Acute effect of cigarette smoking on glucose tolerance and other cardiovascular risk factors.

OBJECTIVE: To investigate the acute effect of cigarette smoking on glucose tolerance, insulin sensitivity, serum lipids, blood pressure, and heart rate. RESEARCH DESIGN AND METHODS: This nonrandomized experimental control trial in a tertiary care center included 20 healthy chronic smokers and 20 age-, sex-, and BMI-matched healthy volunteers. Two oral glucose tolerance tests (OGTTs) were performed on each subject. Three cigarettes were smoked during the first 30 min in one of the tests. Serum glucose, insulin, and C-peptide levels were measured every 30 min; the area under the curve (AUC) and the insulin sensitivity index (ISI) were calculated; serum total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride levels were measured at 0 and 180 min; and blood pressure and heart rate were recorded every 5 min throughout 180 min. RESULTS: Smoking acutely impaired glucose tolerance: the AUC for glucose in smokers was 25.5 +/- 1.03 mmol/l (mean +/- SE) (95% CI 22.9-28) during the smoking OGTT and 21.8 +/- 0.85 mmol/l (CI 19.2-24.3) in the control OGTT (P < 0.01); in nonsmokers, it was 19.7 +/- 0.3 mmol/l (CI 18.8-20.5) in the smoking OGTT and 18.7 +/- 0.35 mmol/l (CI 17.8-19.5) in the control OGTT (P < 0.05). Smoking acutely increased serum insulin and C-peptide levels and decreased ISI only in smokers: ISI in smokers was 55 +/- 2.8 (CI 47.4-62.6) in the control OGTT and 43 +/- 2.7 (CI 35.4-50.6) in the smoking OGTT (P < 0.05). Smoking acutely caused a rise of serum total cholesterol levels in both groups and increased LDL cholesterol and triglyceride serum levels significantly only in smokers (P < 0.05). A significant rise of blood pressure and heart rate while smoking was present in all the subjects. CONCLUSIONS: Smoking acutely impaired glucose tolerance and insulin sensitivity, enhanced serum cholesterol and triglyceride levels, and raised blood pressure and heart rate. These findings support the pathogenetic role of cigarette smoking on cardiovascular risk factors.

Hypoglycemic effect of Opuntia streptacantha Lemaire in NIDDM.

To assess the hypoglycemic effect of the nopal Opuntia streptacantha Lemaire (O. streptacantha Lem.), three groups of patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied. Group one (16 patients) ingested 500 g of broiled nopal stems. Group 2 (10 patients) received only 400 ml of water as a control test. Three tests were performed on group 3 (6 patients): one with nopal, a second with water, and a third with ingestion of 500 g broiled squash. Serum glucose and insulin levels were measured at 0, 60, 120, and 180 min. After the intake of O. streptacantha Lem., serum glucose and serum insulin levels decreased significantly in groups 1 and 3, whereas no similar changes were noticed in group 2. The mean reduction of glucose reached 17.6 +/- 2.2% of basal values at 180 min in group 1 and 16.2 +/- 1.8% in group 3; the reduction of serum insulin at 180 min reached 50.2 +/- 8.0% in group 1 and 40.3 +/- 12.4% in group 3. This study shows that the stems of O. streptacantha Lem. cause a hypoglycemic effect in patients with NIDDM. The mechanism of this effect is unknown, but an increased insulin sensitivity is suggested.

Hyperinsulinemia in patients with coronary heart disease in absence of overt risk factors.

The objective of the study was to determine if male subjects with coronary atherosclerotic heart disease (CHD) without major CHD risk factors have hyperinsulinemia and related metabolic changes. Previous studies suggested that hyperinsulinemia is a CHD risk factor, but they did not entirely exclude concurrent metabolic abnormalities. A prospective, comparative, cross-sectional study in a tertiary care teaching hospital in Mexico City was conducted in 15 men who had suffered myocardial infarction 6 to 24 months before and had significant coronary occlusion on angiography. Control group was formed by 15 age-matched healthy men. None had hypertension, obesity, diabetes, gout, glucose intolerance or hyperlipidemia. Body mass index (BMI), waist/hip ratio (WHR), blood pressure (BP); oral glucose tolerance test (OGTT) with measurement of serum glucose, insulin and C-peptide every 30 min for 2 h, fasting serum cholesterol, triglycerides and uric acid, areas under curve (AUC) of glucose and insulin, insulin/glucose ratio and insulin sensitivity index were calculated. BMI, WHR and BP were similar in both groups. Fasting and post-load serum glucose and insulin concentrations were significantly higher in CHD than in control group (p < 0.01); fasting glucose 5.9 +/- 0.6 vs. 4.8 +/- 0.7 nmol/1, 2-h glucose 8.3 +/- 0.6 vs. 7.3 +/- 0.9 mmol/l, fasting insulin 17.5 +/- 1.2 vs. 15.3 +/- 1.7 pmol/l, 2 h insulin 448 +/- 108 vs. 282 +/- 87 pmol/l in CHD and control group, respectively. AUC of glucose, AUC of insulin, insulin/glucose ratio, post load C-peptide, serum cholesterol, triglycerides and uric acid levels were also significantly higher in CHD than in healthy controls. Insulin sensitivity index was significantly lower in patients with CHD (27.7 +/- 8.3) than in healthy control subjects (73.9 +/- 18) (p < 0.001). Patients with CHD have hyperinsulinemia and subtle metabolic abnormalities related with insulin resistance even in absence of overt risk factors.

Influence of acute hyperglycemia on left ventricular function in diabetics assessed by echocardiography.

Myocardial dysfunction in diabetes mellitus is reversed by proper correction of metabolic changes. To assess the role of hyperglycemia on cardiac dysfunction, 50 g of dextrose were intravenously infused to 15 subjects with stable type 2 diabetes. Echocardiographic measurements were made at 0, 60, 120, 180, and 240 minutes. In spite of the high levels of blood glucose reached in diabetics, left ventricular ejection fraction, fractional shortening, and stroke volume did not experience significant changes. Moreover, cardiac output significantly (p less than 0.01) increased in diabetics secondary to an increase in heart rate. No cardiac changes were noticed in 7 healthy subjects studied in a similar fashion. However, their induced hyperglycemia was not as elevated as in the diabetic patients. These results suggest that acute induced hyperglycemia per se does not appear to impair left ventricular contractility in diabetics at resting conditions.

[The effect of acute hyperinsulinemia on arterial pressure in healthy individuals]. / Effecto de la hiperinsulinemia aguda en la tensión arterial de individuos sanos.

To assess if induced hyperinsulinemia enhances blood pressure (BP), three tests were performed to nine healthy volunteers as follows: A. After an oral dextrose load (75 g), 250 ml of 0.9% NaCl plus 25 g dextrose were infused in three hours. B. The same procedure, plus 15 U of regular insulin in the intravenous solution. C. (control) The same procedure but without insulin and dextrose. Pulse and BP were measured every 15 minutes, serum glucose and insulin were determined hourly. Hyperinsulinemia from 2 to 7-fold the basal value was induced in the test A, and from 7 to 30-fold in the test B (P less than 0.01). BP did not rise with hyperinsulinemia, but a slight and nonsignificant decrease of mean BP and higher heart rate (P less than 0.05) were noticed at the third hour in the test B. Acute hyperinsulinemia do not cause high BP. A cause-effect relationship between hyperinsulinemia and hypertension is still unproved.

Influence of nopal intake upon fasting glycemia in type II diabetics and healthy subjects.

To assess if the acute hypoglycemic effect of nopal which occurs in diabetic patients also appears in healthy individuals, 500 g of nopal stems (O. streptacantha Lem.) were given orally to 14 healthy volunteers and to 14 patients with NIDDM. Serum glucose and insulin levels were measured at 0, 60, 120 and 180 minutes after nopal ingestion. A control test was performed with the intake of 400 ml of water. The intake of nopal by the NIDDM group was followed by a significant reduction of serum glucose and insulin concentration reaching 40.8 + 4.6 mg/dl (n = 14) (mean+SEM) and 7.8 + 1.5 uU/ml (n = 7) less than basal value, respectively, at 180 minutes. (P less than 0.001 vs control test). No significant changes were noticed in the healthy group as compared with the control test (P greater than 0.05). Acute hypoglycemic effect of nopal was observed in patients with NIDDM but not in healthy subjects, thus the mechanisms of this effect differs from current hypoglycemic agents.

[Changes in ventricular function in diabetes mellitus. Relation to the duration of the diabetes and its complications]. / Alteraciones de la función ventricular en la diabetes mellitus. Relación con la duración de la diabetes y sus complicaciones.

To find out if ventricular dysfunction is related with diabetes duration or diabetic chronic complications, resting and exercise electrocardiograms, chest X-ray, echocardiograms and dynamic scintigraphy with left ventricular ejection fraction measurement (LVEF) were performed to three groups of diabetic subjects without known cardiopathy or hypertension: (I) twelve subjects with less than five-years diabetes, (II) eleven with five to ten years, (III) nineteen with diabetes lasting more than ten years. Results were compared with ten healthy volunteers. 90.4% of diabetics had at least one abnormality. LVEF was significantly lower in diabetics (P less than 0.001) than in control group. No important differences were found according to diabetes duration. Lower fractional shortening and lower cardiac output were found in group III than in control group (P less than 0.05). Impaired ventricular function in group III was related (P less than 0.05) with the evidence of diabetic late complications. Relationship between ventricular dysfunction and other microvascular abnormalities might suggest that microangiopathy participates in some extent to the pathogenesis of ventricular disorder.