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Hepatic cyclooxygenase-2 expression protects against diet-induced steatosis, obesity, and insulin resistance

AuthorsFrancés, Daniel E.; Motiño, Omar; Agra, Noelia CSIC; González-Rodríguez, Águeda; Fernández-Alvarez, Ana Julia CSIC ORCID; Cucarella, Carme CSIC ; Mayoral, Rafael CSIC; Castro-Sánchez, Luis; García-Casarrubios, Ester; Boscá, Lisardo CSIC ORCID CVN; Carnovale, Cristina E.; Casado, Marta CSIC ORCID ; Valverde, Ángela M. ; Martín-Sanz, Paloma CSIC ORCID
Issue Date2015
PublisherAmerican Diabetes Association
CitationDiabetes 64(5): 1522-1531 (2015)
AbstractAccumulation evidence links obesity-induced inflammation as an important contributor to the development of insulin resistance, which plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes and nonalcoholic fatty liver disease. Cyclooxygenase (COX)-1 and -2 catalyze the first step in prostanoid biosynthesis. Because adult hepatocytes fail to induce COX-2 expression regardless of the proinflammatory stimuli used, we have evaluated whether this lack of expression under mild proinflammatory conditions might constitute a permissive condition for the onset of insulin resistance. Our results show that constitutive expression of human COX-2 (hCOX-2) in hepatocytes protects against adiposity, inflammation, and, hence, insulin resistance induced by a high-fat diet, as demonstrated by decreased hepatic steatosis, adiposity, plasmatic and hepatic triglycerides and free fatty acids, increased adiponectin-to-leptin ratio, and decreased levels of proinflammatory cytokines, together with an enhancement of insulin sensitivity and glucose tolerance. Furthermore, hCOX-2 transgenic mice exhibited increased whole-body energy expenditure due in part by induction of thermogenesis and fatty acid oxidation. The analysis of hepatic insulin signaling revealed an increase in insulin receptor-mediated Akt phosphorylation in hCOX-2 transgenic mice. In conclusion, our results point to COX-2 as a potential therapeutic target against obesity-associated metabolic dysfunction.
Identifiersdoi: 10.2337/db14-0979
issn: 0012-1797
e-issn: 1939-327X
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