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Cited by 155Growth Hormone and Insulin-like Growth FactorsPancreatic function and diabetesPituitary Gland Disorders and Treatments

Both Human Pituitary Growth Hormone and Recombinant DNA-Derived Human Growth Hormone Cause Insulin Resistance at a Postreceptor Site*

ROSENFELD, RON G., WILSON, DARRELL M., DOLLAR, LAURA A., BENNETT, ANN, HINTZ, RAYMOND L.·1982·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem-54-5-1033
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Abstract

We have investigated the effects on carbohydrate metabolism of human GH produced by recombinant DNA technology (methionyl-hGH) compared with pituitary hGH. Twelve normal adult male subjects received four daily im injections of either methionyl-hGH or pituitary hGH in a double blind, crossover study. Oral glucose tolerance tests and assays of insulin binding to peripheral monocytes were performed before th initial administration and 12 h after the fourth injection of both hGH preparations. Both methionyl-hGH and pituitary hGH resulted in significant carbohydrate intolerance, with a rise in fasting plasma glucose from 96.6 +/- 2.9 to 105.9 +/- 3.0 mg/ml (mean +/- SEM) after pituitary hGH and from 96.2 +/- 1.5 to 107.5 +/- 3.3 mg/dl after methionyl-hGH (P less than 0.01). The area under the glucose tolerance curve increased by 34% after pituitary hGH and by 37% after methionyl-hGH. With both hGH preparations, carbohydrate intolerance was associated with marked hyperinsulinemia, with a rise in fasting plasma insulin levels from 9.4 +/- 1.2 to 33.2 +/- 7.8 microU/ml after pituitary hGH and from 7.4 +/- 1.1 to 45.8 +/- 11.1 microU/ml after methionyl-hGH (P less than 0.01). The integrated plasma insulin levels during the oral glucose tolerance test tripled after both hGH preparations. The pronounced insulin resistance could not be attributed to an alteration in insulin receptor concentrations. Both hGH preparations were associated with small reductions in insulin binding to monocytes at tracer concentrations, but the decline in binding was not statistically significant. The calculated binding sites per cell and Ke were not significantly altered by hGH administration. We conclude that methionyl-hGH and pituitary hGH are indistinguishable in their ability to induce insulin-resistant carbohydrate intolerance. This decrease in insulin sensitivity cannot be attributed to an alteration in insulin binding, and presumably represents a postreceptor defect in insulin action.

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Crossref · 10.1210/jcem-54-5-1033

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Authors
ROSENFELD, R. G., WILSON, D. M., DOLLAR, L. A., BENNETT, A., & HINTZ, R. L.
Affiliations
Stanford Medicine (US)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
1982-05
Volume
54
Issue
5
Pages
1033-1038
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem-54-5-1033
OpenAlex
W1980214906
Cited by
155
References
26
Citations by year
2019: 2 · 2018: 1 · 2016: 2 · 2015: 2 · 2014: 1
FWCI
6.34
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
Keywords
growth hormone, recombinant human growth hormone, pituitary growth hormone, insulin resistance, carbohydrate intolerance, hyperinsulinemia, insulin receptor binding, monocytes, oral glucose tolerance
MeSH terms
Adult, Blood Glucose, DNA, Recombinant, Double-Blind Method, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Male, Monocytes, Growth Hormone

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