Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients

A. Garg, W. E. Grizzle, P. C. Kansal, T. V. Stabler, L. R. Boots

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Patients with hypopituitarism are predisposed to fasting hypoglycemia and are considered unusually sensitive to insulin-induced acute hypoglycemia. However, whether impaired response of counter-regulatory hormones, such as glucagon, epinephrine (E), and nor-epinephrine (NE) contribute to the susceptibility to acute hypoglycemia in hypopituitary patients has not been systematically evaluated. Therefore, we compared counter-regulatory hormone responses to insulin-induced acute hypoglycemia in 9 patients with hypopituitarism who were off hormone replacement therapy and 13 normal healthy subjects. All subjects received a prime-continuous intravenous infusion of insulin (0.1 Unit/kg body weight · h) till plasma glucose declined to less than 2.5 mmol/l or occurrence of hypoglycemic symptoms. All normal subjects and 7 out of 9 hypopituitary patients recovered spontaneously from hypoglycemia. Two hypopituitary patients with hypothalamic pathology however needed intravenous glucose, glucagon and hydrocortisone to assist recovery from hypoglycemia. Overall, patients with hypopituitarism showed a slower rate of recovery of plasma glucose after hypoglycemia than normal subjects (0.78 ± 0.33 mmol/l · h vs. 1.72 ± 0.15 mmol/l · h, respectively; p = 0.02). The responses of key counter-regulatory hormones, glucagon, E and NE, to hypoglycemia however were essentially similar in both the groups. We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired.

Original languageEnglish (US)
Pages (from-to)276-282
Number of pages7
JournalHormone and Metabolic Research
Volume26
Issue number6
StatePublished - 1994

Fingerprint

Norepinephrine
Glucagon
Hypoglycemia
Hormones
Insulin
Plasmas
Glucose
Recovery
Hydrocortisone
Hypopituitarism
Epinephrine
Pathology
Hypoglycemic Agents
Adrenocorticotropic Hormone
Hormone Replacement Therapy
Intravenous Infusions
Healthy Volunteers
Body Weight

Keywords

  • cortisol
  • epinephrine
  • glucagon
  • hypoglycemia
  • hypopituitarism
  • insulin
  • norepinephri ne

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Garg, A., Grizzle, W. E., Kansal, P. C., Stabler, T. V., & Boots, L. R. (1994). Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients. Hormone and Metabolic Research, 26(6), 276-282.

Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients. / Garg, A.; Grizzle, W. E.; Kansal, P. C.; Stabler, T. V.; Boots, L. R.

In: Hormone and Metabolic Research, Vol. 26, No. 6, 1994, p. 276-282.

Research output: Contribution to journalArticle

Garg, A. ; Grizzle, W. E. ; Kansal, P. C. ; Stabler, T. V. ; Boots, L. R. / Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients. In: Hormone and Metabolic Research. 1994 ; Vol. 26, No. 6. pp. 276-282.
@article{4852b4677a87482295b3974ae3312c8a,
title = "Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients",
abstract = "Patients with hypopituitarism are predisposed to fasting hypoglycemia and are considered unusually sensitive to insulin-induced acute hypoglycemia. However, whether impaired response of counter-regulatory hormones, such as glucagon, epinephrine (E), and nor-epinephrine (NE) contribute to the susceptibility to acute hypoglycemia in hypopituitary patients has not been systematically evaluated. Therefore, we compared counter-regulatory hormone responses to insulin-induced acute hypoglycemia in 9 patients with hypopituitarism who were off hormone replacement therapy and 13 normal healthy subjects. All subjects received a prime-continuous intravenous infusion of insulin (0.1 Unit/kg body weight · h) till plasma glucose declined to less than 2.5 mmol/l or occurrence of hypoglycemic symptoms. All normal subjects and 7 out of 9 hypopituitary patients recovered spontaneously from hypoglycemia. Two hypopituitary patients with hypothalamic pathology however needed intravenous glucose, glucagon and hydrocortisone to assist recovery from hypoglycemia. Overall, patients with hypopituitarism showed a slower rate of recovery of plasma glucose after hypoglycemia than normal subjects (0.78 ± 0.33 mmol/l · h vs. 1.72 ± 0.15 mmol/l · h, respectively; p = 0.02). The responses of key counter-regulatory hormones, glucagon, E and NE, to hypoglycemia however were essentially similar in both the groups. We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired.",
keywords = "cortisol, epinephrine, glucagon, hypoglycemia, hypopituitarism, insulin, norepinephri ne",
author = "A. Garg and Grizzle, {W. E.} and Kansal, {P. C.} and Stabler, {T. V.} and Boots, {L. R.}",
year = "1994",
language = "English (US)",
volume = "26",
pages = "276--282",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "Georg Thieme Verlag",
number = "6",

}

TY - JOUR

T1 - Counter-regulatory hormone responses to insulin-induced acute hypoglycemia in hypopituitary patients

AU - Garg, A.

AU - Grizzle, W. E.

AU - Kansal, P. C.

AU - Stabler, T. V.

AU - Boots, L. R.

PY - 1994

Y1 - 1994

N2 - Patients with hypopituitarism are predisposed to fasting hypoglycemia and are considered unusually sensitive to insulin-induced acute hypoglycemia. However, whether impaired response of counter-regulatory hormones, such as glucagon, epinephrine (E), and nor-epinephrine (NE) contribute to the susceptibility to acute hypoglycemia in hypopituitary patients has not been systematically evaluated. Therefore, we compared counter-regulatory hormone responses to insulin-induced acute hypoglycemia in 9 patients with hypopituitarism who were off hormone replacement therapy and 13 normal healthy subjects. All subjects received a prime-continuous intravenous infusion of insulin (0.1 Unit/kg body weight · h) till plasma glucose declined to less than 2.5 mmol/l or occurrence of hypoglycemic symptoms. All normal subjects and 7 out of 9 hypopituitary patients recovered spontaneously from hypoglycemia. Two hypopituitary patients with hypothalamic pathology however needed intravenous glucose, glucagon and hydrocortisone to assist recovery from hypoglycemia. Overall, patients with hypopituitarism showed a slower rate of recovery of plasma glucose after hypoglycemia than normal subjects (0.78 ± 0.33 mmol/l · h vs. 1.72 ± 0.15 mmol/l · h, respectively; p = 0.02). The responses of key counter-regulatory hormones, glucagon, E and NE, to hypoglycemia however were essentially similar in both the groups. We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired.

AB - Patients with hypopituitarism are predisposed to fasting hypoglycemia and are considered unusually sensitive to insulin-induced acute hypoglycemia. However, whether impaired response of counter-regulatory hormones, such as glucagon, epinephrine (E), and nor-epinephrine (NE) contribute to the susceptibility to acute hypoglycemia in hypopituitary patients has not been systematically evaluated. Therefore, we compared counter-regulatory hormone responses to insulin-induced acute hypoglycemia in 9 patients with hypopituitarism who were off hormone replacement therapy and 13 normal healthy subjects. All subjects received a prime-continuous intravenous infusion of insulin (0.1 Unit/kg body weight · h) till plasma glucose declined to less than 2.5 mmol/l or occurrence of hypoglycemic symptoms. All normal subjects and 7 out of 9 hypopituitary patients recovered spontaneously from hypoglycemia. Two hypopituitary patients with hypothalamic pathology however needed intravenous glucose, glucagon and hydrocortisone to assist recovery from hypoglycemia. Overall, patients with hypopituitarism showed a slower rate of recovery of plasma glucose after hypoglycemia than normal subjects (0.78 ± 0.33 mmol/l · h vs. 1.72 ± 0.15 mmol/l · h, respectively; p = 0.02). The responses of key counter-regulatory hormones, glucagon, E and NE, to hypoglycemia however were essentially similar in both the groups. We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired.

KW - cortisol

KW - epinephrine

KW - glucagon

KW - hypoglycemia

KW - hypopituitarism

KW - insulin

KW - norepinephri ne

UR - http://www.scopus.com/inward/record.url?scp=0028300860&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028300860&partnerID=8YFLogxK

M3 - Article

VL - 26

SP - 276

EP - 282

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 6

ER -