hypoglycemia question

[MCsoundt]

Having LOTS of trouble with this concept, so maybe some of you could help me out. What exactly are the roles of glucagon, NE/epi, cortisol, and GH in times of hypoglycemia?

Basically, most of my confusion stems from this: FA says b2 adrenergic receptors increase insulin release, but I always thought the purpose of sympathetic nervous system in times of hypoglycemia was to stimulate gluconeogenesis and INHIBIT insulin so that glucose could get to the glucose-independent organs (e.g. brain, RBCs). And then what about all those other hormones... I'm horribly confused by the physiology and regulation of hypoglycemia and have no clue where my missing link is. Any help would be awesome, ty.

---

Members don't see this ad.

 

[herewego]

First of all, insulin is needed to get glucose into adipose and skeletal muscles. So think of it this way, if you're sympathetic fight or flight is going off, you want to get glucose into where its needed. You do want gluconeogenesis in fight or flight, because glycogenolysis only lasts so long. If you have increased insulin, your cAMP decrease->decrease protein kinase A-> increased phosphofructokinase-2 because its inactive when phosphorylated-> leading to more glycolysis in the end. Glucagon does pretty much the opposite, increasing cAMP, increase protein kinase A, phosphorykating fructose bisphosphatase 2 (active), and pushing things to gluconeogenesis.

Glucagon, NE, and EPI will activate adenyly cyclase-> eventually leading to insulin release. Cortisol (stress hormone) increases PNMT which is the enzyme for conversion of NE->Epi-> same mechanism as above.

Hope that helps.

 

[MCsoundt]

First of all, insulin is needed to get glucose into adipose and skeletal muscles. So think of it this way, if you're sympathetic fight or flight is going off, you want to get glucose into where its needed. You do want gluconeogenesis in fight or flight, because glycogenolysis only lasts so long. If you have increased insulin, your cAMP decrease->decrease protein kinase A-> increased phosphofructokinase-2 because its inactive when phosphorylated-> leading to more glycolysis in the end. Glucagon does pretty much the opposite, increasing cAMP, increase protein kinase A, phosphorykating fructose bisphosphatase 2 (active), and pushing things to gluconeogenesis.

Glucagon, NE, and EPI will activate adenyly cyclase-> eventually leading to insulin release. Cortisol (stress hormone) increases PNMT which is the enzyme for conversion of NE->Epi-> same mechanism as above.

Hope that helps.

That does make sense. I think one of my biggest issues is that I've got conflicting info on what a lot of the hormones do, so I wanted to solidify them once and for all, and then maybe that will help me complete my understanding of this issue.

Glucagon: inc gluconeogenesis/lipolysis/proteolysis, stimulate insulin release

Cortisol: inc gluconeogenesis/lipolysis/proteolysis, inhibit the effects of insulin (diabetogenic)

GH: ??? inhibit the effects of insulin???

beta2 receptors: ???? my guess is stimulate gluconeogenesis/lipolysis/proteolysis, stimulate insulin release, idk!

alpha2: ??? inhibit insulin release?

Yeah, so you can see my knowledge is a wee-bit deficient. would love if someone could fill in those blanks for me and/or correct my mistakes. Muchas gracias