title: Insulin sensitivity in cardiological syndrome X.
abstract: OBJECTIVE
  To test whether cardiological syndrome X is an insulin-resistant state. SETTING, DESIGN AND SUBJECTS: The coronary care unit of a referral centre for angina pectoris in Pisa, Italy. A case-control study, involving 10 patients with unequivocal (angiographycally proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects.
  
  
  METHODS
  Insulin sensitivity and pattern of substrate oxidation (assessed by the euglycaemic insulin clamp technique in combination with indirect calorimetry).
  
  
  RESULTS
  Fasting plasma glucose and insulin levels were 5.05 +/- 0.11 versus 4.88 +/- 0.11 mmol l-1 and 68 +/- 10 versus 56 +/- 6 pmol l-1, respectively (controls versus patients, ns). During the insulin clamp, glucose disposal rate was nearly identical in patients and controls (25.9 +/- 1.8 and 27.2 +/- 1.8 mumol kg-1 min-1, respectively. P = 0.88). Non-oxidative glucose disposal accounted for similar proportions of total glucose uptake (59 versus 53%, patients versus controls, ns). Resting energy expenditure (13.7 +/- 0.6 versus 13.8 +/- 0.8 cal kg-1 min-1, ns) and insulin-induced thermogenesis were similar in the two groups. Fasting plasma NEFA concentrations (0.64 +/- 0.09 and 0.64 +/- 0.06 mmol l-1, patients and controls, ns) fell in a similar time-course and to virtually identical nadirs (0.13 +/- 0.02 and 0.14 +/- 0.02 mmol l-1) after insulin infusion. Fasting plasma potassium was similar in patients and controls (3.99 +/- 0.10 and 4.16 +/- 0.04 mmol l-1, ns), and insulin induced equivalent hypokalaemia (-14 versus -19%).
  
  
  CONCLUSIONS
  None of the in vivo actions of insulin were impaired in patients with 'pure' syndrome X when compared to matched controls. Therefore, we conclude that cardiological syndrome X is not an insulin resistant state per se, and that any decrease in insulin sensitivity found in this condition is likely to be secondary.
authors.affiliation: Metabolism Unit, National Research Council (CNR), Institute of Clinical Physiology, Pisa, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Quiønones Galvan
authors.forename: A
authors.initials: A
authors.lastname: Natali
authors.forename: E
authors.initials: E
authors.lastname: Muscelli
authors.forename: D
authors.initials: D
authors.lastname: Ciociaro
authors.forename: N
authors.initials: N
authors.lastname: Pecori
authors.forename: P G
authors.initials: PG
authors.lastname: Camici
authors.forename: E
authors.initials: E
authors.lastname: Ferrannini
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D002153:Calorimetry, Indirect; D016022:Case-Control Studies; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D017566:Microvascular Angina / Q000378:metabolism*; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D011188:Potassium