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Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT.
Am J Physiol Endocrinol Metab 2003; 284(6):E1156-61AJ

Abstract

High concentrations of nonesterified fatty acids (NEFA) are a risk factor for developing type 2 diabetes in Pima Indians. In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians. To test this hypothesis, fasting plasma NEFA concentrations, body composition, insulin action (M), acute insulin response (AIR, 25-g IVGTT), and glucose tolerance (75-g OGTT) were measured in 151 Pima Indians [107 normal glucose tolerant (NGT), 44 impaired glucose tolerant (IGT)] at the initial visit. These subjects, participants in ongoing studies of the pathogenesis of obesity and type 2 diabetes, had follow-up measurements of body composition, glucose tolerance, M, and AIR. In NGT individuals, cross-sectionally, high fasting plasma NEFA concentrations at the initial visit were negatively associated with AIR after adjustment for age, sex, percent body fat, and M (P = 0.03). Longitudinally, high fasting plasma NEFA concentrations at the initial visit were not associated with change in AIR. In individuals with IGT, cross-sectionally, high fasting plasma NEFA concentrations at the initial visit were not associated with AIR. Longitudinally, high fasting plasma NEFA concentrations at the initial visit were associated with a decrease in AIR before (P < 0.0001) and after adjustment for sex, age at follow-up, time of follow-up, change in percent body fat and insulin sensitivity, and AIR at the initial visit (P = 0.0006). In conclusion, findings in people with NGT indicate that fasting plasma NEFA concentrations are not a primary etiologic factor for beta-cell failure. However, in subjects who have progressed to a state of IGT, chronically elevated NEFA seem to have a deleterious effect on insulin-secretory capacity.

Authors+Show Affiliations

Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona 85016, USA. nstefan@mail.nih.govNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12582008

Citation

Stefan, Norbert, et al. "Elevated Plasma Nonesterified Fatty Acids Are Associated With Deterioration of Acute Insulin Response in IGT but Not NGT." American Journal of Physiology. Endocrinology and Metabolism, vol. 284, no. 6, 2003, pp. E1156-61.
Stefan N, Stumvoll M, Bogardus C, et al. Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT. Am J Physiol Endocrinol Metab. 2003;284(6):E1156-61.
Stefan, N., Stumvoll, M., Bogardus, C., & Tataranni, P. A. (2003). Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT. American Journal of Physiology. Endocrinology and Metabolism, 284(6), pp. E1156-61.
Stefan N, et al. Elevated Plasma Nonesterified Fatty Acids Are Associated With Deterioration of Acute Insulin Response in IGT but Not NGT. Am J Physiol Endocrinol Metab. 2003;284(6):E1156-61. PubMed PMID: 12582008.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT. AU - Stefan,Norbert, AU - Stumvoll,Michael, AU - Bogardus,Clifton, AU - Tataranni,P Antonio, Y1 - 2003/02/11/ PY - 2003/2/13/pubmed PY - 2003/6/20/medline PY - 2003/2/13/entrez SP - E1156 EP - 61 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 284 IS - 6 N2 - High concentrations of nonesterified fatty acids (NEFA) are a risk factor for developing type 2 diabetes in Pima Indians. In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians. To test this hypothesis, fasting plasma NEFA concentrations, body composition, insulin action (M), acute insulin response (AIR, 25-g IVGTT), and glucose tolerance (75-g OGTT) were measured in 151 Pima Indians [107 normal glucose tolerant (NGT), 44 impaired glucose tolerant (IGT)] at the initial visit. These subjects, participants in ongoing studies of the pathogenesis of obesity and type 2 diabetes, had follow-up measurements of body composition, glucose tolerance, M, and AIR. In NGT individuals, cross-sectionally, high fasting plasma NEFA concentrations at the initial visit were negatively associated with AIR after adjustment for age, sex, percent body fat, and M (P = 0.03). Longitudinally, high fasting plasma NEFA concentrations at the initial visit were not associated with change in AIR. In individuals with IGT, cross-sectionally, high fasting plasma NEFA concentrations at the initial visit were not associated with AIR. Longitudinally, high fasting plasma NEFA concentrations at the initial visit were associated with a decrease in AIR before (P < 0.0001) and after adjustment for sex, age at follow-up, time of follow-up, change in percent body fat and insulin sensitivity, and AIR at the initial visit (P = 0.0006). In conclusion, findings in people with NGT indicate that fasting plasma NEFA concentrations are not a primary etiologic factor for beta-cell failure. However, in subjects who have progressed to a state of IGT, chronically elevated NEFA seem to have a deleterious effect on insulin-secretory capacity. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/12582008/Elevated_plasma_nonesterified_fatty_acids_are_associated_with_deterioration_of_acute_insulin_response_in_IGT_but_not_NGT_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00427.2002?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -