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Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus.
J Clin Endocrinol Metab. 1985 Aug; 61(2):313-21.JC

Abstract

Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. The Caucasians were normal weight, averaging 101 +/- 3% (+/-SEM) ideal BW (IBW), or were obese (168 +/- 21% IBW) and had normal glucose tolerance (n = 77), impaired glucose tolerance (IGT; n = 12), or noninsulin-dependent diabetes mellitus (NIDDM; n = 19). The American Indians were all obese (144 +/- 6% IBW) and had either normal glucose tolerance (n = 22) or NIDDM (n = 11). In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. Exceptions were two groups with the most severe diabetes in whom incremental insulin values after oral glucose were only 70% (thin Caucasians) and 110% (obese Indians) that of lean normal subjects. The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. High fasting GIP and exaggerated GIP increments in response to nutrients could be attributed to neither obesity nor diabetes alone nor to the type of nutrient used to stimulate its release, but, instead, may be genetic or dietary in origin or may be due to other as yet unidentified factors. High basal GIP and exaggerated nutrient-stimulated GIP release were associated with hyperinsulinemia, except in the most severe diabetic patients. These observations suggest that exaggerated GIP release, along with a greater rise in serum glucose in response to nutrients, may play a role in the pathogenesis of the hyperinsulinemia of obesity and early NIDDM.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

4008608

Citation

Mazzaferri, E L., et al. "Gastric Inhibitory Polypeptide Responses to Nutrients in Caucasians and American Indians With Obesity and Noninsulin-dependent Diabetes Mellitus." The Journal of Clinical Endocrinology and Metabolism, vol. 61, no. 2, 1985, pp. 313-21.
Mazzaferri EL, Starich GH, Lardinois CK, et al. Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab. 1985;61(2):313-21.
Mazzaferri, E. L., Starich, G. H., Lardinois, C. K., & Bowen, G. D. (1985). Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus. The Journal of Clinical Endocrinology and Metabolism, 61(2), 313-21.
Mazzaferri EL, et al. Gastric Inhibitory Polypeptide Responses to Nutrients in Caucasians and American Indians With Obesity and Noninsulin-dependent Diabetes Mellitus. J Clin Endocrinol Metab. 1985;61(2):313-21. PubMed PMID: 4008608.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus. AU - Mazzaferri,E L, AU - Starich,G H, AU - Lardinois,C K, AU - Bowen,G D, PY - 1985/8/1/pubmed PY - 1985/8/1/medline PY - 1985/8/1/entrez SP - 313 EP - 21 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 61 IS - 2 N2 - Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. The Caucasians were normal weight, averaging 101 +/- 3% (+/-SEM) ideal BW (IBW), or were obese (168 +/- 21% IBW) and had normal glucose tolerance (n = 77), impaired glucose tolerance (IGT; n = 12), or noninsulin-dependent diabetes mellitus (NIDDM; n = 19). The American Indians were all obese (144 +/- 6% IBW) and had either normal glucose tolerance (n = 22) or NIDDM (n = 11). In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. Exceptions were two groups with the most severe diabetes in whom incremental insulin values after oral glucose were only 70% (thin Caucasians) and 110% (obese Indians) that of lean normal subjects. The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. High fasting GIP and exaggerated GIP increments in response to nutrients could be attributed to neither obesity nor diabetes alone nor to the type of nutrient used to stimulate its release, but, instead, may be genetic or dietary in origin or may be due to other as yet unidentified factors. High basal GIP and exaggerated nutrient-stimulated GIP release were associated with hyperinsulinemia, except in the most severe diabetic patients. These observations suggest that exaggerated GIP release, along with a greater rise in serum glucose in response to nutrients, may play a role in the pathogenesis of the hyperinsulinemia of obesity and early NIDDM. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/4008608/Gastric_inhibitory_polypeptide_responses_to_nutrients_in_Caucasians_and_American_Indians_with_obesity_and_noninsulin_dependent_diabetes_mellitus_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jcem-61-2-313 DB - PRIME DP - Unbound Medicine ER -