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Cited by 139Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsMetabolism, Diabetes, and Cancer

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

Hormonal control of substrate cycling in humans.

Open access
Miyoshi, H, Shulman, G I, Peters, E J, Wolfe, M H, Elahi, D, Wolfe, R R·1988·Journal of Clinical Investigation
DOI 10.1172/jci113487PMC PMC442588
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Abstract

Recent studies have established the existence of substrate cycles in humans, but factors regulating the rate of cycling have not been identified. We have therefore investigated the acute response of glucose/glucose-6P-glucose (glucose) and triglyceride/fatty acid (TG/FA) substrate cycling to the infusion of epinephrine (0.03 microgram/kg.min) and glucagon. The response to a high dose glucagon infusion (2 micrograms/kg.min) was tested, as well as the response to a low dose infusion (5 ng/kg.min), with and without the simultaneous infusion of somatostatin (0.1 microgram/kg.min) and insulin (0.1 mU/kg.min). Additionally, the response to chronic prednisone (50 mg/d) was evaluated, both alone and during glucagon (low dose) and epinephrine infusion. Finally, the response to hyperglycemia, with insulin and glucagon held constant by somatostatin infusion and constant replacement of glucagon and insulin at basal rates, was investigated. Glucose cycling was calculated as the difference between the rate of appearance (Ra) of glucose as determined using 2-d1- and 6,6-d2-glucose as tracers. TG/FA cycling was calculated by first determining the Ra glycerol with d5-glycerol and the Ra FFA with [1-13C]palmitate, then subtracting Ra FFA from three times Ra glycerol. The results indicate that glucagon stimulates glucose cycling, and this stimulatory effect is augmented when the insulin response to glucagon infusion is blocked. Glucagon had minimal effect on TG/FA cycling. In contrast, epinephrine stimulated TG/FA cycling, but affected glucose cycling minimally. Prednisone had no direct effect on either glucose or TG/FA cycling, but blunted the stimulatory effect of glucagon on glucose cycling. Hyperglycemia, per se, had no direct effect on glucose or TG/FA cycling. Calculations revealed that stimulation of TG/FA cycling theoretically amplified the sensitivity of control of fatty acid flux, but no such amplification was evident as a result of the stimulation of glucose cycling by glucagon.

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Crossref · 10.1172/jci113487

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Metadata

Authors
Miyoshi, H., Shulman, G. I., Peters, E. J., Wolfe, M. H., Elahi, D., & Wolfe, R. R.
Affiliations
  • Shriners Hospitals for Children - Galveston (US)
  • Harvard University (US)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1988-05-01
Volume
81
Issue
5
Pages
1545-1555
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci113487
PMC
PMC442588
OpenAlex
W2007418665
Cited by
139
References
35
Citations by year
2025: 2 · 2024: 2 · 2023: 2 · 2022: 6 · 2021: 1 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 5
FWCI
13.12
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Deutsches Krebsforschungszentrum
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK040936, DK34817)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
substrate cycling, glucagon, epinephrine, insulin, somatostatin, prednisone, hyperglycemia, fatty acid flux, hormonal regulation of metabolism
MeSH terms
Adult, Blood Glucose, Epinephrine, Fatty Acids, Glucagon, Glucose, Humans, Hyperglycemia, Insulin, Prednisone, Triglycerides

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