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Old 10-21-2014
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Default beta blocker and diabetes

On a uworld question it states in the explanation that "Additionally, blockade of Beta 2 adrenergic receptors inhibits hepatic gluconeogenesis and peripheral glycogenolysis and lipolysis. For this reason, non-selective Beta-blockers should not be used in diabetic patients."

From this I take it that it is saying if you were to STIMULATE beta 2 then you would increase hepatic gluconeogenesis and peripheral glycogenolysis --> increasing blood sugar.

In First AID 2014 on page 244 it says that Beta 2 increases insulin release. Wouldn't the insulin release due to beta 2 receptor stimulation lower hepatic gluconeogenesis and glycogenolysis and promote storage and metabolism instead?

The QID for this is 1492 if anyone wants to look it up. Please clear this up for me if you can. I understand the answer to the question, but that specific part of the explanation confused me a bit. Thanks!
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Old 10-21-2014
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An inhibition of hepatic gluconeogenesis and peripheral glycogenolysis and lipolysis = inhibition of glucagon effects, why?

Glucagon works through Gs receptor, just as Beta-receptors do, so it increases cAMP too. When a beta 2 blocker is used, which would decrease cAMP, that receptor is occupied but the glucagon bypass that limitation and causes an opposite effect (increase cAMP) . That's why is used in beta blocker overdose and also increases HR and myocardial contractility.

As you said, B2 stimulation increase insuline releasing, but when the receptor is busy with a beta blocker a beta agonist won't do nothing on that receptor, that means insuline secretion won't be increased.

In summary:

B2 blockage (or any Gs receptor blockage) = busy receptor = decreased cAMP = inhibition of hepatic gluconeogenesis and peripheral glycogenolysis and lipolysis

However keep in mind glucagon and glucagon like peptide also increase insuline relea via Gs/Gq and beta 2 receptor respectively .
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