Endocrine Abstracts

Background and aims: Mechanism underlying the IR (Insulin-resistance) remains yet to be identified. Resistin has been shown to antagonize insulin action, and thus might be implicated in the pathogenesis of IR. In contrast, adiponectin has been shown to increase insulin sensitivity and improve glucose tolerance. We aimed to test the hypothesis that resistin levels might correlate positively with the indices of insulin resistance, while the opposite might be true for adiponectin.

Materials and methods: The study included 18 patients with established insulin-resistance: (W-16, M-2), age-35.8±11.6 years, BMI-30.23±10.1 kg/m². IR was assessed both in a fasting state: HOMA-R, QUICKI and during the oral glucose tolerance test (OGTT); this allows the assessment of compensatory hyperinsulinaemia, sometimes observed only in response to meals. Insulin Resistance Index (IRI) was calculated through the formula: 2/[1/(INSp×GLYp)]+1, where INSp and GLYp are the measured insulin and glycaemic areas. The concentrations of: adiponectin, resistin, insulin, glucose were assessed using kits dedicated to clinical purposes.

Results: The concentrations of: (G)lucose (mmol/l), (I)nsulin (mU/l), (A)diponectin (μg/ml), (R)esistin (ng/ml) in 0, 60, 120 minutes during the OGTT are presented below: (G)- 4.88±0.88, 8.69±3.72, 6.99±2.60, (I)- 14.33±10.12, 122.33±64.84, 87.94±65.03, (A)- 11.49±4.71, 12.61±5.73, 14.92±7.58, (R)- 7.29±1.59, 7.36±1.14, 7.18±1.26, (A/R)- 1.58, 1.71, 2.08, (IRI): 1.34±0.29, HOMA-R: 2.99±1.74, QUICKI: 0.58±0.09.

There was a significant correlation (P<0.05) among those 3 methods of insulin-resistance assessment. A negative correlation between fasting serum adiponectin and resistin was observed (−0.56; P<0.05). There was no correlation between indices of IR and the levels of adiponectin and resistin.

Conclusions: We raise the hypothesis that fasting serum adiponectin/resistin ratio may be useful in prediction of future cardiovascular risk among people with established IR.