[Guar gum in the treatment of diabetes and hypercholesterolemia].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Uusitupa.
Explore the source record for details and available documents.
The pharmacokinetic properties of two new HB 420 glibenclamide preparations, Semi-Euglucon N 1.75 mg and Daonil N 1.75 mg, and of two older HB 419 glibenclamide preparations, Semi-Euglucon 2.5 mg and Daonil 2.5 mg, were compared in a randomized cross-over study in eight healthy volunteers. The HB 420 glibenclamide preparations induced peak plasma glibenclamide concentrations up to about 90 ng/ml at 1.3 to 1.4 hours after ingestion. Administration of the HB 419 preparations induced significantly lower peak plasma glibenclamide concentrations at 1.8 to 2.3 hours after ingestion. Glibenclamide was absorbed and eliminated more rapidly after administration of both HB 420 preparations than after administration of the HB 419 preparations. The mean elimination half-life of glibenclamide was 1.3 +/- 0.1 hours in the case of both HB 420 preparations and 2.0 to 2.5 +/- 0.2 hours in the case of HB 419 preparations. Although the HB 420 preparations contained lower doses of glibenclamide than the HB 419 preparations, the AUC values after administration of the former were similar to the AUC value obtained after administration of one of the HB 419 preparations, indicating improved absorption of glibenclamide from the newly developed preparations. However, the other HB 419 preparation was associated with the greatest AUC value of all, suggesting that glibenclamide was absorbed from this preparation almost as completely as from the HB 420 preparations.
The post-prandial blood glucose and serum insulin responses to test meals, each including 300 ml fat-free milk taken separately with the meal or premixed before cooking into the meal consisting of oatmeal porridge, were studied in 10 diet-treated Type 2 (non-insulin-dependent) diabetic subjects. The modifying effect of guar gum on the responses was also studied by supplementing both types of test meals with 5 g granulated guar gum taken at the beginning of the meal. The blood glucose response was higher after the meal which contained cooked milk than after the respective meal with milk taken separately. The guar gum supplementation attenuated the blood glucose response after the meals, but the effect was more pronounced after the meal containing cooked milk. Post-prandial serum insulin responses were similar after all test meals. The results suggest that cooking may facilitate the absorption of lactose from milk-containing foods, and that supplementation with guar gum may counteract this response.
Fourteen male subjects with hypercholesterolemia received daily supplementation with granulated guar gum or placebo, 15 g/day, during 12 wk in a double-blind, cross-over trial. A statistically significant reduction in serum total cholesterol (7.27 +/- 0.24 versus 8.23 +/- 0.26 mmol/l, mean +/- SEM, p less than 0.01) which was mainly due to a reduction in low-density lipoprotein cholesterol concentration (4.70 +/- 0.19 versus 5.32 +/- 0.23 mmol/l, p less than 0.05) was observed after 6 wk on guar gum as compared with placebo. Between 6 and 12 wk on guar gum the serum cholesterol and low-density lipoprotein cholesterol levels increased in most subjects, and after 12 wk the difference from placebo was no longer statistically significant. Serum high-density lipoprotein cholesterol levels were unaffected by guar gum. Serum and lipoprotein triglycerides showed no significant changes during the study, and the body weight of the subjects remained unchanged. Serum calcium, magnesium, phosphate, and iron levels, and urinary calcium excretion were not affected by guar gum supplementation. No severe side effects were observed, necessitating reduction of the dose or stopping the treatment. It is concluded that the hypocholesterolemic effect of guar gum seems to decrease during prolonged dietary supplementation. Further controlled studies are needed before the dose response and the long-term effects of guar gum in hypercholesterolemia can be evaluated.
Systolic time intervals (STI) were recorded six times in 12 male students. All 72 recordings were measured twice by a physician and once by two nurses. By comparing these measurements an intra- and interobserver (= methodological) variation was obtained. For measured parameters (QS2- interval and LVET) variation was less than 2%. For calculated parameters the variation was larger, but did not reach the level of statistical significance. Methodological variation was smaller than physiologic variation. The internal consistency was almost perfect for measured parameters and only slightly worse for calculated parameters.
Explore the source record for details and available documents.
A double-blind, placebo-controlled trial was carried out in 17 Type 2 (non-insulin-dependent) diabetic patients, treated with diet therapy alone to study the effects of guar gum on metabolic control, serum lipids, and blood pressure levels. Thirteen of the patients had drug treatment for hypertension. Guar gum was taken with meals three times a day, and the dose was gradually increased to 21 g per day. A slight, but not significant improvement was found in the metabolic control of the patients after the guar gum treatment compared to the placebo. Serum total cholesterol was 11% (p greater than 0.01) lower after the guar gum but no significant differences were found in HDL-cholesterol or serum triglycerides during the guar gum treatment compared to the placebo. Diastolic blood pressure level was significantly lower during the guar gum treatment compared to placebo. No difference was observed in systolic blood pressure levels between the guar gum and placebo treatments. The reduction of diastolic blood pressure was independent of changes in fasting blood glucose level or body weight, but could in part be due to simultaneous reduction in serum cholesterol concentration. The changes associated with guar gum supplementation suggest a reduction in the risk for cardiovascular complications in diabetic patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In the present study a Perkin-Elmer 5000 atomic absorption spectrometer equipped with a tungsten--iodide lamp for improved background correction at the 357.9 nm chromium absorption line and an HGA 500 graphite furnace were employed for the direct determination of chromium in human serum, milk and urine. The method of standard additions was used: 0.25-0.75 ng Cr was added to 1 ml samples. Except for urine samples, a dilution of 1 + 1 to 1 + 2 with H2O was necessary in order to obtain correct calibration curves. The average concentration of chromium in all the samples of normal subjects was less than 0.5 ng Cr ml-1. The day-to-day variation for all of the pooled samples was around 10% (relative standard deviation). For urine, the accuracy of the method was tested by comparing the results of another laboratory for the same two round robin samples. Excellent agreement was found between the present method and those of the other laboratory that had used isotope dilution--mass spectrometry and continuum source wavelength modulated echelle--atomic absorption spectrometry to define the chromium concentration in the samples. The detection limit of the method, 0.05 ng Cr ml-1 for urine and serum and 0.1 ng Cr ml-1 for human milk, was sufficient for the biological fluids analyzed. The method was employed for the determination of chromium in 24-h urine samples of maturity onset diabetics supplemented with 20 or 200 micrograms Cr3+ d-1 for six weeks. It was shown that the 24-h urinary chromium excretion accurately indicates the daily dietary chromium intake of these patients.
Systolic time intervals (STI) were recorded in 33 newly diagnosed non-insulin-dependent diabetics (19 men, 14 women, aged 44-64 years) before and after 3-8 months' dietary therapy. The mean (+/- SD) fasting blood glucose was 11.1 +/- 2.6 mmol/l before treatment and 7.8 +/- 1.8 at the second examination (p less than 0.001). Concomitantly with the decline in blood glucose concentration, the heart rate corrected pre-ejection period (PEP) decreased from 139 +/- 11.9 to 135 +/- 14.4 msec (mean +/- SD) (p less than 0.05), the heart rate corrected left ventricular ejection time (LVET) increased from 400 +/- 15.1 to 410 +/- 20.7 msec (p less than 0.0025) and the PEP/LVET ratio decreased from 0.39 +/- 0.06 to 0.36 +/- 0.06 (p less than 0.005). When the diabetics were divided into two groups according to the degree of the decline in blood glucose concentration, only those whose fasting blood glucose decreased by greater than or equal to 3 mmol/l showed significant changes in STI. No significant changes were observed in the mean heart rate or systolic blood pressure during the treatment. Cardiac dysfunction occurring in untreated non-insulin-dependent diabetics may be caused by metabolic factors and it may be reversed at least partially by correction of hyperglycemia.
The effects of two different beta-receptor blocking agents, beta 1-selective metoprolol (150 mg/day) and non-selective propranolol (120 mg/day), on hormonal responses to physical exercise (30 min bicycle ergometer test) were compared with placebo within a double-blind, cross-over design in 7 healthy male volunteers. Plasma prolactin levels decreased from the initial values during and after exercise during treatments with placebo and beta-receptor blocking agents, but they were constantly higher with the two beta-blocking agents than with placebo. Exercise did not affect plasma testosterone levels, but during propranolol they remained higher than during placebo and metoprolol. The plasma LH and FSH levels were not affected by exercise, nor were they significantly modified by beta-blockade. The results of this study as well as those of previous studies indicate that beta-receptor blocking agents interfere with physiological endocrine functions and that the non-selective agents may have more distinct effects in this respect.
In a double-blind crossover study the effect of ingested guar gum granules, 15 g/d for 3 months, on blood lipids was evaluated in twelve obese hypercholesterolaemic patients. Serum total cholesterol decreased during the guar gum period in eight of the ten patients who completed the study. The mean serum cholesterol was 8.5 +/- 0.4 mmol/l after the guar gum period as compared to 8.9 +/- 0.3 mmol/l after the placebo period. The mean HDL-cholesterol or body weight showed no significant changes during either treatment period. Guar gum administration did not cause any significant changes in 24-h urinary excretion of sodium, potassium, calcium or magnesium. It is concluded that the administration of guar gum granules seems to reduce serum total cholesterol in hypercholesterolaemic patients without exerting an effect on HDL-cholesterol. The beneficial effect of guar gum is independent of the changes in body weight.
Explore the source record for details and available documents.
A double-blind cross-over study was performed to compare the efficacy in maturity-onset (type 2) diabetes of two glibenclamide preparations, HB 419, currently in general use, and HB 420, a new product with more complete absorption. Nineteen diabetic outpatients participated in the study. Seventeen completed the trial. Before the trial, fasting blood glucose levels in all patients were over 7.0 mmol/l, relative body weights were below 130% and daily glibenclamide doses ranged from 10 to 15 mg. The study was made up of two periods, each lasting for two months. The trial dosage of HB 419 was 5 mg twice a day and of HB 420 3.5 mg twice a day. Fasting blood glucose levels, diurnal glucose excretion, glycohaemoglobin A1 (GHbA1) levels, body weight and blood pressure levels were determined. The mean (+/- SEM) fasting blood glucose concentration was 11.5 +/- 0.6 mmol/l at the end of the baseline period. After one month of treatment, the mean fasting blood glucose level was 11.4 +/- 0.6 mmol/l in patients on HB 419 and 12.5 +/- 0.7 mmol/l in patients on HB 420 (p less than 0.01) but at the end of the two treatment periods the mean fasting blood glucose value was the same (11.6 +/- 0.5 mmol/l) for both glibenclamide preparations. No significant differences were found in GHbA1 values, diurnal glucose excretion, body weight or blood pressure levels between the treatment regimens.
Explore the source record for details and available documents.