Study of the serum resistin level in elderly patients with essential hypertension

Objective To investigate the serum resistin concentration in elderly patients with essential hypertension and potential role of resisitin in the decline of glucose tolerance . Methods Fasting serum resistin concentration was measured with enzyme immunoassay in 55 patients with essential hypertension (including 25 elderly patients and 30 non elderly patients) and 13 normotensives (control group).Oral glucose tolerance test and insulin release test were performed to calculate glucose area under the curve (AUC G ), the ratio of insulin level change to glucose level change during the first 30 min after glucose ingestion (△I 30 /△G 30 ) and insulin sensitivity index (ISI) according to the Cederholm' formula. Height, body weight, waist and hip circumferencs were measured for calculating body mass index (BMI) and waist hip ratio (WHR). Results The fasting serum resistin concentrations in the elderly group was higher than those in the non elderly group 〔(29 6±12 4) vs (23 1±8 9) μg/L, P 0 05〕 and the control group 〔(29 6±12 4) vs (19 7±5 3) μg/L, P 0 05〕 Fasting plasma glucose (FPG) in the elderly group was higher than that in the non elderly group 〔(6 4±1 2) vs (4 8±0 4) mmol/L, P 0 05〕 and in the control group 〔(6 4±1 2) vs (4 9±0 6) mmol/L, P 0 05〕. The ISI in the elderly group was lower than that in the non elderly group (32 8±10 8 vs 48 8±15 8, P 0 05). △I 30 /△G 30 in the elderly group was lower than that in the non elderly group (8 6±7 2 vs 14 0±10 5, P 0 05). Pearson analysis showed that age was correlated with fasting serum resistin concentrations ( P 0 001), while FPG was correlated with both the age ( P 0 001) and the fasting serum resistin concentrations ( P 0 01). The age and the fasting serum resistin concentrations were negatively correlated with the ISI ( P 0 001, P 0 05) and △I 30 /△G 30 ( P 0 05 and P 0 05). Conclusions The increase of fasting serum resistin level in the elderly patients with essential hypertension may cause the decline in glucose tolerance. A possible mechanism is that the excessive resisitin leads to the development of insulin resistance and an impairment of β cell secretory function.