independently of insulin resistance and hepatic steatosis in obese patients. The elevated OPN expression in AT was paralleled with the AT macrophage infiltration, and both phenomena were reversed after weight loss. The circulating OPN level was slightly elevated in obese patients and was not related to liver steatosis. Further, AT did not appear to secrete OPN. In contrast, bariatric surgery–induced weight loss induced a strong increase in circulating OPN. CONCLUSIONS—The modestly elevated circulating OPN levels in morbidly obese patients were not related to liver steatosis and did not appear to result from adipose tissue secretion. In subcutaneous AT, expression of OPN was directly related to macrophage accumulation independently from liver complications. In contrast, hepatic OPN and CD44 expressions were related to insulin resistance and steatosis, suggesting their local implication in the progression of liver injury.

Abstract

International audience

Additional details

Created:
March 10, 2024
Modified:
March 10, 2024