11 September 2007
Comment: "Hypoxia is a potential risk factor for chronic inflammation..."
Since hyperglycaemia and obesity go seemingly hand-in-hand, I am assuming that it is safe to say that VEGF transcription is inhibited in obese individuals, just as it is in those with a high glucose level. If this is true, then as the adipocytes of an obese patient increase in diameter (without dietary restrictions), the blood vessels cannot adequately supply nutrients to the fatty tissue, thus inducing a hypoxic state. Proinflammatory cytokines are released in this hypoxic state roughly two hours after the hypoxia is detected, and hypoxia response genes are then released about eight hours after the initial detection. Could this vicious cycle be prevented by somehow increasing VEGF expression to adequately perfuse blood (oxygen) to the growing masses of adipose tissue?
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2 comments:
VEGF is important in a negative way for cancer patients and those with macular degeneration. Keep in mind that there are always side effects that need to be looked at.
Jessica, I'm not sure if it is accurate to assume that VEGF is inhibited in obese people. In my opinion, it's always dangerous to assume ANYTHING in science. But given that the assumption IS true and what you're exploring here is inducing VEGF in obese patients to alleviate inflammation caused by hypoxia, I think my concern would be how to target this therapy strictly to the adipose tissue. Also, expression of VEGF is probably implicated in tons of other pathways which may cause side effects or problems, as mentioned by stephen.
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