Does syndrome X exist in hypertensive elderly persons with impaired glycemic control?

Citation
Kc. Johnson et al., Does syndrome X exist in hypertensive elderly persons with impaired glycemic control?, J GERONT A, 54(11), 1999, pp. M571-M576
Citations number
38
Categorie Soggetti
Public Health & Health Care Science","Medical Research General Topics
Journal title
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
ISSN journal
10795006 → ACNP
Volume
54
Issue
11
Year of publication
1999
Pages
M571 - M576
Database
ISI
SICI code
1079-5006(199911)54:11<M571:DSXEIH>2.0.ZU;2-Q
Abstract
Background. This report focuses on the glycemic stale in relation to insuli n and lipid levels of a cohort of elderly hypertensive persons to estimate the prevalence of syndrome X. Methods. ii cross-sectional study was performed at the University of Tennes see, Memphis, and the General Clinical Research Center (GCRC) on 95 partici pants in the Trial of Nonpharmacologic Interventions in the Elderly (TONE) study who agreed to participate in an ancillary study. A standard oral gluc ose tolerance test (OGTT) with insulin and C-peptide levels and a fasting l ipid profile were obtained. Results. In this sample of healthy elderly participants with hypertension w ho were taking an antihypertensive medication, 43 (45.3%) had normal glucos e tolerance (NGT), 41 (43.2%) had impaired glucose tolerance (IGT), and 11 (11.6%) had undiagnosed non-insulin-dependent diabetes mellitus (NIDDM). Fa sting hyperinsulinemia occurred in only one participant, who was in the IGT group. Hypertriglyceridemia and low high density lipoprotein (HDL) occurre d in four persons, none of whom had hyperinsulinemia. Persons in the NIDDM and IGT groups had decreased beta cell function compared to persons in the NGT group, but did not have increased peripheral insulin resistance as esti mated from the OGTT data. Conclusions. Our data demonstrated that in this cohort of elderly hypertens ive participants with a high prevalence of central obesity, impaired glycem ic control was common, but was not associated with Fasting hyperinsulinemia or peripheral insulin resistance. Furthermore, we conclude that syndrome X essentially did not occur in these participants and postulate that the pri mary etiology fur their impaired glycemic control is beta cell dysfunction. Further research is needed to elucidate these relationships.