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Tumor hypoglycemia: deficient splanchnic glucose output and deficient glucagon secretion
Abstract:
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.
Insights
A benign mesothelioma caused fasting hypoglycemia by decreasing splanchnic glucose output and impairing glucagon secretion. This study offers a new approach to analyzing hypoglycemia unrelated to excess insulin.
Area of Science:
- Endocrinology
- Oncology
- Metabolic Research
Background:
- Fasting hypoglycemia can present diagnostic challenges, particularly when not caused by insulinoma.
- Mesothelioma, a rare cancer, is not typically associated with metabolic disturbances like hypoglycemia.
Observation:
- A patient with benign mesothelioma experienced severe fasting hypoglycemia.
- Serum insulin and glucose utilization were low, while splanchnic glucose output was markedly reduced.
- Glucagon levels were low-normal and showed a poor response to alanine stimulation.
Findings:
- The primary cause of hypoglycemia was decreased splanchnic glucose output, linked to reduced glycogenolysis.
- Deficient glucagon secretion contributed to the impaired glucose production.
- Neither insulin-like activity nor somatostatin was detected in the tumor, and serum levels of NSILA-s were not elevated.
Implications:
- This case highlights an unusual paraneoplastic syndrome where a benign tumor disrupts glucose homeostasis.
- The findings suggest a potential novel mechanism involving an unknown tumor-secreted factor affecting hepatic glucose production and/or pancreatic alpha-cell function.
- The analytical approach may serve as a model for investigating other cases of non-insulin-mediated hypoglycemia.