Insulin resistance [b][url=http://diabetesdestroyersystemreview.com/]Diabetes 
Destroyer[/url][/b] often leads to Beta-Cell destruction through various 
mechanism listed below. However, some individuals may have limited 
Beta-Cellmass early in life because of genetic factors predisposing them to 
diabetes.

Central Obesity is the main risk factor for the development of diabetes. It is 
often accompanied by an elevation of lipids in the blood (dyslipidemia) and 
increased circulating leptin and cytokine levels. All of these factors have 
been shown to modulate Beta-cell function and survival. The influence of 
dyslipidemia on the Beta-cells of an individual will depend on his or her 
specific lipid profile. Whereas some free fatty acids and lipoproteins have 
been shown to be pro-apoptotic for the Beta-cell, others are protective. Thus, 
long-term exposure to saturated fatty acids such as palmitate (a saturated 
fatty acid that is found in humans, animals and plants and is a major component 
of palm oil) appears highly toxic, whereas monounsaturated fatty acids such as 
oleate protect against both palmitate- and glucose-induced Beta-Cellapoptosis. 
It is interesting to note that similar toxic effects are also observed in 
non-Beta-cells such as cardiac cells. Lipoproteins may affect Beta-Cellsurvival 
in a similar way, whereby VLDL and LDL are pro-apoptotic and HDL is protective.

[b][url=http://diabetesdestroyersystemviews.com/]http://diabetesdestroyersystemviews.com/[/url][/b]

Mitochondrial dysfunction has also been proposed as a common feature of both 
impaired insulin responsiveness of peripheral tissues and defective 
Beta-Cellsecretory function and survival.

-- 
Context is everything: 
http://forum.magnolia-cms.com/forum/thread.html?threadId=4acac53c-7839-436c-9bc1-9df4c8437a5c


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