CoChat
Sign Up
Cited by 321Growth Hormone and Insulin-like Growth FactorsPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

The Effect of Growth Hormone on Glucose Metabolism and Insulin Secretion in Man*

BRATUSCH-MARRAIN, PAUL R., SMITH, DOUGLAS, DEFRONZO, RALPH A.·1982·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem-55-5-973
Open this paper in CoChat — free account

Abstract

Pharmacological doses of GH are known to impair glucose tolerance. In the present study we have employed the euglycemic insulin and hyperglycemic clamp techniques to examine the effect of physiological elevations in plasma GH concentrations (27 ± 2 ng/ml) on the tissue responses to insulin and on glucose-stimulated insulin secretion. Three types of studies (low dose insulin clamp, high dose insulin clamp, and hyperglycemic clamp) were performed in young healthy volunteers before and after the infusion of GH (2 μg/kg-h) for 2 and 12 h. In the low dose insulin clamp studies, the plasma insulin concentration was acutely raised and was maintained at 59 ±4 μU/ml, while plasma glucose was maintained at basal levels. After 2 h of GH infusion, insulin-mediated glucose metabolism was slightly, although not significantly, decreased (4.48 ± 0.56 vs. 5.04 ± 0.39 mg/kg-min) in the control study. After 12 h of GH infusion, however, insulin-mediated glucose uptake decreased by 32 ± 9% (3.36 ± 0.40 mg/kg-min; P < 0.01). Basal endogenous glucose production (2.02 ± 0.07 mg/kg-min) was suppressed by 89 ± 4% in the control study. After short term GH infusion, the degree of suppression (90 ± 5%) was similar to the control value. After 12 h of GH infusion, however, suppression of endogenous glucose production (78 ± 5%) was slightly less than that in controls (P < 0.05). In the high dose insulin clamp studies, GH was infused for either 2 or 12 h, after which plasma insulin levels were increased to 2292 ± 96 μU/ml while maintaining euglycemia (high dose insulin clamp study). Insulin-mediated glucose uptake was 11.22 ± 0.53 mg/kg-min in the control study, slightly lower during short term GH infusion (9.56 ± 1.00 mg/kg-min) and significantly diminished after long term GH infusion (7.16 ± 1.12 mg/kg-min; P <0.02). In the hyperglycemic clamp studies, plasma glucose was raised and maintained at 125 mg/dl above the basal level. Glucose metabolism in controls (8.68 ± 0.53 mg/ kg-min) was decreased by 31 ± 7% after 2 h and by 44 ± 6% after 12 h of GH infusion. The mean increment in plasma insulin in response to hyperglycemia (control, 56 ± 10 μU/ml) was unaltered after 2 and 12 h of GH administration. Total binding of [125I]insulin to monocytes was 7.0 ± 0.5% before GH infusion. After 2 h of GH administration, no change in total specific insulin binding (7.4 ± 0.4%) occurred. After 12 h of exposure to GH, however, total binding was decreased (5.9 ± 0.4% P < 0.02) due to a decrease in receptor affinity. We conclude that physiological elevations in GH 1) induce state a of insulin resistance within 2–12 h, 2) only slightly impair insulin's suppressive effect on endogenous glucose production, indicating that the primary site of insulin resistance resides in peripheral tissues, 3) do not alter the plasma insulin response to hyperglycemia, and 4) cause a decrease in insulin binding that results from a decrease in receptor affinity. The inability to overcome the defect in glucose metabolism at high plasma insulin concentrations suggests that a significant postreceptor defect (in addition to the receptor defect) contributes to the observed insulin resistance. (J Clin Endocrinol Metab55: 973, 1982)

Overview

Integrity signals

Registry

Crossref · 10.1210/jcem-55-5-973

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

1 retracted

Show all 54 references

Cited by

Sorted by citations

Related

See all

Metadata

Authors
BRATUSCH-MARRAIN, P. R., SMITH, D., & DEFRONZO, R. A.
Affiliations
Yale University (US)
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
1982-11
Volume
55
Issue
5
Pages
973-982
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem-55-5-973
OpenAlex
W2171960002
Semantic Scholar
c4e4067abc17770df77f7da924aa42c745bebe94
Cited by
321
References
54
Citations by year
2026: 1 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 5 · 2014: 3 · 2013: 4 · 2012: 2
FWCI
7.51
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 › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
growth hormone, glucose metabolism, insulin secretion, glucose-stimulated insulin secretion, insulin-stimulated glucose uptake, endogenous glucose production, glucose tolerance, hyperglycemic clamp, hyperinsulinemic-euglycemic clamp, insulin sensitivity, insulin resistance
MeSH terms
Adult, Amino Acids, Blood Glucose, Fatty Acids, Nonesterified, Glucose, Humans, Insulin, Kinetics, Liver, Male, Monocytes, Receptor, Insulin, Growth Hormone

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review