The effect of serum insulin on the blood pressure responses after oral glucose load in lean and centrally obese adult male subjects

• Published in: Asian Journal of Medical Sciences Vol. 12; no. 5; pp. 65 - 68
• Main Authors: Htein, Thiri Win, Thant, Zarli, Mar, Ohn
• Format: Journal Article
• Language: English
• Published: Manipal College of Medical Sciences, Pokhara 01.05.2021
• Subjects: blood pressure responses; centrally obese; oral glucose load; serum insulin
• ISSN: 2467-9100; 2091-0576
• DOI: 10.3126/ajms.v12i5.34248

Background: The vasodilator action of insulin might contribute to the reduction of blood pressure in the postprandial state and it remains to be clarified whether this action is impaired in the insulin- resistant obese state or not. Aims and Objective: The present study aimed to determine the blood pressure responses after an oral glucose load in lean and insulin resistant centrally obese adult male subjects. Materials and Methods: This study was carried out in eleven lean and eleven centrally obese adult male subjects. After a 75 g oral glucose load, blood pressures were measured at 15-minute intervals and the serum insulin level was determined at 30-minute intervals for two hours. Blood pressure was measured by indirect sphygmomanometry and serum insulin concentration was analyzed by ELISA method. Results: All centrally obese subjects were insulin resistant (HOMA-IR≥2.6). After oral glucose load, the per cent change in glucose-stimulated insulin responses at 30 minutes (626% vs 344%, p<0.05) and at 60 minutes (756% vs 417%, p<0.01) were significantly greater in the lean group than the centrally obese group. The fall in postprandial blood pressures started at 15 minutes and returned to baseline values at 120 minutes. The per cent change in SBP at 15 minutes (-2.2% vs -1.2%, p<0.05) and at 30 minutes (-3.2% vs -2.1%, p<0.05) were significantly greater in the lean group than the centrally obese group. Conclusion: The present findings suggest that attenuation in BP responses as well as a lesser change in glucose-stimulated insulin responses in the centrally obese subjects might be attributable to the presence of insulin resistance.