title: Insulin resistance in hypertensives: effect of salt sensitivity, renin status and sodium intake.
abstract: OBJECTIVE
  Homeostasis Model Assessment (HOMA index) is predictive of insulin sensitivity in normal and diabetic patients. This study was designed to see if insulin resistance in hypertensives, measured using the HOMA index, differs, based on salt sensitivity, renin status and sodium intake.
  
  
  METHODS
  Fasting insulin and glucose were determined in subsets of 426 essential hypertensives, and normotensives. HOMA was calculated as fasting glucose (mmol) x fasting insulin (muU/ml)/22.5.
  
  
  RESULTS
  Four hundred and twenty-six essential hypertensives and normotensives from four HERMES centers form the basis of this report. There was no difference in the HOMA index between hypertensives and normotensives (P= 0.291) or between hypertensives grouped according to blood pressure salt sensitivity (P = 0.153). However, when essential hypertensives were subgrouped by renin status, the low-renin group had significantly lower (P< 0.01) HOMA index than the normal/high-renin group. When normal/high-renin group was divided into modulators and non-modulators, the nonmodulators had significantly higher HOMA index (P< 0.001) than other hypertensive subsets. The effect of sodium intake on the HOMA index was significant only for non-modulators (P< 0.002), with salt restriction increasing insulin resistance.
  
  
  CONCLUSIONS
  Insulin sensitivity differs among subsets of essential hypertension, non-modulators being most insulin resistant and the low-renin subset insulin sensitive. Salt restriction might have an adverse effect on insulin sensitivity in non-modulators. The reduction in cardiovascular risk seen in low-renin hypertensives may be related to their increased insulin sensitivity; in contrast, the clustering of cardiovascular risk factors seen in nonmodulators may be due to increased insulin resistance.
authors.affiliation: Endocrine--Hypertension Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. araji@rics.bwh.harvard.edu
authors.forename: A
authors.initials: A
authors.lastname: Raji
authors.forename: G H
authors.initials: GH
authors.lastname: Williams
authors.forename: X
authors.initials: X
authors.lastname: Jeunemaitre
authors.forename: P N
authors.initials: PN
authors.lastname: Hopkins
authors.forename: S C
authors.initials: SC
authors.lastname: Hunt
authors.forename: N K
authors.initials: NK
authors.lastname: Hollenberg
authors.forename: E W
authors.initials: EW
authors.lastname: Seely
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006706:Homeostasis / Q000187:drug effects*; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000235:genetics / Q000503:physiopathology; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011379:Prognosis; D012083:Renin / Q000097:blood*; D012307:Risk Factors; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D017673:Sodium Chloride, Dietary; D012083:Renin