Acute hypoglycemic effect of Opuntia streptacantha Lemaire in NIDDM.
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Biomedical subjects
Publications and source records attributed to A C Frati.
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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.
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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.
To find out if a second dose of O. streptacantha may enhance its hypoglycemic effect, three tests were performed in fasting condition to 8 type II diabetic subjects and 6 healthy individuals. The tests were as follows: A. 500 g of broiled stems of O. streptacantha were given orally initially and two hours later. B. Only the initial dose. C. Control test with water. Serum glucose and C peptide were measured every two hours from 0 to 6 hours. In diabetic patients a significant (P < 0.01 vs control) decrease of serum glucose reaching from 41 to 46% less than initial value, was noticed in tests A and B, without differences between them. C peptide did not change. In healthy subjects serum glucose and C peptide did not significantly differ between tests. A second dose of O. streptacantha, two hours after the first one, did not improve its hypoglycemic activity.
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.
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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.
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Familial frequency of malignant neoplasms from 20 children with dermatomyositis was investigated and compared with 225 controls. Eight patients with dermatomyositis (40 per cent) had nine family members with a malignant tumour; this frequency is significantly higher than those found in the controls with juvenile rheumatoid arthritis (P less than 0.01), neoplasms (P less than 0.01), and a variety of diseases (P less than 0.05). This finding and the known association of neoplasm-dermatomyositis might suggest an hereditary predisposing factor, possibly a subtle inmune deficiency, common for tumours and dermatomyositis.