Impaired fasting glucose is not a risk factor for atherosclerosis

Citation
M. Hanefeld et al., Impaired fasting glucose is not a risk factor for atherosclerosis, DIABET MED, 16(3), 1999, pp. 212-218
Citations number
30
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
DIABETIC MEDICINE
ISSN journal
07423071 → ACNP
Volume
16
Issue
3
Year of publication
1999
Pages
212 - 218
Database
ISI
SICI code
0742-3071(199903)16:3<212:IFGINA>2.0.ZU;2-L
Abstract
Aim To determine a new category of dysfunctional glucose homeostasis - impa ired fasting glucose (IFG) - introduced by the American Diabetes Associatio n (ADA) and the World Health Organization (WHO) defining those with abnorma l but nondiabetic fasting glucose values and with a possible risk for devel oping diabetes. It is not known whether IFG is a risk factor for atheroscle rosis, as is impaired glucose tolerance (IGT). Methods In this case-control cross-sectional study in which the oral glucos e tolerance (75-g OGTT) and the carotid intima-media thickness (IMT) with B mode ultrasound, as a marker of atherosclerosis, were measured, together w ith IIbA(1c), lipids, plasminogen activator (PAI), insulin and proinsulin c oncentrations In blood plasma. Out of 788 subjects of the risk factors in I GT for Atherosclerosis and Diabetes (RIAD) study we found 104 IFG cases tha t were compared to 104 controls with fasting plasma glucose (FPG) < 6.1 mmo l/l, matched for age, sex and body mass index. Subjects with 2h postprandia l (pp) plasma glucose greater than or equal to 11.1 mmol/l were excluded. T he rest were subdivided into those with 2h plasma glucose < 7.8 mmol/l (63 pairs, NGT) and those with plasma glucose > 7.8 mmol/l and < 11.1 mmol/l (4 1 pairs, IGT). Results The case and control groups showed no significant differences in th e major risk factors except for waist-to-hip ratio (WHR) which was higher i n the IFG with NGT. IFG with NGT exhibited significantly higher levels of H bA(1c), true insulin and proinsulin. In IFG with IGT, only HbA(1c) and proi nsulin were significantly increased vs. controls. IMT was in the same range for cases and controls in both subgroups. However, IMT mean and IMTmax wer e significantly increased in IFG with IGT vs. IFG with NGT (0.95 mm vs. 0.8 0 mm and 1.10 mm vs. 0.90 mm). Cumulative distribution analysis of IMT illu strates that IMT in IFG with IGT is more shifted to higher artery wall thic kness than in IFG with NGT. Conclusions In our case-control study IFG alone was not related to increase d IMT. Only IFG in a combination with IGT exhibited atherosclerotic changes of the carotid arteries. IFG is not analogous to IGT as a risk factor for atherosclerosis.