Epinephrine exerts opposite effects on peripheral glucose disposal and glucose-stimulated insulin secretion. A stable label intravenous glucose tolerance test minimal model study
Abstract
Epinephrine (EPI) plays a pivotal role in regulating glucose metabolism both in splanchnic and peripheral tissues. Nevertheless, previous studies did not clarify the mechanisms by which EPI affect both glucose disposal processes in peripheral tissues and beta-cell secretion. The aim of this study was to investigate, in six normal volunteers, the effects of elevated EPI concentration on peripheral glucose disposal and insulin secretion by using the stable labeled (either [6,6-2H2] or [2-2H1]glucose) intravenous glucose tolerance test (IVGTT) in conjunction with the minimal models of labeled glucose disappearance and C-peptide secretion. Elevated plasma EPI concentration significantly decreased glucose effectiveness (SG*) by 29% (0.0059 +/- 0.0013 vs. 0.0083 +/- 0.0011 min-1, P < 0.05), and even more, 61%, insulin sensitivity (SI*); (22 +/- 6 x 10(4) vs. 54 +/- 20 x 10(4) min-1.pmol.l-1; P < 0.01). These findings are not due to an isotopic effect induced by an enhanced glycogen breakdown, because the [2-2H1]glucose tracer, which is not incorporated into glycogen, gave results similar to those of [6,6-2H2]glucose tracer. No differences were observed in first phase cell sensitivity, phi 1, in the EPI study (199 +/- 91 vs. 245 +/- 144 10(9), NS), but there was a significant increase in the second-phase cell sensitivity to glucose phi 2, (15.2 +/- 1.7 vs. 17.7 +/- 4.4 10(9).min-1, P < 0.05). In conclusion, EPI selectively impairs peripheral glucose metabolism because of its unique ability to simultaneously and independently decrease glucose effectiveness and insulin sensitivity. Furthermore, EPI enhances phi 2, the ratio between the C-peptide amount secreted during the second phase and the area under the curve of the glucose signal, indicating that the observed increase of C-peptide concentration is due not only to the augmented glucose signal but also to a specific EPI-mediated enhancement of beta-cell responsivity to glucose.
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Activation of the sympathetic nervous system and inhibition of the parasympathetic nerves decreases insulin secretion.
“Furthermore, activation of the sympathetic nervous system and inhibition of the parasympathetic nerves decreases insulin secretion; thus, changes in the autonomic nervous system could explain the absence of a compensatory insulin response after sleep curtailment.132”
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- Authors
- Avogaro, A., Toffolo, G., Valerio, A., & Cobelli, C.
- Affiliations
- Azienda Ospedale - Università Padova (IT)
- University of Padua (IT)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1996-10-01
- Volume
- 45
- Issue
- 10
- Pages
- 1373-1378
- ISSN
- 0012-1797 (ISSN-L)
- OpenAlex
- W2105732055
- Cited by
- 55
- References
- 0
- Citations by year
- 2022: 2 · 2020: 3 · 2019: 2 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 1 · 2013: 4 · 2012: 1
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Consiglio Nazionale delle Ricerche
- National Institutes of Health (5p41rr002176-11)
- National Center for Research Resources (RR 02176)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- epinephrine, glucose-stimulated insulin secretion, beta-cell function, glucose effectiveness, insulin sensitivity, C-peptide secretion, second-phase insulin response, intravenous glucose tolerance test, minimal model analysis, glucose metabolism, glycogenolysis
- MeSH terms
- Insulin Secretion, Adult, Blood Glucose, C-Peptide, Epinephrine, Glucose, Glucose Tolerance Test, Humans, Insulin, Islets of Langerhans, Kinetics, Male, Models, Biological, Reference Values, Time Factors
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