Insulin to Impact on Protein and Amino Acid Metabolism

Abstract

The syndrome of cancer cachexia is characterized by severe weakness, debilitation and generalized host wasting. This malnourished state is associated with decreased survival1 and in up to one half of cancer patients, cancer cachexia has been implicated as the sole cause of death.2 The etiology of this syndrome is multifactorial in nature. While decreased nutrient intake is partly responsible, a major contribution comes from the well described abnormalities in host intermediary metabolism of carbohydrate, protein, and fat.3 Cancer patients have been reported to have abnormal peripheral glucose disposal,4 gluconeogenesis5 and whole body glucose turnover6 which confirm alterations in carbohydrate metabolism in these patients. Fat metabolism is also modified as evidenced by abnormal host lipids stores,7 and free fatty acid and glycerol turnover rates.8,9 Abnormalities of protein metabolism have been reported at the whole body level10,11 as well as in skeletal muscle11 and liver.11 The cachectic cancer patient ineffectively utilizes nutrients and furthermore seems to be unable to adapt to the malnourished state as normal man does by conserving lean body mass.12 In normal man, insulin is a major anabolic hormone which acts as a regulator of glucose, fat and protein metabolism. The role of insulin is one of conservation of mass either by decreasing catabolism or by increasing anabolism.