Why the study?
Are aldosterone levels associated with insulin-mediated muscle microvascular recruitment, insulin sensitivity, and blood pressure in lean and abdominally obese men, and does weight loss affect this?
Are aldosterone levels associated with insulin-mediated muscle microvascular recruitment, insulin sensitivity, and blood pressure in lean and abdominally obese men, and does weight loss affect this?
Absolute aldosterone levels do not explain differences in microvascular and metabolic insulin sensitivity or blood pressure between lean and moderately abdominally obese men.
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Aldosterone unrelated to insulin sensitivity, BP, or microvascular function in abdominal obesity; leaves open differential sodium-aldosterone links by adiposity.
Context: Impaired insulin-mediated muscle microvascular recruitment (IMMR) may add to the development of insulin resistance and hypertension. Increased aldosterone levels have been linked to these obesity-related complications in severely to morbidly obese individuals and to impaired microvascular function in experimental studies. Objectives: To investigate whether aldosterone levels are associated with IMMR, insulin sensitivity, and blood pressure in lean and moderately abdominally obese men, and to study the effect of weight loss. Design, Setting, Participants, Intervention, Main Outcome Measures: In 25 lean and 53 abdominally obese men, 24-hour blood pressure measurement was performed, and aldosterone levels were measured using ultra-performance liquid chromatography tandem mass spectrometry. Insulin sensitivity was assessed by determining whole-body glucose disposal during a hyperinsulinemic clamp. IMMR in forearm skeletal muscle was measured with contrast-enhanced ultrasonography. These assessments were repeated in the abdominally obese men following an 8-week weight loss or weight stable period. Results: Sodium excretion and aldosterone levels were similar in lean and abdominally obese participants, but sodium excretion was inversely associated with aldosterone concentration only in the lean individuals [lean, β/100 mmol sodium excretion (adjusted for age and urinary potassium excretion) = -0.481 (95% confidence interval, -0.949 to -0.013); abdominally obese, β/100 mmol sodium excretion = -0.081 (95% confidence interval, -0.433 to 0.271); P for interaction = 0.02]. Aldosterone was not associated with IMMR, insulin sensitivity, or blood pressure and was unaffected by weight loss. Conclusion: In moderately abdominally obese men, the inverse relationship between sodium excretion and aldosterone concentration is less than that in lean men but does not translate into higher aldosterone levels. The absolute aldosterone level does not explain differences in microvascular and metabolic insulin sensitivity and blood pressure between lean and moderately abdominally obese men.
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Schütten et al. (2017) studied this question.
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