Novel Insights Into Effects of Cortisol and Glucagon on Nocturnal Glucose Production in Type 2 Diabetes.
cortisol
endogenous glucose production
glucagon
gluconeogenesis
glycogenolysis
type 2 diabetes
Journal
The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
received:
07
02
2020
accepted:
30
04
2020
pubmed:
7
5
2020
medline:
4
2
2021
entrez:
7
5
2020
Statut:
ppublish
Résumé
The effect of physiological changes in night-time cortisol and glucagon on endogenous glucose production (EGP) and nocturnal glycemia are unknown. To determine the effects of changes in cortisol and glucagon on EGP during the night. Two overnight protocols were conducted. In Protocol 1, endogenous cortisol was blocked with metyrapone and hydrocortisone infused either at constant (constant) or increasing (variable) rates to mimic basal or physiological nocturnal cortisol concentrations. In Protocol 2, endogenous glucagon was blocked with somatostatin and exogenous glucagon was infused at either basal or elevated rates to mimic nocturnal glucagon concentrations observed in nondiabetic (ND) and type 2 diabetes (T2D) individuals. EGP was measured using [3-3H] glucose and gluconeogenesis estimated with 2H2O in all studies. Mayo Clinic Clinical Research Trials Unit, Rochester, MN, US. In Protocol 1, 34 subjects (17 ND and 17 T2D) and in Protocol 2, 39 subjects (21 ND and 18 T2D) were studied. Endogenous glucose production. EGP, gluconeogenesis, and glycogenolysis were higher with variable than with constant cortisol at 7 am in T2D subjects. In contrast, nocturnal EGP did not differ in ND subjects between variable and constant cortisol. While elevated glucagon increased EGP, glycogenolysis, and gluconeogenesis in ND, the data in T2D subjects indicated that EGP and gluconeogenesis but not glycogenolysis were higher during the early part of the night. Nocturnal hyperglucagonemia, but not physiological rise in cortisol, contributes to nocturnal hyperglycemia in T2D due to increased gluconeogenesis.
Identifiants
pubmed: 32374825
pii: 5831336
doi: 10.1210/clinem/dgaa241
pmc: PMC7274493
pii:
doi:
Substances chimiques
Blood Glucose
0
Glucagon
9007-92-5
Hydrocortisone
WI4X0X7BPJ
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK029953
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK085516
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000135
Pays : United States
Informations de copyright
© Endocrine Society 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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