Author:
Serre-Beinier Véronique,Toso Christian,Morel Philippe,Gonelle-Gispert Carmen,Veyrat-Durebex Christelle,Rohner-Jeanrenaud Françoise,Calandra Thierry,Roger Thierry,James Richard W,Montet Xavier,Bühler Léo,Bosco Domenico,Berney Thierry
Abstract
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine produced by many cells and tissues including pancreatic β-cells, liver, skeletal muscle, and adipocytes. This study investigates the potential role of MIF in carbohydrate homeostasis in a physiological setting outside of severe inflammation, utilizing Mif knockout (MIF−/−) mice. Compared with wild-type (WT) mice, MIF−/− mice had a lower body weight, from birth until 4 months of age, but subsequently gained weight faster, resulting in a higher body weight at 12 months of age. The lower weight in young mice was related to a higher energy expenditure, and the higher weight in older mice was related to an increased food intake and a higher fat mass. Fasting blood insulin level was higher in MIF−/− mice compared with WT mice at any age. After i.p. glucose injection, the elevation of blood insulin level was higher in MIF−/− mice compared with WT mice, at 2 months of age, but was lower in 12-month-old MIF−/− mice. As a result, the glucose clearance during intraperitoneal glucose tolerance tests was higher in MIF−/− mice compared with WT mice until 4 months of age, and was lower in 12-month-old MIF−/− mice. Insulin resistance was estimated (euglycemic–hyperinsulinemic clamp tests), and the phosphorylation activity of AKT was similar in MIF−/− mice and WT mice. In conclusion, this mouse model provides evidence for the role of MIF in the control of glucose homeostasis.
Subject
Endocrinology,Endocrinology, Diabetes and Metabolism
Cited by
25 articles.
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