engleski

Increased β-cell and liver functions are responsible for glucose homeostasis in patients with glucose intolerance

Introduction: The study compared insulin resistance (IR), inflammation and other markers of the metabolic syndrome (MS) between groups with glucose intolerance (GI) and type 2 diabetes (DM2). Methods: IR, β-cell function, C-reactive protein (CRP), homocysteine (HCY), fibrinogen (FIB), liver function, albumin/creatinine (A/C) ratio and MS parameters were assessed in patients with DM2 (n=150), GI (n=82) and a control group (CG) (n=96). GI was diagnosed based on oral glucose tolerance test (OGTT). IR and β-cell function were assessed using computer homeostatic model assessment (HOMA2). Results: Significant differences in β-cell function (p<0.0001) [DM2 (75.29±43.62), GI (117.12±58.43) and CG (149.48±58.45)], BMI (p=0.03), aspartate aminotransferase (AST) (p=0.01) and A/C (p<0.01) were found among the tested groups. The groups did not differ regarding IR (p=0.58)], CRP (p=0.11), FIB (p=0.58) and HCY (p=0.97). β-cell function correlated significantly (p<0.001) with BMI (r=0.193), fasting plasma glucose (fPG) (r=-0.705), postprandial PG (r=-0.485), and glycated haemoglobin (r=-0.418) in DM2, and with BMI (r=0.448) and fPG (r=-0.553) in GI. The best model for IR in DM2 (R2=37.83) included triglycerides (R2=16.19), age (R2=6.99), low- density lipoprotein (R2=9.63) and CRP (R2=5.01), and in GI (R2=80.28) it included GGT (R2=26.13), age (R2=13.97), BMI (R2=11.79), alanine aminotransferase (ALT) (R2=17.67), and CRP (R2=10.72). Conclusion: There was no difference in IR between patients with GI and those with DM2, suggesting a similar risk for vascular disease in the two groups. Increased β-cell function, and AST, GGT and CRP as predictors of IR maintain glucose homeostasis in patients with GI.

beta-cell function; liver function; insulin resistance; glucose intolerance

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