Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?

To: Miljenko Zuanic who wrote (527)	5/21/2001 8:09:49 PM
From: Miljenko Zuanic	Read Replies (1) \| Respond to of 3557

Leptin and Insulin Regulate Cholesterol Metabolism in Macrophages -------------------------------------------------------------------------------- WESTPORT, CT (Reuters Health) May 18 - The effects of leptin and insulin on cholesterol ester metabolism in macrophages may contribute to the increased risk of atherosclerosis seen with type 2 diabetes and obesity, according to a report published in the May issue of Diabetes. Dr. Peter R. Shepherd from the University College London in the UK and colleagues used cell culture techniques to study the interaction between leptin and a murine macrophage cell line. The authors found that the macrophages expressed a functional form of the leptin receptor that became tyrosine-phosphorylated after low-dose leptin stimulation. Leptin also stimulated phosphoinositide 3-kinase (PI 3-kinase) activity and tyrosine phosphorylation of JAK2 and STAT3 in the macrophages. Leptin significantly increased the activity of hormone-sensitive lipase (HSL), a neutral cholesterol esterase present in macrophages, the researchers note. Cyclic AMP added to this effect, while PI 3-kinase inhibitors appeared to block it. In macrophages, unlike in adipocytes, insulin inhibited HSL activity independent of PI 3-kinase. "There is accumulating evidence that hyperleptinemia and the combination of hyperinsulinemia and hyperglycemia play direct roles in the development of atherosclerosis," the investigators state. Based on the current findings, "we suggest that leptin and insulin could play counteracting roles in regulating cholesterol ester homeostasis in macrophages," they add. Dr. Shepherd's team believes that "either leptin resistance or increased insulin action could contribute to the increased formation of foam cells and atherosclerosis in obese and diabetic individuals." Diabetes 2001;50:955-961.