|Can you clarify?
Aug 2, 2002
I've noticed alot of diabetics develop the central obesity similar to what I'm going through with PIs.My question involves glucose intolerance/insulin resistance. Are they the same thing? Can this occur and your fasting glucose levels still be in line? Is isulin resistance when the body (pancreas)produces too little insulin and then carbs can't be broken down? Could this be related also to the nukes that cause mitochondrial toxcity particularly in the pancreas? Also, if sugars can't enter into a cell to be burned as energy what happens to the sugar in the body?Finally I've been reading up and see things like chromium picolinate etc can help to burn sugars more efficiently, what do you think? Lastly is there a state where the body produces too much insulin? I know I've asked alot of questions,but I'm just trying to make some sense of why this is happening. Thanks....
Response from Ms. Fields-Gardner
Glucose intolerance reflects the body's reduced ability to appropriately metabolize glucose. One reason why this can happen is insulin resistance. Insulin resistance can be a problem in any injury or disease, even with normal fasting blood glucose. After eating, glucose levels rise and insulin responds to deliver glucose for use and storage.
In the case of insulin resistance, lack of production is not the real problem. In an effort to keep up with rising glucose, insulin levels may continue to rise with less effectiveness in reducing glucose levels. The result we are concerned about is the resulting lack of storage in normal subcutaneous fat stores and potential increase in inappropriate fat deposits.
The question about chromium picolinate is an interesting one. First you should know that there has been some suggestion that this supplement may be associated with DNA fragmentation and mutagenic effects. While these reports are controversial, studies of the potential benefits in carbohydrate and lipid metabolism improvements are ongoing. Rat studies suggest an improvement in triglyceride levels, insulin sensitivity, and catabolism with corticosteroid use. How this translates to HIV-infected humans will be interesting to see.
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