title: Dietary sodium restriction decreases insulin secretion without affecting insulin sensitivity in humans.
abstract: BACKGROUND
  Interruption of the renin-angiotensin-aldosterone system prevents incident diabetes in high-risk individuals, although the mechanism remains unclear.
  
  
  OBJECTIVE
  To test the hypothesis that activation of the endogenous renin-angiotensin-aldosterone system or exogenous aldosterone impairs insulin secretion in humans.
  
  
  METHODS
  We conducted a randomized, blinded crossover study of aldosterone vs vehicle and compared the effects of a low-sodium versus a high-sodium diet.
  
  
  METHODS
  Academic clinical research center.
  
  
  METHODS
  Healthy, nondiabetic, normotensive volunteers.
  
  
  METHODS
  Infusion of exogenous aldosterone (0.7 μg/kg/h for 12.5 h) or vehicle during low or high sodium intake. Low sodium (20 mmol/d; n = 12) vs high sodium (160 mmol/d; n = 17) intake for 5-7 days.
  
  
  METHODS
  Change in acute insulin secretory response assessed during hyperglycemic clamps while in sodium balance during a low-sodium vs high-sodium diet during aldosterone vs vehicle.
  
  
  RESULTS
  A low-sodium diet increased endogenous aldosterone and plasma renin activity, and acute glucose-stimulated insulin (-16.0 ± 5.6%; P = .007) and C-peptide responses (-21.8 ± 8.4%; P = .014) were decreased, whereas the insulin sensitivity index was unchanged (-1.0 ± 10.7%; P = .98). Aldosterone infusion did not affect the acute insulin response (+1.8 ± 4.8%; P = .72) or insulin sensitivity index (+2.0 ± 8.8%; P = .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.
authors.affiliation: Divisions of Clinical Pharmacology, Department of Medicine (J.M.L., L.M.B., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (T.J.W.), and Departments of Biostatistics (C.Y.) and Pharmacology (J.M.L.), Vanderbilt University Medical Center, Nashville, Tennessee 37232-6602.
authors.forename: James M
authors.initials: JM
authors.lastname: Luther
authors.forename: Loretta M
authors.initials: LM
authors.lastname: Byrne
authors.forename: Chang
authors.initials: C
authors.lastname: Yu
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wang
authors.forename: Nancy J
authors.initials: NJ
authors.lastname: Brown
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000008:administration & dosage / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D018592:Cross-Over Studies; D004039:Diet, Sodium-Restricted; D004311:Double-Blind Method; D005260:Female; D015309:Glucose Clamp Technique; D064368:Healthy Volunteers; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D008297:Male; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology; D012982:Sodium, Dietary / Q000008:administration & dosage*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D012982:Sodium, Dietary; D000450:Aldosterone; D012083:Renin