Plasma lipoprotein(a) (Lp(a)) is known to be a strong independent risk factor for ischemic heart disease. However, it is not easily modulated by drugs that are presently available. Lp(a) is not present in many experim...Plasma lipoprotein(a) (Lp(a)) is known to be a strong independent risk factor for ischemic heart disease. However, it is not easily modulated by drugs that are presently available. Lp(a) is not present in many experimental animals except for Old World monkeys. In this study, we examined whether cynomolgus monkeys are useful model for research of human plasma Lp(a), and observed that plasma Lp(a) in cynomolgus monkeys varied as much as humans. As a result of 4 day-fasting in cynomolgus monkeys, the plasma Lp(a) level decreased in a monkey with originally high Lp(a) level. The Lp(a) level continued to decrease even 3 days after banana feeding, but returned to the original level 3 days after monkey chow feeding. On the other hand, in a monkey with low Lp(a) level, fasting had no effect on the Lp(a) level. However, in the third monkey having originally high Lp(a) level, the Lp(a) was not affected by decreasing the amount of monkey chow feeding by 50%. In summary, we found that cynomolgus monkeys may be an useful model for studying the effects of food on plasma Lp(a) in place of humans, and that high Lp(a) level may be controllable by strict diet regulation.展开更多
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 o...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.展开更多
文摘Plasma lipoprotein(a) (Lp(a)) is known to be a strong independent risk factor for ischemic heart disease. However, it is not easily modulated by drugs that are presently available. Lp(a) is not present in many experimental animals except for Old World monkeys. In this study, we examined whether cynomolgus monkeys are useful model for research of human plasma Lp(a), and observed that plasma Lp(a) in cynomolgus monkeys varied as much as humans. As a result of 4 day-fasting in cynomolgus monkeys, the plasma Lp(a) level decreased in a monkey with originally high Lp(a) level. The Lp(a) level continued to decrease even 3 days after banana feeding, but returned to the original level 3 days after monkey chow feeding. On the other hand, in a monkey with low Lp(a) level, fasting had no effect on the Lp(a) level. However, in the third monkey having originally high Lp(a) level, the Lp(a) was not affected by decreasing the amount of monkey chow feeding by 50%. In summary, we found that cynomolgus monkeys may be an useful model for studying the effects of food on plasma Lp(a) in place of humans, and that high Lp(a) level may be controllable by strict diet regulation.
文摘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.
