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Cited by 54Pancreatic function and diabetesDiabetes and associated disordersDiabetes Management and Research

Serum glucagon counterregulatory hormonal response to hypoglycemia is blunted in congenital hyperinsulinism

Hussain, Khalid, Bryan, Joseph, Christesen, Henrick T., Brusgaard, Klaus, Aguilar-Bryan, Lydia·2005·Diabetes
DOI 10.2337/diabetes.54.10.2946
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Abstract

The mechanisms involved in the release of glucagon in response to hypoglycemia are unclear. Proposed mechanisms include the activation of the autonomic nervous system via glucose-sensing neurons in the central nervous system, via the regulation of glucagon secretion by intra-islet insulin and zinc concentrations, or via direct ionic control, all mechanisms that involve high-affinity sulfonylurea receptor/inwardly rectifying potassium channel-type ATP-sensitive K(+) channels. Patients with congenital hyperinsulinism provide a unique physiological model to understand glucagon regulation. In this study, we compare serum glucagon responses to hyperinsulinemic hypoglycemia versus nonhyperinsulinemic hypoglycemia. In the patient group (n = 20), the mean serum glucagon value during hyperinsulinemic hypoglycemia was 17.6 +/- 5.7 ng/l compared with 59.4 +/- 7.8 ng/l in the control group (n = 15) with nonhyperinsulinemic hypoglycemia (P < 0.01). There was no difference between the serum glucagon responses in children with diffuse, focal, and diazoxide-responsive forms of hyperinsulinism. The mean serum epinephrine and norepinephrine concentrations in the hyperinsulinemic group were 2,779 +/- 431 pmol/l and 2.9 +/- 0.7 nmol/l and appropriately rose despite the blunted glucagon response. In conclusion, the loss of ATP-sensitive K(+) channels and or elevated intraislet insulin cannot explain the blunted glucagon release in all patients with congenital hyperinsulinism. Other possible mechanisms such as the suppressive effect of prolonged hyperinsulinemia on alpha-cell secretion should be considered.

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Authors
Hussain, K., Bryan, J., Christesen, H. T., Brusgaard, K., & Aguilar-Bryan, L.
Affiliations
  • National Health Service (GB)
  • Baylor College of Medicine (US)
  • Department of Pediatrics/Genetics, University Hospital Odense, Denmark
  • Odense University Hospital (DK)
  • Department of Molecular and Cellular Biology, Baylor College of Medicine Houston, Texas
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2005-10-01
Volume
54
Issue
10
Pages
2946-2951
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.54.10.2946
OpenAlex
W2152901707
Cited by
54
References
45
Citations by year
2021: 5 · 2020: 3 · 2019: 3 · 2018: 3 · 2016: 1 · 2015: 3 · 2014: 7 · 2013: 3 · 2012: 1
FWCI
5.39
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (DK-67571, DK52771, R01DK052771)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
Keywords
congenital hyperinsulinism, glucagon secretion, hypoglycemia, hyperinsulinemic hypoglycemia, counterregulatory hormones, epinephrine, norepinephrine, ATP-sensitive potassium channels, sulfonylurea receptor, focal hyperinsulinism
MeSH terms
Adenosine Triphosphate, Child, Preschool, Diazoxide, Epinephrine, Fatty Acids, Nonesterified, Female, Glucagon, Homeostasis, Hormones, Humans, Hyperglycemia, Hyperinsulinism, Infant, Insulin, Islets of Langerhans, Ketone Bodies, Male, Mutation, Norepinephrine, Receptors, Drug, Potassium Channels, ATP-Binding Cassette Transporters, Potassium Channels, Inwardly Rectifying, Sulfonylurea Receptors

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