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Role of Meltrin (ADAM12) in Obesity Induced by High- Fat Diet

Department of Growth Regulation, Institute for Frontier Medical Sciences, Kyoto University (M.M., T.K., A.S.-F.), Sakyo-ku, Kyoto 606-8507, Japan; Mochida Pharmaceutical Co. Ltd. (K.S.), Shizuoka 412-8524, Japan; and Japan Society for the Promotion of Science (M.M.), Tokyo 102-8471, Japan

Address all correspondence and requests for reprints to: Dr. Atsuko Sehara-Fujisawa, Department of Growth Regulation, Institute for Frontier Medical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan. E-mail: asehara{at}frontier.kyoto-u.ac.jp.

Meltrin is a member of the metalloprotease-disintegrin (ADAM) family. In this paper we demonstrate that meltrin is involved in the development of white adipose tissue. Compared with wild-type mice, meltrin ^–/– mice displayed moderate resistance to weight gain induced by a high-fat diet, mainly because of an impaired increase in the number of adipocytes. There was no obvious difference in adipocyte size between wild-type and meltrin ^–/– mice, suggesting normal maturation of adipocytes of the latter under a high-fat diet. Embryonic fibroblasts and stromal-vascular cells lacking meltrin exhibited impaired cell proliferation upon adipogenic stimulation, which was accompanied by moderate defects in adipose differentiation. Addition of culture medium conditioned with wild-type cells in an early phase of adipose differentiation did not restore the defects in the meltrin ^–/– cells. These results uncover the involvement of meltrin in the development of obesity and in adipogenic cell proliferation.