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Some of my customers have asked me about the usage in metformin, as well as insulin with or without GH. Both of these harsh drugs are actually used in most cases in combination with with GH to negate the negative effect of GH on insulin sensitivity. GH by its nature releases glucose (and fatty acids) to the circulation, this is part of it metabolic effect as a stress hormone. The raised blood sugar levels overloads the pancreas which leads in time to insulin resistance at least to some degree. Diet rich in high glycemic carbs has same effect to some extent, this is why some heavy duty athletes, who uses carb loading, especially post workout find the usage in insulin or metformin as helpful, it helps to balance the sugar levels and support the pancreas. Here is where the IGF1 shines, IGF1 is much more healthy and effective for this purpose, the IGF1 naturally balances the insulin levels and increases insulin sensitivity, helps to mobilize fatty acids which helps to reduce fat, in oppose to insulin which directly causes to store fat, and of course optimizes the anabolic, metabolic and anti catabolic effect of the body with or without GH.
For some references -
- http://www.ncbi.nlm.nih.gov/pubmed/9129466
------------conclusions -
GH and IGF-I combined further enhanced fat oxidation while reducing protein catabolism. Serum insulin concentrations were significantly increased by GH but decreased by IGF-I. GH significantly decreased serum total triiodothyronine concentrations and IGF-I significantly decreased serum corticosterone concentrations.
- http://www.ncbi.nlm.nih.gov/pubmed/10571453
-----------results and conclusions
RESULTS:
Administration of IGF-I, but not GH, attenuates dexamethasone-induced protein catabolism and increases insulin sensitivity. Simultaneous treatment with GH and IGF-I additively increases the serum concentration of IGF-I, whole-body anabolism, and lipid oxidation. GH or IGF-I when given alone produces similar increases in the serum concentration of IGF-I. However, GH selectively increases skeletal muscle mass whereas IGF-I selectively attenuates the intestinal atrophy and abnormal intestinal ion transport induced by TPN. These tissue-selective anabolic effects of GH and IGF-I are associated with differential increases in protein synthesis in skeletal muscle and jejunum, respectively.
CONCLUSIONS:
Simultaneous treatment with GH and IGF-I may offer the greatest clinical efficacy because of improved nitrogen retention in association with enhanced lipid oxidation and stimulation of protein synthesis in multiple tissue types.
For some references -
- http://www.ncbi.nlm.nih.gov/pubmed/9129466
------------conclusions -
GH and IGF-I combined further enhanced fat oxidation while reducing protein catabolism. Serum insulin concentrations were significantly increased by GH but decreased by IGF-I. GH significantly decreased serum total triiodothyronine concentrations and IGF-I significantly decreased serum corticosterone concentrations.
- http://www.ncbi.nlm.nih.gov/pubmed/10571453
-----------results and conclusions
RESULTS:
Administration of IGF-I, but not GH, attenuates dexamethasone-induced protein catabolism and increases insulin sensitivity. Simultaneous treatment with GH and IGF-I additively increases the serum concentration of IGF-I, whole-body anabolism, and lipid oxidation. GH or IGF-I when given alone produces similar increases in the serum concentration of IGF-I. However, GH selectively increases skeletal muscle mass whereas IGF-I selectively attenuates the intestinal atrophy and abnormal intestinal ion transport induced by TPN. These tissue-selective anabolic effects of GH and IGF-I are associated with differential increases in protein synthesis in skeletal muscle and jejunum, respectively.
CONCLUSIONS:
Simultaneous treatment with GH and IGF-I may offer the greatest clinical efficacy because of improved nitrogen retention in association with enhanced lipid oxidation and stimulation of protein synthesis in multiple tissue types.