HGH and Diabetes.....

[TRA]

HGH exhibits its effect on pancreatic beta cells, promoting enhanced insulin secretion which usually exhibits itself to some degree as hyperinsulinemia.

This can lead to a degree of insulin resistance and possibly the development of type 2 diabetes. No different really as to the cause of the hyperinsulinemia, either HGH mediated or due to constantly elveated levels of Blood Glucose causing this state...

The best thing is to be able to monitor and manage BG. GDAs, Low GI diet, etc to reduce the possibility.

A nutritional phase aimed at increasing insulin sensitivity certainly could help, as could the chromium, and if one chooses, even metformin.

[Deep_Fried]

A nutritional phase aimed at increasing insulin sensitivity certainly could help, as could the chromium, and if one chooses, even metformin.

I agree except for the Metformin to be used in conjunction with some GH protocols. Maybe not so much for a "fat loss" GH protocol, as much as one for helping gain mass.
The reasons for this are due to the mechanism of action of Metformin. Metformin inhibits the signaling pathways that IGF-1 activates. It also decreases insulin levels which leads to lower synthesis of hepatic IGF-1 as well as a notable increase in IGFBP3 (IGF-1 Binding Protein 3).

A nice snippet of related info by DatBtrue:

<partial cut/paste from the full post on AM>

GH binds with high affinity to its receptor, found in tissues throughout the body, and activation of this receptor stimulates the synthesis and secretion of insulin-like growth factor 1 (IGF-1). Although 90% of circulating IGF-1 is synthesized and secreted by the liver, many types of cells, including some found in the brain, muscle and vasculature, are capable of IGF-1 production.

Binding of the hormone IGF-1 to the IGF-1 receptor (IGFR) causes potent mitogenic effects, including increases in DNA, RNA and protein synthesis.

IGF-1 binding activates the IGF-1 receptor (IGFR), a receptor tyrosine kinase (which in essence means subsequent pathway activation will be by phosphorylation symbolized below by red p). The IGFR subsequently recruits the insulin receptor substrate (IRS-1), which results in the activation of two signaling pathways: the Ras–Raf– MEK–ERK pathway and the PI3K–Akt pathway. The Ras–Raf–MEK–ERK pathway is crucial in mitosis-competent cells for cell proliferation and cell survival. However, in adult skeletal muscle, the function of the Ras–Raf–MEK–ERK pathway is less clear.

The PI3K–Akt pathway has been shown to be both necessary and sufficient to induce skeletal muscle hypertrophy.

Moving down that pathway it has been demonstrated that Akt activity is required for IGF-1- mediated hypertrophy, and expression of activated Akt is sufficient to induce muscle hypertrophy.

Moving further down the pathway we find mTOR has been shown to have an important and central function in integrating a variety of growth signals, from simple nutritional stimulation to activation by protein growth factors, resulting in protein synthesis. Akt phosphorylates (or activates) mTOR and both Akt phosphorylation and mTOR phosphorylation are increased during muscle hypertrophy.



Metformin

Metformin chronically activates AMP-activated kinase (AMPK). AMPK slows liver glucose output by down-regulating expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase; in skeletal muscle, it boosts the efficiency of insulin-stimulated glucose uptake by increasing expression of GLUT-4. These effects mandate a down-regulation of insulin secretion.

The resulting reduction of liver insulin activity will suppress liver production of IGF-I while boosting that of IGFBP-1, thereby decreasing plasma free IGF-I.

Stimulation of AMPK with Metformin also interferes with the Ras–Raf–MEK–ERK pathway of IGF-I signaling by inhibiting the ability of IGF-I to activate ras and its downstream targets.

Stimulation of AMPK with Metformin also blocks the ability of the PI3K-Akt pathway to activate mTOR.

Since the Ras–Raf–MEK–ERK cascade, as well as mTOR and its downstream targets, are key mediators of IGF-I’s ability to increase hypertrophy a systemic increase in AMPK activity as brought about by Metformin will hinder the potential for hypertrophy not only by diminishing plasma levels of insulin and free IGF-I, but also by intervening in the post-receptor intracellular pathways mediated events which bring about these bodybuilding effects.

[TRA]

Great info, deep fried.