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Summary  Earlier findings on the pathogenesis of tumour hypoglycaemia [15] were confirmed and extended in a second patient with this disease. — A block of hepatic glucose release was found to be the main cause of hypoglycaemia in both patients suffering from large tumours of non-endocrine origin. The free fatty acid level failed to increase upon hypoglycaemia. Low free fatty acid levels correlated with an increased rate of glucose assimilation and glucose oxidation. — Immunoreactive, suppressible and nonsuppressible ILA measuredin vitro andin vivo were normal. — However, the serum of patient Z.B. inhibited lipolysis of adipose tissuein vitro to a greater extent than serum of normal subjects. This difference was no longer present after dialysis of the sera and the antilipolytic activity was now found in the diffusate. — The block of hepatic glucose release may be overcome by a pharmacological dose of intravenous glucagon. The block of hepatic glucose release is of paramount importance for the development of hypoglycaemia since the pharmacological blocking of lipolysis alone does not lead to hypoglycaemia, although it may increase glucose assimilation and glucose oxidation. — An attempt is being made to characterize further the antilipolytic substance which is present in increased amounts in the serum of patients with tumour hypoglycaemia.

The pathogenesis of tumour hypoglycaemia: Blocks of hepatic glucose release and of adipose tissue lipolysis