Cited by 59Pancreatic function and diabetesDiabetes Treatment and ManagementNeuropeptides and Animal Physiology

Reduced postprandial cholecystokinin (CCK) secretion in patients with noninsulin-dependent diabetes mellitus: evidence for a role for CCK in regulating postprandial hyperglycemia.

Rushakoff, R A, Goldfine, I D, Beccaria, L J, Mathur, A, Brand, R J, Liddle, R A·1993·The Journal of Clinical Endocrinology & Metabolism

Abstract

The plasma cholecystokinin (CCK) response to a test meal was studied in 16 control subjects and 15 patients with noninsulin-dependent diabetes mellitus (NIDDM). Basal CCK levels were approximately 1 pmol in both groups. However, after the test meal, plasma CCK levels were 2-fold greater in the controls when compared to the diabetics. In controls, CCK levels maximally increased by 5.6 +/- 0.8 pmol (mean +/- SEM) 10 min after feeding, whereas in the NIDDM patients this value was 1.9 +/- 0.6 pmol (P < 0.001). After the test meal, the normal subjects showed no postprandial rise in blood glucose, whereas the diabetic patient showed a rise of 2.6 +/- 0.7 mmol. To determine whether the decreased CCK levels may have been related to the postprandial hyperglycemia, 7 diabetic subjects were infused with CCK. With this CCK infusion, postprandial glucose levels did not rise. These data suggest, therefore: 1) a role for cholecystokinin in regulating postprandial hyperglycemia in man, 2) abnormalities in CCK secretion occur in NIDDM and may contribute to the hyperglycemia seen in this disease.

Integrity signals

Registry

Crossref · 10.1210/jcem.76.2.8432795

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21 of 21 references verified0 citation errors · 0 not checkable

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  • Reduced CCK plasma levels in noninsulin-dependent diabetes mellitus cause postprandial hyperglycemia.

    “The pivotal role of CCK in modulating glucose homeostasis is reflected in postprandial hyperglycemia, which is due to reduced CCK plasma levels in noninsulin-dependent diabetes mellitus.240”

    From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [240]

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Authors
Rushakoff, R. A., Goldfine, I. D., Beccaria, L. J., Mathur, A., Brand, R. J., & Liddle, R. A.
Affiliations
University of California, San Francisco (US)
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
1993-02
Volume
76
Issue
2
Pages
489-493
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2089449544
Cited by
59
References
21
Citations by year
2026: 1 · 2025: 5 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 4 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
0.90
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1p01dk038985-01a1, 5r01dk027626-19)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK38626, DK-27626, P01-DK-38985)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
cholecystokinin, type 2 diabetes, postprandial hyperglycemia, plasma CCK levels, test meal, glucose regulation
MeSH terms
Adult, Aged, Blood Glucose, Cholecystokinin, Diabetes Mellitus, Type 2, Female, Food, Humans, Hyperglycemia, Insulin, Male, Middle Aged

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