Measurement of plasma calcitonin gene-related peptide concentration in healthy humans and patients with type II diabetes mellitus: Responses to meal ingestion and hyperinsulinemia

W. Bradford Carter, H. Heath, R. A. Rizza, P. C. Butler

Research output: Contribution to journalArticle

Abstract

Calcitonin gene-related peptide (CGRP) has been shown to cause insulin resistance and impaired insulin secretion in animal studies. Because Type II diabetes mellitus is characterized by these abnormalities, CGRP has been implicated in the pathogenesis of this disease. However, it is not known whether the concentration of circulating CGRP responds to meal ingestion or hyperinsulinemia, and it remains to be determined whether plasma CGRP concentrations are increased in patients with Type II diabetes mellitus. We applied a new, highly-specific and sensitive immunochemiluminometric assay to measure the concentration of circulating CGRP in patients with Type II diabetes mellitus and matched healthy control subjects both before and following ingestion of a mixed meal. Plasma CGRP concentrations did not change in response to meal ingestion in either healthy subjects or patients with Type II diabetes mellitus and was not increased in patients with Type II diabetes mellitus versus control subjects either before (2.4 ± 0.9 vs 5.0 ± 2.3 pmol/l, P = 0.35) or following (0.4 ± 0.2 vs 0.9 ± 0.34 pmol/l/3 h [area above fasting concentration] P = 0.311 meal ingestion. To determine if hyper insulinemia increased circulating CGRP concentrations in healthy humans, plasma insulin was increased from fasting (40 pmol/l) to high physiological concentrations (200 pmol/l) and supraphysiologic concentrations (600 pmol/l) by a constant low dose (0.6 mU/kg/min) or high dose insulin (2 mU/kg/min) infusion while plasma glucose was maintained constant with a variable glucose infusion. There was no increase in circulating CGRP from fasting levels during either the low dose (3.9 ± 1.5 vs 3.5 ± 1.5 pmol/l) or high dose (2.3 ± 0.7 vs 1.9 ± 0.6 pmol/l) insulin infusion. We conclude that circulating concentrations of CGRP do not change in response to meal ingestion or hyperinsulinemia, and that increased circulating CGRP concentrations are not responsible for the insulin resistance or impaired insulin secretion characteristic of patients with Type II diabetes mellitus.

Original languageEnglish (US)
Pages (from-to)99-103
Number of pages5
JournalEndocrinology and Metabolism
Volume2
Issue number2
StatePublished - 1995

Fingerprint

Calcitonin Gene-Related Peptide
Hyperinsulinism
Type 2 Diabetes Mellitus
Meals
Eating
Insulin
Fasting
Insulin Resistance
Healthy Volunteers
Glucose

ASJC Scopus subject areas

  • Endocrinology

Cite this

Measurement of plasma calcitonin gene-related peptide concentration in healthy humans and patients with type II diabetes mellitus : Responses to meal ingestion and hyperinsulinemia. / Bradford Carter, W.; Heath, H.; Rizza, R. A.; Butler, P. C.

In: Endocrinology and Metabolism, Vol. 2, No. 2, 1995, p. 99-103.

Research output: Contribution to journalArticle

@article{e70f21c1b37f463ba1465cda113ec0fd,
title = "Measurement of plasma calcitonin gene-related peptide concentration in healthy humans and patients with type II diabetes mellitus: Responses to meal ingestion and hyperinsulinemia",
abstract = "Calcitonin gene-related peptide (CGRP) has been shown to cause insulin resistance and impaired insulin secretion in animal studies. Because Type II diabetes mellitus is characterized by these abnormalities, CGRP has been implicated in the pathogenesis of this disease. However, it is not known whether the concentration of circulating CGRP responds to meal ingestion or hyperinsulinemia, and it remains to be determined whether plasma CGRP concentrations are increased in patients with Type II diabetes mellitus. We applied a new, highly-specific and sensitive immunochemiluminometric assay to measure the concentration of circulating CGRP in patients with Type II diabetes mellitus and matched healthy control subjects both before and following ingestion of a mixed meal. Plasma CGRP concentrations did not change in response to meal ingestion in either healthy subjects or patients with Type II diabetes mellitus and was not increased in patients with Type II diabetes mellitus versus control subjects either before (2.4 ± 0.9 vs 5.0 ± 2.3 pmol/l, P = 0.35) or following (0.4 ± 0.2 vs 0.9 ± 0.34 pmol/l/3 h [area above fasting concentration] P = 0.311 meal ingestion. To determine if hyper insulinemia increased circulating CGRP concentrations in healthy humans, plasma insulin was increased from fasting (40 pmol/l) to high physiological concentrations (200 pmol/l) and supraphysiologic concentrations (600 pmol/l) by a constant low dose (0.6 mU/kg/min) or high dose insulin (2 mU/kg/min) infusion while plasma glucose was maintained constant with a variable glucose infusion. There was no increase in circulating CGRP from fasting levels during either the low dose (3.9 ± 1.5 vs 3.5 ± 1.5 pmol/l) or high dose (2.3 ± 0.7 vs 1.9 ± 0.6 pmol/l) insulin infusion. We conclude that circulating concentrations of CGRP do not change in response to meal ingestion or hyperinsulinemia, and that increased circulating CGRP concentrations are not responsible for the insulin resistance or impaired insulin secretion characteristic of patients with Type II diabetes mellitus.",
author = "{Bradford Carter}, W. and H. Heath and Rizza, {R. A.} and Butler, {P. C.}",
year = "1995",
language = "English (US)",
volume = "2",
pages = "99--103",
journal = "Endocrinology and Metabolism, Supplement",
issn = "1096-6374",
publisher = "Churchill Livingstone",
number = "2",

}

TY - JOUR

T1 - Measurement of plasma calcitonin gene-related peptide concentration in healthy humans and patients with type II diabetes mellitus

T2 - Responses to meal ingestion and hyperinsulinemia

AU - Bradford Carter, W.

AU - Heath, H.

AU - Rizza, R. A.

AU - Butler, P. C.

PY - 1995

Y1 - 1995

N2 - Calcitonin gene-related peptide (CGRP) has been shown to cause insulin resistance and impaired insulin secretion in animal studies. Because Type II diabetes mellitus is characterized by these abnormalities, CGRP has been implicated in the pathogenesis of this disease. However, it is not known whether the concentration of circulating CGRP responds to meal ingestion or hyperinsulinemia, and it remains to be determined whether plasma CGRP concentrations are increased in patients with Type II diabetes mellitus. We applied a new, highly-specific and sensitive immunochemiluminometric assay to measure the concentration of circulating CGRP in patients with Type II diabetes mellitus and matched healthy control subjects both before and following ingestion of a mixed meal. Plasma CGRP concentrations did not change in response to meal ingestion in either healthy subjects or patients with Type II diabetes mellitus and was not increased in patients with Type II diabetes mellitus versus control subjects either before (2.4 ± 0.9 vs 5.0 ± 2.3 pmol/l, P = 0.35) or following (0.4 ± 0.2 vs 0.9 ± 0.34 pmol/l/3 h [area above fasting concentration] P = 0.311 meal ingestion. To determine if hyper insulinemia increased circulating CGRP concentrations in healthy humans, plasma insulin was increased from fasting (40 pmol/l) to high physiological concentrations (200 pmol/l) and supraphysiologic concentrations (600 pmol/l) by a constant low dose (0.6 mU/kg/min) or high dose insulin (2 mU/kg/min) infusion while plasma glucose was maintained constant with a variable glucose infusion. There was no increase in circulating CGRP from fasting levels during either the low dose (3.9 ± 1.5 vs 3.5 ± 1.5 pmol/l) or high dose (2.3 ± 0.7 vs 1.9 ± 0.6 pmol/l) insulin infusion. We conclude that circulating concentrations of CGRP do not change in response to meal ingestion or hyperinsulinemia, and that increased circulating CGRP concentrations are not responsible for the insulin resistance or impaired insulin secretion characteristic of patients with Type II diabetes mellitus.

AB - Calcitonin gene-related peptide (CGRP) has been shown to cause insulin resistance and impaired insulin secretion in animal studies. Because Type II diabetes mellitus is characterized by these abnormalities, CGRP has been implicated in the pathogenesis of this disease. However, it is not known whether the concentration of circulating CGRP responds to meal ingestion or hyperinsulinemia, and it remains to be determined whether plasma CGRP concentrations are increased in patients with Type II diabetes mellitus. We applied a new, highly-specific and sensitive immunochemiluminometric assay to measure the concentration of circulating CGRP in patients with Type II diabetes mellitus and matched healthy control subjects both before and following ingestion of a mixed meal. Plasma CGRP concentrations did not change in response to meal ingestion in either healthy subjects or patients with Type II diabetes mellitus and was not increased in patients with Type II diabetes mellitus versus control subjects either before (2.4 ± 0.9 vs 5.0 ± 2.3 pmol/l, P = 0.35) or following (0.4 ± 0.2 vs 0.9 ± 0.34 pmol/l/3 h [area above fasting concentration] P = 0.311 meal ingestion. To determine if hyper insulinemia increased circulating CGRP concentrations in healthy humans, plasma insulin was increased from fasting (40 pmol/l) to high physiological concentrations (200 pmol/l) and supraphysiologic concentrations (600 pmol/l) by a constant low dose (0.6 mU/kg/min) or high dose insulin (2 mU/kg/min) infusion while plasma glucose was maintained constant with a variable glucose infusion. There was no increase in circulating CGRP from fasting levels during either the low dose (3.9 ± 1.5 vs 3.5 ± 1.5 pmol/l) or high dose (2.3 ± 0.7 vs 1.9 ± 0.6 pmol/l) insulin infusion. We conclude that circulating concentrations of CGRP do not change in response to meal ingestion or hyperinsulinemia, and that increased circulating CGRP concentrations are not responsible for the insulin resistance or impaired insulin secretion characteristic of patients with Type II diabetes mellitus.

UR - http://www.scopus.com/inward/record.url?scp=0029025390&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029025390&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0029025390

VL - 2

SP - 99

EP - 103

JO - Endocrinology and Metabolism, Supplement

JF - Endocrinology and Metabolism, Supplement

SN - 1096-6374

IS - 2

ER -