King Grub
2014-07-18, 17:11
Context:
Interruption of the renin-angiotensin-aldosterone system (RAAS) prevents incident diabetes in high risk individuals, although the mechanism remains unclear.
Objective:
To test the hypothesis that activation of the endogenous RAAS or exogenous aldosterone impairs insulin secretion in humans.
Design:
Randomized, blinded cross-over study of aldosterone versus vehicle, and comparison of the effects of low sodium versus high sodium diet
Setting:
Academic clinical research center
Participants:
Healthy, non-diabetic, normotensive volunteers
Interventions:
Infusion of exogenous aldosterone (0.7 μ g/kg/hr for 12.5 hrs) or vehicle during low or high sodium intake. Low sodium (20mmol/d, n=12) versus high sodium (160mmol/d, n=17) intake for 5–7 days.
Main Outcome Measures:
Change in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during low sodium versus high sodium diet during aldosterone versus vehicle.
Results:
Low sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0±5.6%, P=0.007) and C-peptide responses (-21.8±8.4%, P=0.014) were decreased, while the insulin sensitivity index was unchanged (-1.0±10.7%, P=0.98). Aldosterone infusion did not affect the acute insulin response (+1.8±4.8%, P=0.72) or insulin sensitivity index (+2.0±8.8%, P=0.78). Systolic blood pressure and serum potassium were similar during low and high sodium intake and during aldosterone infusion.
Conclusions:
Low dietary sodium intake reduces insulin secretion in humans independent of insulin sensitivity.
Dietary sodium restriction decreases insulin secretion without affecting insulin sensitivity in humans. The Journal of Clinical Endocrinology & Metabolism July 16, 2014.
http://press.endocrine.org/doi/pdf/10.1210/jc.2014-2122
Interruption of the renin-angiotensin-aldosterone system (RAAS) prevents incident diabetes in high risk individuals, although the mechanism remains unclear.
Objective:
To test the hypothesis that activation of the endogenous RAAS or exogenous aldosterone impairs insulin secretion in humans.
Design:
Randomized, blinded cross-over study of aldosterone versus vehicle, and comparison of the effects of low sodium versus high sodium diet
Setting:
Academic clinical research center
Participants:
Healthy, non-diabetic, normotensive volunteers
Interventions:
Infusion of exogenous aldosterone (0.7 μ g/kg/hr for 12.5 hrs) or vehicle during low or high sodium intake. Low sodium (20mmol/d, n=12) versus high sodium (160mmol/d, n=17) intake for 5–7 days.
Main Outcome Measures:
Change in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during low sodium versus high sodium diet during aldosterone versus vehicle.
Results:
Low sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0±5.6%, P=0.007) and C-peptide responses (-21.8±8.4%, P=0.014) were decreased, while the insulin sensitivity index was unchanged (-1.0±10.7%, P=0.98). Aldosterone infusion did not affect the acute insulin response (+1.8±4.8%, P=0.72) or insulin sensitivity index (+2.0±8.8%, P=0.78). Systolic blood pressure and serum potassium were similar during low and high sodium intake and during aldosterone infusion.
Conclusions:
Low dietary sodium intake reduces insulin secretion in humans independent of insulin sensitivity.
Dietary sodium restriction decreases insulin secretion without affecting insulin sensitivity in humans. The Journal of Clinical Endocrinology & Metabolism July 16, 2014.
http://press.endocrine.org/doi/pdf/10.1210/jc.2014-2122