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MEDLINE Abstracts: Insulin Sensitivity in Patients With Syndrome X
Epidemiological Investigation of Insulin Resistance Syndrome (Syndrome X) in a City in Japan
Imamura M, Kishitani Y, Saika T, Iio K, Ikami H, Kagita A, Nishimura A, Masuda K, Ohno Y, Aoki N
Clinical & Experimental Pharmacology & Physiology 22 Suppl 1:S30-1, Dec 1995
In order to study the prevalence of insulin resistance syndrome (syndrome X) in Japanese subjects, inhabitants aged above 40 years living in Osaka-Sayama city from September 1992 through December 1993 were investigated. The population-based study was performed on 2498 subjects (661 males and 1837 females) constituting 10.9% of the total population aged above 40 years.
The prevalence of glucose intolerance was 8.7% (n = 218) in 2498 subjects. The prevalence of hypertension was 36.9% (n = 923) and that of hypertriglyceridaemia was 19.0% (n = 475). The prevalence of syndrome X as characterized by an association of glucose intolerance, hypertension and hypertriglyceridaemia was 1.6% (n = 39) in all subjects examined and 17.4% in subjects showing glucose intolerance.
Fasting serum insulin levels were significantly higher in patients with syndrome X than in normal subjects. Furthermore, the levels were significantly correlated with blood levels of frucutosamine, fasting glucose and triglyceride, and with body mass index as well.
In conclusion, insulin resistance syndrome (syndrome X) is also found among the larger Japanese population, and fasting serum insulin levels can be a useful marker of this metabolic disorder.
Insulin-Resistant Glucose Metabolism in Patients With Microvascular Angina -- Syndrome X
Vestergaard H, Skott P, Steffensen R, Wroblewski H, Pedersen O, Kastrup J
Metabolism: Clinical & Experimental 44(7):876-82, Jul 1995
Studies in patients with microvascular angina (MA) or the cardiologic syndrome X have shown a hyperinsulinemic response to an oral glucose challenge, suggesting insulin resistance and a role for increased serum insulin in coronary microvascular dysfunction. The aim of the present study was to examine whether patients with MA are insulin-resistant. Nine patients with MA and seven control subjects were studied. All were sedentary and glucose-tolerant. Coronary arteriography was normal in all participants, and exercise-induced coronary ischemia was demonstrated in all MA patients. A euglycemic, hyperinsulinemic clamp was performed in combination with indirect calorimetry. Biopsy of vastus lateralis muscle was taken in the basal state and after 4 hours of euglycemia and hyperinsulinemia (2 mU.kg-1.min-1). The fasting level of "true" serum insulin was significantly higher (43 ± 6 v 22 ± 3 pmol/L, P < .02) and the rate of insulin-stimulated glucose disposal to peripheral tissues was lower in patients with MA (13.4 ± 1.0 v 18.2 ± 1.4 mg.kg fat-free mass [FFM]-1.min-1, P < .02) due to a decrease in nonoxidative glucose metabolism (8.4 ± 0.9 v 12.5 ± 1.3 mg.kg FFM-1.min-1, P < .02). No difference was found in glucose or lipid oxidation rates between the two groups.
Effects of Diabetes and Level of Glycemia on All-Cause and Cardiovascular Mortality. The San Antonio Heart Study.
Wei M, Gaskill SP, Haffner SM, Stern MP
Diabetes Care 21(7):1167-72, Jul 1998
Objective: Although the level of hyperglycemia is clearly a risk factor for microvascular complications in diabetic patients, its role in macrovascular complications remains controversial. We followed 4,875 subjects (65% Mexican-American) for 7-8 years to investigate the effects of diabetes and hyperglycemia on all-cause and cardiovascular disease (CVD) mortality. These end points were also analyzed according to quartiles of baseline fasting plasma glucose among diabetic participants.
Research Design and Methods: The Cox proportional hazards model was used to estimate the relative risks (RRs) for all-cause and CVD mortality.
Results: Diabetes was significantly associated with increased all-cause mortality (RR [95% CI] = 2.1 [1.3-3.5] in men; 3.2 [1.9-5.4] in women) and increased CVD mortality (3.2 [1.4-7.1] in men; 8.5 [2.8-25.2] in women). Among diabetic subjects, those in quartile 4 had a 4.2-fold greater risk of all-cause mortality (P < 0.001) and a 4.7-fold greater risk of CVD mortality (P = 0.01) than those in quartiles 1 and 2 combined. After further adjustment for other potential risk factors, subjects in quartile 4 had a 4.9-fold greater risk of all-cause mortality and a 4.9-fold greater risk of CVD mortality than those in quartiles 1 and 2. In addition, hypertension, current smoking, and cholesterol > 6.2 mmol/l were significant predictors of CVD mortality using Cox models.
Conclusions: We conclude that diabetes is a predictor of both all-cause and CVD mortality in the general population and that both hyperglycemia and common CVD risk factors are important predictors of all-cause and CVD mortality in diabetic subjects.
Myocardial Insulin Resistance in Patients With Syndrome X
Botker HE, Moller N, Schmitz O, Bagger JP, Nielsen TT
Journal of Clinical Investigation 100(8):1919-27, Oct 1997
Insulin resistance is common in patients with angina pectoris, a positive exercise electrocardiogram, and normal coronary angiograms (syndrome X). It is still not known whether insulin resistance affects the cardiac muscle itself and, if so, whether insulin resistance involves myocardial hemodynamics and energy metabolism. We investigated hemodynamics as well as metabolite exchanges across the heart and the forearm in eight patients with syndrome X and eight control subjects during a baseline period after an overnight fast and during a hyperinsulinemic-euglycemic clamp. Myocardial hemodynamics and metabolism were studied at rest, during pace stress, and in the recovery period after pacing. Neither coronary sinus blood flow nor forearm blood flow differed between the groups before and during the clamp. Whole body insulin-stimulated glucose uptake was decreased in the patients (15.6±2.1 vs. 23.1±2.0 micromol x kg-1 x min-1). Insulin-stimulated glucose uptake in the forearm and the cardiac muscle was equally reduced in the patients (46±5 and 48±5%). Myocardial glucose uptake correlated with total arterial delivery in the control subjects (r = 0.63, P < 0.01), but not in patients (r = 0.22, P = 0.13). Carbohydrate and lipid oxidation was similar in the two groups at rest, and changes during the clamp were not different in control subjects and patients either at rest, during pacing, or in the recovery period. Patients with syndrome X exhibit myocardial insulin resistance, but cardiac energy metabolism remains unaffected. In patients with syndrome X, insulin-stimulated glucose uptake is independent from myocardial blood flow.
Insulin-like Growth Factor-I, Insulin, and Angina Pectoris Secondary to Coronary Atherosclerosis, Vasospasm, and Syndrome X
Botker HE, Skjaerbaek C, Eriksen UH, Schmitz O, Orskov H
American Journal of Cardiology 79(7):961-3, Apr 1997
We measured growth hormone-related substances in patients with angina pectoris precipitated by different underlying disorders. Although hyperinsulinemia was more pronounced in patients with angina pectoris secondary to atherosclerotic coronary disease than in patients with syndrome X and variant angina, we found no evidence that growth hormone-related substances including insulin-like growth factor-I are associated with coronary atherosclerosis.
Insulin Resistance in Cardiac Syndrome X and Variant Angina: Influence of Physical Capacity and Circulating Lipids
Botker HE, Frobert O, Moller N, Christiansen E, Schmitz O, Bagger JP
American Heart Journal 134(2 Pt 1):229-37, Aug 1997
Insulin resistance has been demonstrated in patients with angina pectoris irrespective of detectable atherosclerosis at coronary angiograms. We compared insulin sensitivity, lipid profiles, and exercise capacity in 20 patients with syndrome X, 15 patients with variant angina, and 20 healthy controls to investigate whether the presentation of the insulin resistance syndrome differs between the two patient groups with disparate vascular abnormalities. All patients had angiographically normal coronary arteries. Maximal oxygen uptake (VO2 max) was determined at bicycle exercise testing. Insulin sensitivity (SI) was assessed by the minimal model analysis of the intravenous glucose tolerance test. Patients with variant angina had significantly lower VO2 max than controls (mean ± SE, 25.6 ± 1.5 vs 30.6 ± 1.4 ml x kg-1 x min-1, p < 0.05), whereas VO2 max in patients with syndrome X was intermediate (27.1 ± 1.3 ml x kg-1 x min-1). Compared with controls, patients with syndrome X and variant angina had reduced insulin sensitivity (controls, 1.47 ± 0.16 10(-4) x min-1/per pmol/L vs syndrome X, 0.86 ± 0.11 10(-4) x min-1 per pmol/L and variant angina, 0.96 ± 0.15 x 10(-4) x min-1 per pmol/L; analysis of variance, p < 0.05). Only patients with syndrome X exhibited fasting hyperinsulinemia. Patients with syndrome X also had higher fasting concentrations of triglycerides and total cholesterol and lower concentrations of high-density lipoprotein cholesterol than controls. When adjusting SI for variances of VO2 max, differences in SI vanished between controls and patients with variant angina but not between controls and patients with syndrome X. Thus syndrome X and variant angina are both associated with insulin resistance, but lipid abnormalities are only prominent in patients with syndrome X. A variable expression in terms of concomitant disturbances of lipid profiles and disparate influences of physical capacity suggests different underlying mechanisms.
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