Insulin sensitivity in cardiological syndrome X

A. Quiñones Galvan, A. Natali, E. Muscelli, D. Ciociaro, N. Pecori, P. G. Camici, E. Ferrannini

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Objectives. 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 (angiographically proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects. Main outcome measures. 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 μmol 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.

Original languageEnglish
Pages (from-to)241-247
Number of pages7
JournalJournal of Internal Medicine
Volume239
Issue number3
Publication statusPublished - 1996

Fingerprint

Insulin Resistance
Insulin
Glucose
Fasting
Coronary Care Units
Indirect Calorimetry
Glucose Clamp Technique
Hypokalemia
Thermogenesis
Angina Pectoris
Nonesterified Fatty Acids
Energy Metabolism
Italy
Case-Control Studies
Healthy Volunteers
Potassium
Referral and Consultation
Outcome Assessment (Health Care)
Blood Pressure
Lipids

Keywords

  • Insulin resistance
  • Microvascular angina
  • Syndrome X

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Quiñones Galvan, A., Natali, A., Muscelli, E., Ciociaro, D., Pecori, N., Camici, P. G., & Ferrannini, E. (1996). Insulin sensitivity in cardiological syndrome X. Journal of Internal Medicine, 239(3), 241-247.

Insulin sensitivity in cardiological syndrome X. / Quiñones Galvan, A.; Natali, A.; Muscelli, E.; Ciociaro, D.; Pecori, N.; Camici, P. G.; Ferrannini, E.

In: Journal of Internal Medicine, Vol. 239, No. 3, 1996, p. 241-247.

Research output: Contribution to journalArticle

Quiñones Galvan, A, Natali, A, Muscelli, E, Ciociaro, D, Pecori, N, Camici, PG & Ferrannini, E 1996, 'Insulin sensitivity in cardiological syndrome X', Journal of Internal Medicine, vol. 239, no. 3, pp. 241-247.
Quiñones Galvan A, Natali A, Muscelli E, Ciociaro D, Pecori N, Camici PG et al. Insulin sensitivity in cardiological syndrome X. Journal of Internal Medicine. 1996;239(3):241-247.
Quiñones Galvan, A. ; Natali, A. ; Muscelli, E. ; Ciociaro, D. ; Pecori, N. ; Camici, P. G. ; Ferrannini, E. / Insulin sensitivity in cardiological syndrome X. In: Journal of Internal Medicine. 1996 ; Vol. 239, No. 3. pp. 241-247.
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abstract = "Objectives. 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 (angiographically proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects. Main outcome measures. 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 μmol 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.",
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AU - Camici, P. G.

AU - Ferrannini, E.

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N2 - Objectives. 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 (angiographically proven) cardiological syndrome X, but normal glucose tolerance, blood pressure and lipid levels, and 13 matched healthy subjects. Main outcome measures. 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 μmol 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.

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