Circulating ghrelin levels in obese women: a possible association with hypertension

Abstract

Objective. The orexigenic hormone ghrelin induces weight gain by stimulating food intake. Ghrelin has been shown to modulate sympathetic activity, to exert vasodilative effects and to counterreact with leptin on both food intake and blood pressure. Of these two hormones, ghrelin levels are decreased in obesity, whereas leptin levels are increased. In this cross‐sectional study, differences in serum ghrelin and leptin levels were examined in normotensive and hypertensive obese women. Material and methods. Sixty‐one normotensive and hypertensive women were classified according to the body mass indices as follows: (a) 18 healthy subjects with BMI 21.5–27.5 kg/m²; (b) 22 normotensive subjects with BMI 30–47 kg/m²; (c) 21 hypertensive obese subjects (BMI 30–48 kg/m²) with systolic blood pressure ⩾140 mmHg or diastolic blood pressure ⩾90 mmHg. Anthropometric measurements including height, weight, BMI, waist and hip circumferences and blood pressure were recorded. The levels of ghrelin and leptin were determined in sera using the commercial ELISA kits. Results. In normotensive obese subjects, ghrelin levels were significantly lower than in controls (0.21±0.13 vs 0.60±0.3 ng/mL), whereas hypertensive obese women had elevated ghrelin levels (0.64±0.36 ng/mL). Ghrelin concentration was decreased despite the presence of hypertension in the patients who had BMIs above 35 kg/m². Leptin levels were significantly higher in both normotensive and hypertensive obese groups (19.54±11.19 and 21.61±12.7 ng/mL, respectively) than in controls (7.61±3.3 ng/mL), and were not affected by the presence of hypertension in obese subjects. Conclusion. Ghrelin was positively associated with hypertension in obese women and this association was inversely influenced by the increase of BMI.

• Blood pressure
• body mass index
• ghrelin
• hypertension
• leptin
• obesity

Acknowledgement

The present work was supported by the research fund of Istanbul University through project no. BYP‐756/02082005.