It is proposed that the raised serum glutamic pyruvic transaminase activity (SGPT) in viral hepatitis reflects an adaptive increase in glutamic pyruvic transminase in muscle for the increased transamination of alanine for post-absorptive glucose homeostasis. However, in a disease where the SGPT is elevated for four to six weeks, muscle cannot be an indefinite source of alanine unless it could, concurrently, resynthesize alanine. Since the two substrates of muscle are glucose and fat, fasting blood sugars, serum triglycerides and SGPT were estimated weekly, for one month, in 12 children with viral hepatitis. This was done to see if there was evidence of increased substrate availability for alanine synthesis, and whether any relationship existed between increased substrate availability and SGPT. The results show that there is a relationship between triglycerides and SGPT. This suggests that the hypertriglyceridaemia, by providing substrate to meet the energy requirements of muscle, spares glucose for alanine synthesis to maintain the alanine content of muscle. The paper suggests the existence of a glucose-alanine-pyruvate-glucose cycle in viral hepatitis and also reviews evidence for increased ammonia uptake by muscle, in liver diseases associated with raised SGPT, to support the concept of amino acid synthesis.
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