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PubMedDate not supplied

Low dose metformin in the treatment of type II non-insulin-dependent diabetes: clinical and metabolic evaluations.

Low doses of metformin (500 mg twice daily) were administered to 20 diabetic patients, combined with the original sulfonylurea treatment which had become ineffective even at full dosage. After 1 and 5 weeks, the effects of the drug on glycemic control, blood intermediate metabolites and monocyte insulin receptors were monitored. Metformin clearly improved glycemic control by reducing both fasting blood glucose from 189.88 +/- 21.11 mg/dl to 131.12 +/- 16.02 mg/dl after 1 week and to 130.11 +/- 13.29 mg/dl after 5 weeks (p less than 0.025 both after 1 and 5 weeks); the diurnal blood glucose average fell from 235.33 +/- 24.11 mg/dl to 174.66 +/- 23.45 mg/dl (p less than 0.0025) after 1 week and to 177.65 +/- 21.71 mg/dl (p less than 0.0005) after 5 weeks. Consequently both blood glycosylated hemoglobin (p = n.s. after 1 week, p less than 0.025 after 5 weeks) and serum fructosamine (p less than 0.0025 after both 1 and 5 weeks) also decreased after metformin treatment. No change in plasma insulin and C-peptide levels was reported and no modification in diurnal rhythms of blood lactate, pyruvate, alanine glycerol and beta-OH-butyrate was detected at any time during metformin treatment. All the changes documented in the binding values were already complete at the end of the first week; insulin binding to monocytes increased slightly but significantly (p less than 0.05) and the number of receptors per cell rose (p less than 0.05) but could not be correlated to any index of glycemic control. These data suggest that the antidiabetic action of metformin is neither related to its lactate-increasing activity nor does it depend upon its inducing an increase in insulin binding values. This metformin-related hypoglycemic effect might be the result, at least in part, of a reduced oxidative phosphorylation without inhibition of hepatic gluconeogenesis and/or of decreased hepatic glucose output. Moreover, our data are also consistent with the hypothesis that metformin might affect insulin action at a post-receptor level.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Effect of insulin treatment on osteocalcin levels in diabetic children and adolescents.

To investigate bone mineral metabolism in insulin-dependent diabetes mellitus, serum osteocalcin, a marker of bone formation, was measured in 31 diabetic children at onset of disease and 15 days after metabolic improvement by insulin therapy. As a control group for osteocalcin levels we studied 31 healthy sex- and age-matched children. Mean values of serum osteocalcin at onset of diabetes were significantly lower than in control group (p < 0.001), but we did not find any difference after 15 days of insulin therapy. Osteocalcin and parathyroid hormone concentrations were significantly greater after 15 days of insulin treatment than at onset of disease (p < 0.001 and p < 0.01, respectively). The osteocalcin levels were negatively correlated both with fructosamine and with glycosylated hemoglobin (p < 0.01 and p < 0.001, respectively), and positively correlated with the degree of metabolic acidosis at onset (p < 0.05). Therefore we postulate that during glycometabolic imbalance there is a decrease in bone turnover that could be one of the etiological factors of diabetic osteopenia.

Child↗
PubMed2005

The inflammatory properties of electronegative low-density lipoprotein from type 1 diabetic patients are related to increased platelet-activating factor acetylhydrolase activity.

AIMS/HYPOTHESIS: Chemical and biological characteristics of LDL(-) from type 1 diabetic subjects were analysed. The diabetic patients were studied during poor and optimised glycaemic control. MATERIALS AND METHODS: Total LDL was subfractionated into electropositive LDL(+) and electronegative LDL(-) by anion exchange chromatography and the lipid and protein composition of the two determined. RESULTS: LDL(-) differed from LDL(+) in that it had higher triglyceride, non-esterified fatty acids, apoE, apoC-III and platelet-activating factor acetylhydrolase (PAF-AH), as well as lower apoB relative content. No evidence of increased oxidation was observed in LDL(-). LDL(-) increased two-fold the release of interleukin 8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) in endothelial cells, suggesting an inflammatory role. Optimisation of glycaemic control after insulin therapy decreased the proportion of LDL(-), but did not modify the composition of LDL subfractions, except for a decrease in PAF-AH activity in LDL(-). The possibility that LDL(-) could be generated by non-enzymatic glycosylation was studied. Fructosamine and glycated LDL content in LDL subfractions from type 1 diabetic patients was greater than in LDL subfractions isolated from normoglycaemic subjects, and decreased after glycaemic optimisation in both subfractions. However, no difference was observed between LDL(+) and LDL(-) before and after insulin therapy. CONCLUSIONS/INTERPRETATION: These results provide evidence that LDL(-) is not produced by glycosylation. Nevertheless, LDL(-) from diabetic patients displays inflammatory potential reflected by the induction of chemokine release in endothelial cells. This proatherogenic effect could be related to the high PAF-AH activity in LDL(-).

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1996

Electronegative low density lipoprotein subform is increased in patients with short-duration IDDM and is closely related to glycaemic control.

We evaluated the effect of improving glycaemic control with intensive insulin therapy on LDL susceptibility to oxidation, electronegative LDL proportion, and LDL subfraction phenotype in a group of 25 patients with short-duration insulin-dependent diabetes mellitus (IDDM); 25 matched healthy control subjects were also studied. LDL susceptibility to oxidation was measured by continuous monitoring of conjugated diene formation. Electronegative LDL was isolated by anion exchange chromatography, and quantified as percentage of total LDL. Six LDL subfractions were isolated by density gradient ultracentrifugation and phenotype A or B classified as the quotient (LDL1-LDL3)/(LDL4-LDL6). Compared to the control group, IDDM subjects with poor glycaemic control showed higher electronegative LDL (19.03 +/- 10.09 vs 9.59 +/- 2.98%, p < 0.001), similar LDL subfraction phenotype and lower susceptibility to oxidation (lag phase 45.6 +/- 8.8 vs 41.2 +/- 4.7 min, p < 0.05). After three months of intensive insulin therapy, HbA1c decreased from 10.88 +/- 2.43 to 5.69 +/- 1.54% (p < 0.001), and electronegative LDL to 13.84 +/- 5.15% (p < 0.05). No changes in LDL susceptibility to oxidation or LDL subfraction phenotype were observed. Electronegative LDL appeared significantly correlated to HbA1c and fructosamine (p < 0.01 and p < 0.001) only in poorly controlled IDDM patients. These findings suggest that high electronegative LDL in IDDM subjects is related to the degree of glycaemic control, and could therefore be due to LDL glycation rather than to LDL oxidation or changes in LDL subfraction phenotype.

Adolescent↗
PubMed1997

The effect of portal and peripheral insulin delivery on carbohydrate and lipid metabolism in a miniature pig model of human IDDM.

A pig model of insulin-dependent diabetes was used to examine the importance of the portal-systemic insulin gradient for whole-body metabolic control. Six pigs had jugular vein, portal vein, and carotid artery cannulae implanted before being made diabetic (150 mg kg[-1] streptozotocin). Each animal received 4 weeks of portal and 4 weeks of peripheral insulin delivery in random order. The blood glucose target range was 5-10 mmol x l(-1), and serum fructosamine and fasting and postprandial blood glucose concentrations were not different between peripheral and portal insulin infusion. Insulin requirement was not different between the 4 week infusion periods, but fasting peripheral insulin levels after peripheral delivery (124 +/- 16 (mean +/- SEM) pmol x l[-1]) were significantly higher (p < 0.05) than in portally infused (73.8 +/- 5.4 pmol x l[-1]) or pre-diabetic control animals (68.4 +/- 3.6 pmol x l[-1]). Basal hepatic glucose output was also higher (p < 0.05) in peripherally (4.2 +/- 0.4 mg x kg[-1] x min[-1]) than in portally infused animals (2.9 +/- 0.4 mg x kg[-1] x min[-1]) or controls (3.0 +/- 0.3 mg x kg[-1] x min[-1]). Clamp glucose metabolic clearance rate was, however, not different between the peripheral and portal insulin delivery routes (8.1 +/- 1.0 vs 9.0 +/- 0.7 ml x kg[-1] x min[-1]), although both were significantly lower (p < 0.05) than that measured in prediabetic control animals (11.7 +/- 1.0 ml x kg[-1] x min[-1]). Lipid profiles and subfractions were similar in all three groups. It is concluded that the portal route of delivery is superior to the peripheral in maintaining more appropriate insulin concentrations and control of hepatic glucose output, although in the absence of euglycaemia it is still associated with significant metabolic abnormalities.

Animals↗
PubMed2000

Erythromycin improves glycaemic control in patients with Type II diabetes mellitus.

AIMS/HYPOTHESIS: Erythromycin mimics the effect of the gastrointestinal hormone motilin by binding to its receptor and acting as a motilin agonist. We recently found that motilin stimulates insulin secretion at lower doses than doses required to stimulate gastric contractile activity. We studied the effects of erythromycin on insulin secretion and glycaemic control in patients with diabetes mellitus. METHODS: Inpatients (n = 34) with Type II (non-insulin-dependent) diabetes mellitus were randomly assigned to receive either erythromycin (400 mg orally three times a day, n = 19) or a placebo (n = 15) for 1 week (first study). Another 34 outpatients with Type II diabetes were also treated with erythromycin (200 mg orally three times a day, n = 17) or a placebo (n = 17) for 4 weeks (second study). Finally, nine inpatients with Type II diabetes and eight normal control subjects received intravenous erythromycin (10 mg x kg(-1) x h(-1)) or saline infusion and insulin secretion was examined (third study). RESULTS: Erythromycin lowered fasting blood glucose and fructosamine concentrations (p < 0.01) and increased basal as well as glucose-stimulated insulin secretion (p <0.05-0.01) (first study). Low doses of erythromycin treatment for 4 weeks also significantly improved glycaemic control in Type II diabetic patients (second study). Erythromycin infusion significantly increased plasma insulin and decreased glucose concentrations in Type II diabetic and control subjects and greatly potentiated glucose-induced insulin secretion in the latter (third study). CONCLUSION/INTERPRETATION: These results indicate that erythromycin given orally has an antidiabetogenic effect and therefore erythromycin derivatives that lack the antibacterial activity could have a therapeutic value in Type II diabetic patients.

Blood Glucose↗
PubMed1999

A comparison of repaglinide and glibenclamide in the treatment of type 2 diabetic patients previously treated with sulphonylureas.

OBJECTIVE: To compare the efficacy and safety of repaglinide, a novel oral prandial glucose regulator, with that of glibenclamide, an oral hypoglycaemic agent, in the treatment of patients with type 2 diabetes. METHODS: This was a 14-week, double-blind, parallel-group trail in which a total of 195 type 2 diabetic patients treated with oral hypoglycaemic agents were randomized to receive either repaglinide, administered preprandially three times daily, or glibenclamide, given preprandially once or twice daily, as per manufacturer's recommendations. RESULTS: By the end of the study, the 2-h postprandial blood glucose values were lower in the repaglinide group than in the glibenclamide group, with the difference approaching statistical significance (repaglinide, 8.1 (0.6) mol x l(-1) vs glibenclamide, 9.1 (0.6)mmol x l(-1); P = 0.07). There was no statistically significant difference in the mean blood glucose level at the end of the study between the two groups (repaglinide, 7.1 (0.5) mmol x l(-1) vs glibenclamide, 7.4 (0.5) mmol x l(-1); P = 0.42), and baseline HbA1c values had decreased to the same degree in both the repaglinide [7.8% (0.1%) to 7.5% 0.1%)] and the glibenclamide groups [8.0 (0.1%) to 7.6 (0.1%)]. There are no significant differences between the repaglinide and glibenclamide treatment groups in the levels of fasting blood glucose, fructosamine, fasting C-peptide, insulin and proinsulin. Neither treatment group showed any clinically significant changes in blood lipid profiles. Repaglinide and glibenclamide were both well tolerated. No significant differences were observed between the two treatment groups with respect to adverse events, including hypoglycaemic episodes and weight change. No accumulation of repaglinide was apparent during the maintenance period. CONCLUSION: Repaglinide is as well tolerated as glibenclamide and is equally effective in the management of type 2 diabetes. Repaglinide may, however, offer an improvement in postprandial blood glucose control compared with glibenclamide, thereby helping to reduce the relative long-term risk of diabetic complications.

Blood Glucose↗
PubMed2000

Effects of troglitazone on insulin sensitivity in HIV-infected patients with protease inhibitor-associated diabetes mellitus.

Antiretroviral therapy (ART) is frequently associated with metabolic alterations, including insulin resistance and diabetes mellitus. In this pilot study, we evaluated the effect of the PPARgamma activator troglitazone on ART-associated insulin resistance in HIV-infected patients with ART-associated diabetes mellitus. Six patients with protease inhibitor (PI)-associated diabetes mellitus, lipodystrophy and dyslipidemia were treated with troglitazone 400 mg q.d. for 3 months. Previous oral antidiabetics were discontinued prior to the study. At baseline and after 3 months, insulin sensitivity (intravenous insulin tolerance test), body composition (multifrequence bioelectrical impedance analysis) and fat distribution (CT scan quantification) were assessed. Glycaemic control (fasting and postprandial blood glucose, fructosamine, glycosylated haemoglobin) and serum lipid status were determined monthly. In four of the six patients, there was a clear improvement in insulin sensitivity, resulting in a reversal of insulin resistance in two of these patients. Overall, there was an increase in lean body mass and a decrease in total body fat. The volume of visceral adipose tissue decreased whilst the volume of subcutaneous adipose tissue increased. Total cholesterol, LDL and HDL cholesterol increased, and total triglycerides and VLDL-cholesterol decreased. No adverse effects such as hepatotoxicity were observed. Treatment with troglitazone 400 mg q.d. can ameliorate and in some cases even reverse ART-associated insulin resistance. Therefore, further studies including non-diabetic patients with ART-associated insulin resistance may be helpful in evaluating the long-term effects of thiazolidinediones on ART-associated insulin resistance and other metabolic complications, such as adipose maldistribution and dyslipidaemia.

Adipose Tissue↗
PubMed2001

Carbohydrate and diabetes: is the source or the amount of more importance?

There have been two approaches to examining the effects of carbohydrate on postprandial glycemia: 1) studies designed to determine the glycemic response of foods containing carbohydrate, regardless of the source, i.e., starch, sugar, or fiber (glycemic index [GI] of carbohydrates), and 2) studies comparing the glycemic response to equivalent amounts of starches or sugars. A number of food factors determine the glycemic response to carbohydrates: food form, digestibility, cooking, sugars, type of starch, presence of antinutrients, and second meal or lente effect. In people with diabetes, the severity of glucose intolerance and premeal glucose concentrations also influence the glycemic response. The GI attempts to classify individual foods (50-g portions) by the extent to which they raise blood glucose levels compared with a standard (reference carbohydrate), initially glucose and in later studies bread. Acute glycemic responses differ, however, when meals containing low GI foods are compared to meals containing high GI foods long term (measured by fructosamine or hemoglobin A1c), the outcomes are mixed. If there is an effect from the GI of foods on glycemia, it is modest at best. In other studies, when sucrose is substituted for a variety of starches--in meals or snacks and both acutely and for up to 6 weeks--the glycemic response is similar if the total amount of carbohydrate is similar. Therefore, the recommendation for persons with diabetes in regard to the glycemic effect of carbohydrates is that the total amount of carbohydrate in meals or snacks is more important than the source or type and is the first priority in the planning of meals or snacks. This has led to the implementation of carbohydrate counting, in which foods are listed as carbohydrate choices based on the amount and not the source of the carbohydrate.

Diabetes Mellitus↗
PubMed1987

Evidence for an increased glycation of IgG in diabetic patients.

The levels of non-enzymatically glycated total plasma proteins, albumin and IgG were determined in diabetic and non-diabetic patients using affinity chromatography on boronate-agarose gels. A significant increase in both glycated albumin and IgG, and in total glycated plasma proteins was demonstrated. A good correlation between glycated albumin and glycated hemoglobin was observed, while the correlation between glycated IgG and glycated albumin (or hemoglobin) was lower. This was found probably related to wide variations of glycated IgG for diabetics patients who have high glycated hemoglobin levels. These variations were inversely correlated with total serum IgG. Determination of fructosamine or 5-hydroxymethylfurfural content of IgG showed a significant increase in diabetics. Glycated IgG was found to contain approximately one mole of glucose. The main site of glycation was determined to be present in the Fab (more precisely the Fd) part of the IgG molecule.

Blood Glucose↗
PubMed1988

Characterisation of a slow component of normal human serum albumin.

A minor component of albumin was isolated from normal human serum. It had reduced electrophoretic mobility, reacted normally with specific albumin antiserum and, in contrast to normal albumin, did not bind nickel. Sequence analysis showed that the minor band contained components with Ala-His-Lys- and His-Lys- N-terminal sequences, indicating removal of Asp and Asp-Ala respectively from the parent albumin which was found to have the expected N-terminal sequence of Asp-Ala-His-Lys. Both normal albumin and the minor component had an average of 0.32 residues of glucose bound as fructosamine.

Amino Acid Sequence↗
PubMed1988

In vitro glycation of dried serum.

In vitro glycation of sera dried on water-resistant medium (Parafilm) and on paper were studied by measuring the change of glucose level, fructosamine:total protein ratio, glycated protein concentration and alteration of electrophoretic mobility of sera before and after drying. The results suggested the instability of glucose in dried sera was due to in vitro glycation which was influenced by surface properties of media on which the sera were deposited. A new method for rapid effective in vitro glycation of sera was also proposed.

Blood Chemical Analysis↗
PubMed1994

ELISA for in vivo assessment of nonenzymatically glycated platelet glutathione peroxidase.

Using a combination of boronate affinity chromatography and ELISA methodology, a simple procedure was devised to selectively determine the in vivo glycated state of the platelet glutathione peroxidase (GSH-Px) from normal and diabetic subjects. The mean total GSH-Px levels in the normal (n = 14) and diabetic (n = 18) platelets were 1167 +/- 97 and 1007 +/- 73 ng/mg protein, respectively. The mean percentage glycated GSH-Px in the normal and diabetic platelets were 5.79 +/- 0.72% and 11.68 +/- 0.95%, respectively. When the percentage glycated GSH-Px was compared with the fructosamine values, a correlation coefficient of 0.71 was obtained. This indicates that the glycation status of platelet GSH-Px can be utilized as a sensitive, short-term index of plasma glucose levels.

Animals↗
PubMed1995

Nonenzymic glycation of apolipoprotein B in patients with insulin- and noninsulin-dependent diabetes mellitus.

OBJECTIVE: To evaluate the level of nonenzymatic glycation of apolipoprotein B in patients with insulin and noninsulin dependent diabetes mellitus. METHODS: Using a method based on a combination of affinity chromatography and immunonephelometry, we measured the concentration of glycated apolipoprotein B (apo B) in serum of 140 diabetic patients, 43 insulin-dependent (IDDM), and 97 noninsulin-dependent (NIDDM), and 45 nondiabetic control subjects. RESULTS: Although total apo B concentration in serum was significantly increased only in NIDDM patients, both groups of diabetics showed higher percentages of glycated apo B (IDDM, 4.84 +/- 0.8%; NIDDM, 5.61 +/- 1.1%) than did control subjects (4.28 +/- 1.0%), the greatest percentage (5.80%) being found in patients with diabetic nephropathy. No significant correlations were found between glycated apo B and the traditional parameters of glycemic control, such as glycated hemoglobin and fructosamines, and direct influence by sudden plasma glucose fluctuations on apo B glycation was not shown either, perhaps for a low inherent glycability of this apolipoprotein. CONCLUSIONS: It is unclear if these low proportions of glycated apo B in vivo may significantly affect lipoprotein metabolism assuming a pathophysiological role in atherogenesis.

Adolescent↗
PubMed1994

Increased erythrocyte aggregation in insulin-dependent diabetes mellitus and its relationship to plasma factors: a multivariate analysis.

Red blood cell aggregation in vitro (kinetics and shear resistance) was studied in 13 healthy controls and 13 type I (insulin-dependent) diabetic patients free of severe degenerative complications who were matched for age, sex, and body mass index. Measurements were performed with a device that analyzes the laser light backscattered by a blood suspension. Both the velocity of rouleau formation and the cohesion of the rouleau network were significantly increased in diabetic patients. Plasma viscosity and whole-blood viscosity measured at low shear rate (0.95 s-1) were also significantly elevated in the diabetic group. Multivariate analyses of the whole population sample and the diabetic patients confirmed the influence of plasma proteins on the kinetics of aggregation. Fibrinogen levels, which were close to normal, affected mainly the shear resistance of the aggregates. Triglyceride and apolipoprotein (apo) B levels and indexes of metabolic control or protein glycation (fasting blood glucose and fructosamine) also appeared to influence markedly both the kinetics of rouleau formation and the cohesion of the rouleau networks. These rheological abnormalities occurred in diabetic patients before the appearance of any severe degenerative complications. We suggest that these rheological abnormalities are linked to plasma or erythrocyte factors, and are not due to angiopathy.

Adult↗
PubMed1992

Critical differences of clinical-chemical parameters in blood from Red Danish dairy cows.

The purpose of the present study was to calculate the critical differences between two analytical results for 23 routinely used bovine clinical-chemical parameters. The critical difference can be used to judge whether the difference between two consecutive analytical results from the same animal is due to natural variation or not. From 20 cows, blood samples were collected once daily for five days, and the interindividual variance, the intra-individual variance, and the analytical variance were calculated using nested analysis of variance. The critical difference both in absolute values and in percentages was calculated from these variances. The main conclusions were that the critical difference in percentages was in general between 10 and 40 per cent but varied from 10.6 per cent for sodium to 280.2 per cent for lactate and that the analytical variation was generally in accordance with accepted standards, although the analytical variation for alkaline phosphatase, total serum protein, urea and fructosamine should be improved.

Analysis of Variance↗
PubMed1991

Placebo-controlled, double-blind, cross-over trial of growth hormone treatment in prepubertal children with chronic renal failure.

Stunted growth is a serious problem for children with chronic renal failure (CRF) despite normal endogenous growth hormone secretion and normal or elevated plasma concentrations of insulin-like growth factors (IGF) I and II. Biosynthetic growth hormone (GH) was given to 20 prepubertal children (eleven boys, nine girls; mean age 9.5 years, range 4-16) with CRF and severe growth retardation in a placebo-controlled, double-blind, cross-over trial. 6 months of subcutaneous injection of GH (4 IU/m2 per day) was either preceded or followed by 6 months of placebo injection. The patients had a full examination every 3 months. Sixteen children completed the study. Height velocity improved significantly with GH therapy (p less than 0.0001) and placebo (p less than 0.04), but the GH-induced height-velocity increase exceeded that of placebo by 2.9 cm per 6 months. There was a positive relationship between prestudy height velocity and height-velocity increase. Bone maturation was not affected. GH caused a significant increase in IGF-I and a moderate increase in IGF-II plasma concentrations. The pretreatment elevation of IGF-binding protein-1 decreased by almost 50% during GH therapy, while IGF-binding protein-3 increased significantly in concentration, although this increase was significantly smaller than the GH-induced increase in IGF-I. Fructosamine, lipid, and parathyroid concentrations remained constant. Renal function deterioration did not accelerate. Impressive height-velocity increase can be achieved with GH therapy in children with CRF and growth retardation without changes in renal function. Bone maturation appears unaffected suggesting improved final height. Treatment is best started before growth retardation becomes considerable.

Adolescent↗
PubMedDate not supplied

Effects of long-term cilazapril treatment on glucose and lipid metabolism in hypertensive patients with non-insulin-dependent diabetes mellitus.

The effects of long-term cilazapril treatment on glucose and lipid metabolism were assessed in 25 hypertensive patients with non-insulin-dependent diabetes mellitus (NIDDM). Patients were treated with 0.5 to 1 mg of cilazapril once daily or a combination of cilazapril and other antihypertensive drugs once daily for 48 weeks. Both systolic and diastolic blood pressures were significantly reduced (P < 0.001) throughout the study with no significant changes in heart rate and no adverse effects such as cough. There were no significant changes in body mass index or serum levels of glycated hemoglobin A1c, fructosamine, total cholesterol, triglycerides, lipoproteins (high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol), or apolipoproteins (apo A-I, apo C-II, apo C-III, apo B, and apo E). Cilazapril caused a significant increase (P < 0.05) in levels of apo A-II and a significant decrease (P < 0.05) in the apo B:apo A-I ratio, an index of arteriosclerosis. These results suggest that cilazapril has favorable effects on glucose and lipid metabolism and that it may be useful as the first or second choice of antihypertensive drugs in hypertensive patients with NIDDM.

Adult↗