Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion.
Fasting hypoglycemia occurred in a patient with a histologically benign mesothelioma; the serum insulin was low (2-4 muU./ml.), as was the glucose utilization rate. Splanchnic glucose output was markedly decreased on direct measurement (21 mg./min.; normal: 108-180 mg./min.). Splanchnic uptake of gluconeogenic substrates plasma glucagon was low normal during hypoglycemia and responded poorly to oral and intravenous alanine. The nonsuppressible insulin-like (NSILA-s) and somatomedin-like activities of the serum were not elevated, and the tumor did not release insulin-like activity on incubation nor did it contain somatostatin. The marked decrease in splanchnic glucose output was the principal cause of hypoglycemia, was associated with an apparent decrease in glycogenolysis, and was at least partly due to deficient glucagon secretion. The relationship of the tumor to these defects is unclear. The tumor may have secreted an unknown insulin-like material affecting primarily the liver and/or pancreatic alpha cell. The approach used here may serve as a paradigm for the analysis of hypoglycemia not caused by excessive insulin.
D005934:Glucagon / Q000097:blood / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D007003:Hypoglycemia / Q000209:etiology*; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism*; D008654:Mesothelioma / Q000150:complications* / Q000503:physiopathology; D010179:Pancreas / Q000378:metabolism*; D013899:Thoracic Neoplasms / Q000150:complications* / Q000503:physiopathology
D007328:Insulin; D005934:Glucagon; D005947:Glucose