Insulin, anabolic resistance

Insulin is a powerful anabolic hormone but it is unlikely that insulin deficiency causes skeletal muscle atrophy by direct action on muscle fibers (as opposed to neurogenic atrophy) except in chronic untreated cases. There is however a close parallel between the catabolic states induced by glucocorticoid excess and by insulin deficiency. Moreover, impaired insulin action is implicated in other endocrine myopathies as a contributory cause of muscle wasting. Both acromegaly and thyrotoxicosis are associated with insulin resistance due to a postreceptor defect, and secondary hyperparathyroidism due to hypophosphatemia also gives rise to insulin insensitivity. 

The production of both anabolic sex hormones and growth hormone decreases in aging and the result is muscle loss. Also the loss of neural motor cells gives rise to atrophy of the muscles. In the aging process an increased inflammatory activity can be seen and it causes degeneration of muscle tissue through insuline resistance and activation of protein breakdown enzymes. The increased inflammatory activity is due to both normal aging as well as the presence of multiple chronic diseases (Dutta 1997. 

Cohen JC, Hickman R. Insulin resistance and diminished glucose tolerance in powerlifters ingesting anabolic steroids. J Clin EndocrinolMetab. 1987 64 960-963. 

Urea, the end product of nitrogen metabolism, accumulates rapidly in ARF. Most patients with ARF have a primary stressful illness that results in ureagenesis, and thus protein breakdown is markedly accelerated. Protein catabolism in ARF may be stimulated as the result of insulin resistance, metabolic acidosis, circulating proteases and inflammatory mediators, and the effects of uremic toxins. The mechanism may be direct, via modulation of protein synthesis, or indirect, by inhibiting the action of anabolic hormones. ... 

Fujita S, Glynn BL, Timmerman KL et al. (2009) Supraphysiological hyperinsuhnaemia is necessary to stimulate skeletal muscle protein anabolism in older adults evidence of a true age-related insulin resistance of musde protein metabolism. Diabetologia 52, 1889-1898. 

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