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If lipolysis was impaired, wouldn't that decrease the breakdown into FFA and decrease plasma levels? I dont understand the mechanism. Thanks!
 

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Actually, that seems paradoxical at first, but note which is the main hormone stimulated to be released with B2 stimulation. Its Insulin. {Remember the mnemonic RIRI, which is alpha1, apha2, beta1, beta2. Stimulation of the first 2 receptors decrease Renin and Insulin respectively, stimulation of the latter 2 receptors increase Renin and Insulin respectively}

So, when u use beta blockers, insulin release in inhibited. The body function as if there is Insulin resistance. Lipolysis gets impaired, since one of the key hormones involved in FFA rotation and storage (not release) is Insulin. That is, storage of FFA as fats require Insulin to be present (Insulin stimulates LPL, the hormone that combines 3 FFA with Glycerol to make a TG molecule ), hence FFA aren't stored as TG's, and their free levels in the blood rises.

In a nutshell, there is diabetes like picture with chronic beta blocker usage. That's why they aren't preferred in diabetic patients. They cause hyperlipidemia, not by impaired breakdown of fats(lipolysis), but because the FFA's aren't stored in the adipose tissues(lipogenesis), and the levels of FFA and other lipids rise in the blood.

Hope that helps!
 
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