Other than causing your body to absorb nutrients, what affects does insulin cause. To clarify I am not concerned with injected insulin, I am more concerned with insulin secreted after meals. Also as a body builder wouldn’t I be more worried about glucagon, the hormone responsible for nutrients being released into the blood stream?
Good question, J Rod. I’ll hit on a few different points, but I’m sure others will have further points to expand upon and questions to raise.
I also want to ask a quick question of you, J-Rod: What do you think–or think you know–that glucagon does?
inhibits lipoylsis (i.e. the breakdown of stored triglyceride) directly by inhibiting hormone-sensitive lipase
inhibits fat oxidation (in addition to inhibiting lipolysis) by affecting carnitine palmitate transferase and entry of fatty acids into the mitochondria
stimulates lipogenesis (i.e. the creation and storage of triglyceride) by directly stimulating lipoprotein lipase
results in high serum triglycerides (i.e. conversion of excess glucose to triglyceride)
results in high total cholesterol, especially bad cholesterol (i.e. LDL), when the ratio of insulin to glucagon is high (regularly)
attenuates the presence of growth hormone when (insulin is) high
Now, these are just some of the actions that might be of interest from a physique or health standpoint. Obviously, there are many other positive issues associated with insulin that I hope others will address (i.e. IGF-1, anti-catabolic, etc.)
I belive glucagon to be the hormone responsible to releasing nutrients into the blood stream (mainly glucose?). I remember this much from bio last year, so if you can fill me in on what im missing, or what is incorrect it would be a big help.
J Rod, I too once believed that glucagon was the primary hormone involved in liver glycogenolysis. However, this appears not to be the case.
According to Michael Kjaer, the primary mechanims responsible for hepatic glucose production in humans are: 1) a decline in plasma insulin, and 2) some “other” factor produced by skeletal muscle.
However, glucagon and the catecholamines likely play a role during prolonged exercise. In addition, epinephrine may play a significant role during intense exercise.
Hey Timbo great Info…
one thiong not clear though:
you mentioned Insulin stimulating Lipase and also de-stimulating it… what is going on?
bumping for timbo
Yes, that’s right. I’ll try to illustrate the best that I can;-)
Adipose and muscle cells have both hormone sensitive lipase (HSL) and lipoprotein lipase (LPL). The former is involved in lipolysis (i.e. the breakdown of stored triglyceride), while the latter is involved in lipogenesis (i.e. the creation of stored triglyceride from free fatty acids).
So, one of the functions of insulin, as previously mentioned, is to inhibit HSL and thus inhibit the breakdown of stored triglyceride–either in the muscle or in adipocytes. In addition, insulin stimulates LPL and thus stimulates the creation and storage of triglyceride in muscle fibers and adipocytes.
While the latter, i.e. body fat, is looked upon unfavorably, the former should not be. While we all know that fat is stored in fat cells, many fail to realize that triglyceride is also stored in muscle cells as intramuscular triglyceride (i.e. IMTGs). IMTGs play a significant role of substrate utilization during exercise.
In addition, using and depleting some of the muscular stores of triglyceride provideds a reservoir for the dietary fat that you eat. This is similar to dietary carbohydrate and muscle and liver glycogen. Interesting, no?
Yes, it is.
Is this intramuscular fat the fat Don Alessi speaks about when he says that IGF-1 induced growth/repair will caus “spot reduction”? I hope not. anyway what do you think of his thoughts (see meltdown I)?
He says (if I got him correctly)
Let’s assume you have a muscle, untrained in the lactic acid/ IGF-1 type of conccentric damage department. releasing of IGF-1 in the muscle site will cause release of GH there (this must be true somehow because you can grow only one muscle if you want) the GH then, IN THAT SITE, will buld muscle/use the fat(inetmuscular?intra?epidermal? the closest available trigliceride?).
Don does not seem to offer any scientific support for his claims. Intramuscular adipose tissue is NOT the adipose tissue we most commonly think of as contributing to “soft” physiques.
Furthermore, Don makes no mention of the different types of adrenoceptors that the intramuscular adipose tissue might be comprised of. Finally, becuase lipolysis and the lipolytic cascade is primarily facilitated by the balance between the chatecholamines and insulin, his thought that GH is the PRIMARY mechanism behind this fat loss is partially flawed.
Spanky, if you don’t mind, I’ll get back to this later. For now, though, I’ll tease you with this.
The paracrine/autocrine IGF-1 system (as opposed to systemic, circulating IGF-1) is likely the most anabolic hormone there is, in terms of building muscle. For real!
When I say autocrine/paracrine system, this refers to a hormone that acts on the tissue(s) that release(s) it or nearby tissues, without entering the bloodstream. For example, IGF-1 released by a myofibril can act on that myofibril or a nearby myofibril in the autocrine/paracrine manner.
I’m going to review some of Coach Alessi’s thoughts on the matter. I don’t know for certain about spot reduction, per se, but this is definitely a site-specific, localized response.