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Abstract
Oral glucose tolerance (GTT) was investigated in 14 patients with liver disease and
in whom IV galactose tolerance (GaTT) was used as a measure of liver function. Impairment
of GTT was found in 1 of 5 patients with hepatitis and in 6 of 9 with cirrhosis. Impairment
was closely correlated with impairment of GaTT. Blood glucose and immunoreactive insulin
(IRI) levels during GTT in the 14 patients were correlated. IRI levels were the same
as in normal subjects but occurred at higher blood glucose levels. The linear regression
of IRI on blood glucose revealed that for similar increments in blood glucose, liver
disease patients had less increase in IEI than that in normal subjects or diabetic
patients with the same blood glucose levels. In cirrhotic subjects with clinical hyperestrogenism
fasting immunoreactive growth hormone (GH) was elevated and did not decrease normally
after glucose administration. IV galactose alone decreased these levels and appeared
to potentiate the effect of glucose on GH. Fasting free fatty acid (FFA) levels were
also elevated and did not decrease normally after glucose administration. In hepatitis
GH and FFA levels were normal. Maturity-onset diabetic persons with the same degree
of impairment of GTT had normal GaTT. Impaired GTT in liver disease is related to
the degree of liver damage and is associated with decreased insulin production. Elevated
GH and FFA levels do not correlate with glucose intolerance. The impaired insulin
production might be explained by a deficiency in the intestinal or hepatic factors
that stimulate insulin secretion during carbohydrate absorption.
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Article info
Publication history
Accepted:
September 16,
1968
Received:
June 4,
1968
Footnotes
☆This study was supported by Grant AM 10632-01A1 and FR 000 96-08, National Institutes of Health, Bethesda, Md.
☆☆Part of this work has been reported in abstract form in the Program of the Twenty-eighth Annual Meeting of the American Diabetes Association, Diabetes 17:327, 1968.
Identification
Copyright
© 1969 Published by Elsevier Inc.
