A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice

Satomi Akagiri; Yuji Naito; Hiroshi Ichikawa; Katsura Mizushima; Tomohisa Takagi; Osamu Handa; Satoshi Kokura; Toshikazu Yoshikawa

doi:10.3164/jcbn.2008022

A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice

J Clin Biochem Nutr. 2008 Mar;42(2):150-7. doi: 10.3164/jcbn.2008022.

Authors

Satomi Akagiri¹, Yuji Naito, Hiroshi Ichikawa, Katsura Mizushima, Tomohisa Takagi, Osamu Handa, Satoshi Kokura, Toshikazu Yoshikawa

Affiliation

¹ Inflammation and Immunology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Abstract

To determine the relative contribution of obesity and visceral white adipose tissue (WAT) to metabolic syndrome, we developed a model that is susceptible to high-fat diet-induced obesity and insulin resistance using male KK/Ta mice. The ratio of WAT weight to body weight was greater in the high-fat diet group compared with the control group in 10-, 14-, and 22-week-old mice. The increase in visceral WAT preceded development of fatty liver and insulin resistance. Adiponectin mRNA expression in WAT was markedly decreased before the decrease in its plasma levels or the development of insulin resistance. Insulin resistance appeared in association with fatty infiltration and TNF-alpha expression in the liver in 22-week-old mice. These data indicate that our mouse model would be useful for future studies that investigate the role of visceral WAT and its products in the development of metabolic syndrome.

Keywords: fatty liver; high-fat diet; metabolic syndrome; white adipose tissue.