Some members have asked me about the usage in metformin, as well as insulin with or without GH. first let me state that insulin is a harsh drug and should be avoided for any athlete performance enhancing purposes. Metformin is used by itself or in combination with with GH to counter balance the negative effect of GH on insulin sensitivity. I'll explain a bit - 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 healthier, carries less side effects then Metformin, and certainly then insulin, and carries some distinct anabolic, metabolic and anti catabolic advantages that Metformin simply doesn't offer. 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 is known as the most anabolic hormone in the body and posses as shown in clinical literature below anti catabolic traits that even GH by itself fails to deliver

For some references to support and explain these -

• 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.