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Shimada, M., Ishibashi, S., Inaba, T., Yagyu, H., Harada, K., et al. (1996) Suppression of diet-induced atherosclerosis in low density lipoprotein receptor knockout mice overexpressing lipoprotein lipase. Proceedings of the National Academy of Sciences of the United States of America, 93, 7242-7246. doi:10.1073/pnas.93.14.7242

has been cited by the following article:

• TITLE: Lipoprotein lipase and obesity

  AUTHORS: Masataka Kusunoki, Kazuhiko Tsutsumi, Daisuke Sato, Takao Nakamura

  KEYWORDS: Lipoprotein Lipase; Lipoprotein Lipase Activator; Insulin Resistance; Lipid Metabolism

  JOURNAL NAME: Health, Vol.4 No.12A, December 31, 2012

  ABSTRACT: Obesity is one of the fast-growing major diseases in developed and developing countries. As has been persuasively argued, long-term imbalance between intake and expenditure of fat is a central factor in the etiology of obesity. Obesity aggravates insulin resistance and promotes cardiovascular diseases and atherosclerosis. We hypothesized that elevating lipoprOtein lipase (LPL) activity in skeletal muscle would cause an improvement of obesity. To test this hypothesis, we studied the effects of the LPL activator NO-1886 inobese animals. NO-1886 elevated LPL activity in skeletal muscle, and improved obesity as well as insulin resistance in obese rats. Furthermore, NO-1886 mitigated body weight gain induced by pioglitazone without suppressive effect on the adiponectin-increasing action of pioglitazone. LPL activators hold a lot of promise of curing several diseases shown above in clinical scene.