Suppression of non-esterified fatty acid concentrations by insulin in patients with hypertension

Recent studies have suggested that insulin resistance may be involved in the development of hypertension. Although skeletal muscle accounts for the majority of peripheral insulin resistance, the effect of insulin on adipose tissue, (i.e., antilipolysis) has rarely been defined in hypertensive patients. To understand the effect of high blood pressure on adipose tissue lipolytic activity in vivo, plasma non-esterified fatty acid (NEFA) concentrations at basal insulin, and during physiological hyperinsulinemic state was compared in patients with essential hypertension and a group of normotensive subjects.

Twenty patients with untreated essential hypertension and 20 age, sex, body mass index (BMI)-matched normotensive subjects were studied. Oral glucose tolerance test (OGTT) in response to a 75-g oral glucose load was carried out for three hours after an overnight fasting. On separate morning, modified insulin suppression test was performed for three hours, which involved a constant infusion of insulin (25 mU/m2/min) glucose (240 mg/m2/min) and somatostatin (350 micrograms/h). The four values obtained every 10 min at last half hour were read as steady state plasma glucose (SSPG), insulin (SSPI) and final NEFA concentrations.

Patients with hypertension had significantly higher fasting plasma insulin (101 +/- 9 vs 69 +/- 8 pmol/L, p < 0.02) and NEFA (543 +/- 38 vs 453 +/- 25 mumol/L, p < 0.05) concentrations compared to normotensive subjects. In response to OGTT, the plasma glucose and insulin concentrations increased significantly in the hypertensive group when compared with normotensive group (p < 0.05 and p < 0.01, respectively), whereas plasma NEFA concentrations were suppressed to a similar extent in these two groups. During modified insulin suppression test, the mean SSPG concentrations were significantly higher (10.1 +/- 0.7 vs 7.8 +/- 0.8 mmol/L, p < 0.01) in patients with hypertension compared with normal subjects despite that the mean SSPI concentrations were similar. Plasma NEFA concentrations fell markedly during the period of physiological hyperinsulinemia and achieved similar levels during the last 30 min of infusion in both hypertensive and normal individuals (92.3 +/- 4.9 vs 86.5 +/- 7.3 mumol/L, p = NS).

Patients with hypertension are glucose intolerant, hyperinsulinemic and insulin resistant compared to a group of normotensive subjects. Hypertensive patients have higher than normal fasting plasma NEFA and insulin concentrations indicating that they might lose the ability to regulate adipocyte metabolism in fasting state.