Naslov
Insulin-resistant patients with type 2 diabetes and glucose intolerance share similar predictors of vascular complications

Autori
Ljubic, Spomenka ; Piljac, Ante ; Novak, Branko ; Kerum, Tanja ; Vucic Lovrencic, Marijana ;

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Diabetes Vol 58, Suppl. 1 / - , 2009, 610-611

Skup
American Diabetes Association 69th Scientific Session

Mjesto i datum
New Orleans (LA), Sjedinjene Američke Države, 05.06.2009. - 09.06.2009

Vrsta sudjelovanja
Ostalo

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
glucose intolerance; inflammation; insulin resistance

Sažetak
Glucose intolerance (GI) and diabetes imply a similar risk of vascular complications, which can be explained by insulin resistance (IR). IR, inflammation and other markers of the metabolic syndrome (MS) were assessed in the groups with GI and type 2 diabetes (DM2). Patients with DM2 (n=150), GI (n=82) and a control group (CG) (n=96) underwent an oral glucose tolerance test (OGTT). Insulin resistance (IR) and &#946; -cell function were assessed by computer homeostatic model assessment (HOMA2) from fasting insulin (FI) and plasma glucose (fPG). The correlation between IR, &#946; -cell function, C-reactive protein (CRP), homocysteine (HCY), fibrinogen (FIB), albumin/creatinine (A/C) ratio and MS parameters were assessed. A significant difference in &#946; -cell function [ANOVA: F60.72, df=2, p<0.0001] was found among the groups with DM2, GI and CG. The groups did not differ in IR, CRP, FIB, HCY, uric acid (UA), gamma-glutamyltransferase (GGT) and body mass index (BMI). Tukey post hoc test pointed to a significant difference in &#946; -cell function between DM2 and GI, DM2 and CG, GI and CG. The &#946; -cell function correlated significantly (p<0.001) with BMI (r=0.193), fPG (r=-0.705), postprandial PG (ppPG) (r=-0.485), glycated hemoglobin (A1c) (r=-0.418) and FI (r=0.618) in DM2, and with BMI (r=0.448), fPG (r=-0.553) and FI (r=0.827) in GI. After stepwise regression procedure the best model for the assessment of IR in DM2 (R&sup2 ; ; =37.83) included triglycerides (partial R&sup2 ; ; =16.19), age (R&sup2 ; ; =6.99), low-density lipoprotein (LDL) (R&sup2 ; ; =9.63) and CRP (R&sup2 ; ; =5.01). The best model for IR in GI (R&sup2 ; ; =80.28) included GGT (R&sup2 ; ; =26.13), age (R&sup2 ; ; =13.97), BMI (R&sup2 ; ; =11.79), alanine aminotransferase (ALT) (R&sup2 ; ; =17.67), and CRP (R&sup2 ; ; =10.72) and for IR in CG (R&sup2 ; ; =83.67) it included BMI (R&sup2 ; ; =30.35), fBG (R&sup2 ; ; =12.74), ALT (R&sup2 ; ; =9.20), aspartate aminotransferase (AST) (R&sup2 ; ; =13.12), high-density lipoprotein (HDL) (R&sup2 ; ; =10.39), age (R&sup2 ; ; =5.94), and UA (R&sup2 ; ; =1.94). IR might be predicted by increased lipid values, liver function parameters and CRP, suggesting a similar mechanism in the pathogenesis of vascular complications in either DM2 or GI. Increased &#946; -cell function in GI is a compensatory mechanism in glucose homeostasis.

Izvorni jezik
Engleski

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