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.