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Old 08-20-2015
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Default Gemfibrozil

Can anyone please explain whether Gemfibrozil (Fibrate used for hypertriglyceridemia) has a final effect of beta oxidation of fatty acids or storage of fat?
Kaplan Biochem says its beta oxidation of fatty acids in peroxisomes. Whereas, in kaplan pharma videos, dr raymon says Gemfibrozil has insulin like effects such as storage of fat.
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Old 08-20-2015
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Gemfibrozil is a fibrate that stimulates proliferation of peroxisomes and increasing gene expression of lipoprotein lipase via PPAR - alpha, hydrolyzing triglycerides into FA for uptake into apidose then storage back into triglycerides

Drugs like Thiazolindiones improves insulin resistance mediated through PPAR - gamma.. Indirectly leads to storage of fats

PPARS are transcription factors that regulate lipid metabolism. Got this from kaplan LNs. Hope this helps

Last edited by charlietc; 08-20-2015 at 10:09 PM.
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Old 08-20-2015
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Quote:
Originally Posted by san.usmle View Post
Can anyone please explain whether Gemfibrozil (Fibrate used for hypertriglyceridemia) has a final effect of beta oxidation of fatty acids or storage of fat?
Kaplan Biochem says its beta oxidation of fatty acids in peroxisomes. Whereas, in kaplan pharma videos, dr raymon says Gemfibrozil has insulin like effects such as storage of fat.
Gemfibrozil acts on ppar - alpha. This is a nuclear receptor found in liver, kidney, heart tissues because the job of ppar-a is to stimulate lipoprotein lipase synthesis and beta oxidation and these tissues r rich in mitochondria where b- oxidation occurs...

TG from blood are taken up by liver broken down and undergo beta oxidation.. This decreases TG in blood.

The only reason why i would think he mentions that in his video is because maybe ppar-a also get stimulated in adipose tissue---> increase LPL and store fat there but dont go throught beta oxidation?? im not sure

Regardless of all the main effect is beta oxidation
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Old 08-21-2015
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Thanks for the explanations guys. It makes sense now
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