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  • 1
    Electronic Resource
    Electronic Resource
    Insulin resistance, hypertension and microalbuminuria in patients with Type 2 (non-insulin-dependent) diabetes mellitus (1993)
    Springer
    Diabetologia 36 (1993), S. 642-647 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin resistance ; hypertension ; lipids ; microalbuminuria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the impact of hypertension and microalbuminuria on insulin sensitivity in patients with Type 2 (non-insulin-dependent) diabetes mellitus using the euglycaemic insulin clamp technique in 52 Type 2 diabetic patients and in 19 healthy control subjects. Twenty-five diabetic patients had hypertension and 19 had microalbuminuria. Hypertension per se was associated with a 27% reduction in the rate of total glucose metabolism and a 40% reduction in the rate of non-oxidative glucose metabolism compared with normotensive Type 2 diabetic patients (both p〈0.001). Glucose metabolism was also impaired in normotensive microalbuminuric patients compared with normotensive normoalbuminuric patients (29.4±2.2 vs 40.5±2.8 μmol · kg lean body mass−1 · min−1; p=0.012), primarily due to a reduction in non-oxidative glucose metabolism (12.7±2.9 vs 21.1±2.6 μmol · kg lean body mass−1 ·min−1; p=0.06). In a factorial ANOVA design, however, only hypertension (p=0.008) and the combination of hypertension and microalbuminuria (p=0.030) were significantly associated with the rate of glucose metabolism. The highest triglyceride and lowest HDL cholesterol concentrations were observed in Type 2 diabetic patients with both hypertension and microalbuminuria. Of note, glucose metabolism was indistinguishable from that in control subjects in Type 2 diabetic patients without hypertension and microalbuminuria (40.5±2.8 vs 44.4±2.8 μmol · kg lean body mass−1 · min−1). We conclude that insulin resistance in Type 2 diabetes is predominantly associated with either hypertension or microalbuminuria or with both.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404074
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  • 2
    Electronic Resource
    Electronic Resource
    LDL subclasses in IDDM patients: relation to diabetic nephropathy (1994)
    Springer
    Diabetologia 37 (1994), S. 681-688 
    Details
    ISSN: 1432-0428
    Keywords: Key words IDDM, diabetic nephropathy, microalbuminuria, proteinuria, lipid metabolism, small dense LDL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To answer the question whether the elevation of LDL-cholesterol in IDDM patients with incipient and established diabetic nephropathy is accompanied by changes in LDL size or composition, we studied distribution of LDL particles in 57 normoalbuminuric [AER 7 (1–19) µg/min, median and range], in 46 microalbuminuric [AER 50 (20–192) µg/min] and in 33 proteinuric [AER 422 (233–1756) µg/min] IDDM patients as well as in 49 non-diabetic control subjects with normoalbuminuria. The three diabetic groups were matched for duration of diabetes and glycaemic control. The mean particle diameter of the major LDL peak was determined by nondenaturing gradient gel electrophoresis. Composition and density distribution of LDL were determined in the subgroups of each patient group by density gradient ultracentrifugation. Normoalbuminuric IDDM patients had larger LDL particles than non-diabetic control subjects (260 Å vs 254 Å, p 〈0.05). LDL particle diameter was inversely correlated with serum triglycerides in all groups (p 〈0.05 for normoalbuminuric and p 〈0.001 for other groups). Triglyceride content of LDL was higher in three IDDM groups compared to control group (p 〈0.05). The elevation of LDL mass in microalbuminuric and proteinuric IDDM groups compared to normoalbuminuric IDDM group (p 〈0.05 for both) was mainly due to the increment of light LDL (density 1.0212–1.0343 g/ml). There were no significant changes in the density distribution or composition of LDL between the three diabetic groups. In conclusion the increase of LDL mass without major compositional changes suggests that the elevation of LDL in incipient and established diabetic nephropathy is primarily due to the increased number of LDL particles. The prevalence of atherogenic small dense LDL particles in IDDM patients with microalbuminuria and proteinuria is closely dependent on plasma triglyceride concentration. [Diabetologia (1994) 37: 681–688]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417692
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  • 3
    Electronic Resource
    Electronic Resource
    The impact of a family history of Type II (non-insulin-dependent) diabetes mellitus on the risk of diabetic nephropathy in patients with Type I (insulin-dependent) diabetes mellitus (1999)
    Springer
    Diabetologia 42 (1999), S. 519-526 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; Type I (insulin-dependent) diabetes mellitus ; familial Type II (non-insulin-dependent) diabetes mellitus ; genetic factors ; risk factor.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. There is substantial evidence for a role of genetic factors in the development of diabetic nephropathy. In Pima Indians, a link between susceptibility to diabetic nephropathy and Type II (non-insulin-dependent) diabetes mellitus has been proposed. In this study, our aim was to examine the association between a family history of Type II diabetes and diabetic nephropathy in patients with Type I (insulin-dependent) diabetes mellitus. Methods. In a cross-sectional case-control study, we assessed the prevalence of Type II diabetes in the parents of 137 Type I diabetic patients with diabetic nephropathy (albuminuria 〉 300 μg/min in two of three overnight urine collections) compared with the parents of 54 Type I diabetic patients without nephropathy (albuminuria 〈 20 μg/min). Results. Thirty-four (25 %) of the patients with nephropathy compared with five (9 %) of the patients without nephropathy had a parental history of Type II diabetes (p = 0.019). A parental history of Type II diabetes was associated with a three-fold risk [odds ratio 2.95 (95 % confidence interval: 1.03 to 8.40), p = 0.043] of diabetic nephropathy after adjustment for sex, glycaemic control and family history of hypertension. Furthermore, there was an excess of risk factors for development of Type II diabetes (higher fasting plasma glucose concentrations, higher prevalence of hypertension, higher waist-hip ratio and a tendency towards more glucose intolerance) among previously non-diabetic parents of patients with nephropathy. Conclusion/interpretation. Genetic or environmental factors or both related to familial Type II diabetes increase susceptibility to diabetic nephropathy in patients with Type I diabetes. [Diabetologia (1999) 42: 519–526]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051189
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  • 4
    Electronic Resource
    Electronic Resource
    LDL subclasses in IDDM patients: relation to diabetic nephropathy (1994)
    Springer
    Diabetologia 37 (1994), S. 681-688 
    Details
    ISSN: 1432-0428
    Keywords: IDDM ; diabetic nephropathy ; microalbuminuria ; proteinuria ; lipid metabolism ; small dense LDL
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To answer the question whether the elevation of LDL-cholesterol in IDDM patients with incipient and established diabetic nephropathy is accompanied by changes in LDL size or composition, we studied distribution of LDL particles in 57 normoalbuminuric [AER 7 (1–19) μg/min, median and range], in 46 microalbuminuric [AER 50 (20–192) μg/min] and in 33 proteinuric [AER 422 (233–1756) μg/min] IDDM patients as well as in 49 non-diabetic control subjects with normoalbuminuria. The three diabetic groups were matched for duration of diabetes and glycaemic control. The mean particle diameter of the major LDL peak was determined by nondenaturing gradient gel electrophoresis. Composition and density distribution of LDL were determined in the subgroups of each patient group by density gradient ultracentrifugation. Normoalbuminuric IDDM patients had larger LDL particles than non-diabetic control subjects (260 Å vs 254 Å, p〈0.05). LDL particle diameter was inversely correlated with serum triglycerides in all groups (p〈0.05 for normoalbuminuric and p〈0.001 for other groups). Triglyceride content of LDL was higher in three IDDM groups compared to control group (p〈0.05). The elevation of LDL mass in microalbuminuric and proteinuric IDDM groups compared to normoalbuminuric IDDM group (p〈0.05 for both) was mainly due to the increment of light LDL (density 1.0212–1.0343 g/ml). There were no significant changes in the density distribution or composition of LDL between the three diabetic groups. In conclusion the increase of LDL mass without major compositional changes suggests that the elevation of LDL in incipient and established diabetic nephropathy is primarily due to the increased number of LDL particles. The prevalence of atherogenic small dense LDL particles in IDDM patients with microalbuminuria and proteinuria is closely dependent on plasma triglyceride concentration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417692
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  • 5
    Electronic Resource
    Electronic Resource
    Risk factors for mortality in Type II (non-insulin-dependent) diabetes: evidence of a role for neuropathy and a protective effect of HLA-DR4 (1998)
    Springer
    Diabetologia 41 (1998), S. 1253-1262 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type II (non-insulin-dependent) diabetes mellitus ; HLA-DR4 ; microalbuminuria ; mortality ; cardiovascular risk factors ; immunological markers ; neuropathy ; NEFA.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To test the hypothesis that interaction between genetic, immunological, clinical and metabolic risk factors influences the outcome of Type II (non-insulin-dependent) diabetes mellitus, we examined which of the above factors present at baseline were associated with mortality in 134 Type II diabetic patients followed for 9 years. Thirty-eight patients (29 %) died during the follow-up period; the majority of whom (68 %) died from cardiovascular disease. At baseline, the deceased patients had higher HbA1 c values (p = 0.002), higher LDL-triglycerides (p = 0.007), lower HDL-cholesterol (p = 0.007), higher non-esterified fatty acid (NEFA) concentrations (p = 0.014), and higher albumin excretion rate (p 〈 0.0001) than the patients who survived. In addition, the frequency of HLA-DR4 (21 vs 39 %, p = 0.048) and of parietal cell antibodies (5 vs 14 %, p = 0.016) were decreased in the deceased as compared to the living patients. Patients who died during follow-up also had more retinopathy (42 vs 16 %, p = 0.002), neuropathy (57 vs 23 %, p 〈 0.001), microalbuminuria (45 vs 6 %, p 〈 0.0001), coronary heart disease (50 vs 13 %, p 〈 0.0001), and peripheral vascular disease (27 vs 9 %, p = 0.005) at baseline than patients who survived. In a multiple logistic regression analysis macroangiopathy (p = 0.004), neuropathy (p = 0.007), HbA1 c (p = 0.018) and albumin excretion rate (p = 0.016) were independent risk factors for death. In patients free of cardiovascular disease at baseline, conventional risk factors such as LDL-cholesterol (p = 0.005) and age (p = 0.003) were associated with subsequent development of cardiovascular disease. In conclusion, in addition to coexisting macroangiopathy, increased albumin excretion rate, poor glycaemic control and neuropathy are risk factors for cardiovascular mortality in patients with Type II diabetes. The presence of HLA-DR4 and signs of autoimmunity may be associated with decreased risk of cardiovascular disease. [Diabetologia (1998) 41: 1253–1262]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051062
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  • 6
    Electronic Resource
    Electronic Resource
    Therapeutic equivalence of once- and thrice-daily glipizide (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 95-99 
    Details
    ISSN: 1432-1041
    Keywords: glipizide ; Type 2 diabetes ; dosing frequency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Two cross-over studies were carried out in 23 patients with Type 2 diabetes, to examine whether glipizide, a potent sulphonylurea with fast and complete absorption and rapid elimination (t1/2〈5 h), can be given once-daily without loss of therapeutic effect. In both studies, patients were randomly assigned to an initial dose of 7.5 mg once daily or 2.5 mg three-times daily, which was increased to 15 mg o.d. or 5 mg t.i.d. if the fasting plasma glucose remained over 10 mmol/l on the lower dosage. In Study 1 (n=11), administration once a day before breakfast was compared with intake before breakfast, lunch and early dinner (5 p.m.) and in Study 2 (n=12) the comparison was between intake once-daily before breakfast and dosing before breakfast, lunch, and at bedtime (10 p.m.). Neither the 24-hour urinary glucose excretion nor HbA1, fasting plasma glucose, insulin or C-peptide levels differed between the once and three times daily administration with the third dose given before early dinner. The nadir plasma levels of glipizide were not significantly different and were often too low to be detected. Postponing the third dose until 10 p.m. did not produce any improvement in HbA1 or in fasting plasma glucose, insulin or C-peptide. The mean nadir glipizide levels following this schedule were twice as high as those after once-daily administration. As expected, the plasma glipizide after breakfast was higher when the whole dose was taken before breakfast than when it was divided. The corresponding plasma level of insulin was higher and that of plasma glucose was lower. The after-lunch levels of glipizide did not differ significantly, and there was no after-lunch difference in plasma insulin or glucose. It appears that the major effect of glipizide is to augment insulin availability following meals, whilst it has little influence on nocturnal glucose control. In a daily dose of 7.5 mg or more, glipizide can be taken once daily without loss of efficacy, at least in areas with Northern European meal schedules.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00870994
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  • 7
    Electronic Resource
    Electronic Resource
    Pharmacokinetics and metabolic effects of glibenclamide and glipizide in type 2 diabetics (1985)
    Springer
    European journal of clinical pharmacology 28 (1985), S. 697-704 
    Details
    ISSN: 1432-1041
    Keywords: glibenclamide ; glipizide ; pharmacokinetics ; metabolic effects ; Type 2 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Fifteen Type 2 diabetics were treated for 4-week periods with once daily (10 mg) glibenclamide, glipizide and placebo according to a double-blind cross-over protocol. Post-dose glipizide concentrations were three times higher than those of glibenclamide, due to the incomplete bioavailability of the latter. On the other hand, pre-dose drug levels were similar, as an expression of the slower absorption and/or elimination of glibenclamide. Both active treatments reduced postprandial blood glucose concentrations and 24-hour urinary glucose excretion to a similar degree, but fasting blood glucose concentrations were slightly lower during glibenclamide treatment. Both active treatments enhanced fasting and postprandial insulin and C-peptide concentrations, the C-peptide response being greater after glipizide than after glibenclamide. Plasma glucagon and GIP concentrations were not significantly affected. Insulin sensitivity was increased by glibenclamide but not by glipizide. Neither therapy affected insulin binding to erythrocytes. It appears that both glibenclamide and glipizide improved glucose metabolism by sustained stimulation of insulin secretion, which was most pronounced with glipizide. Only glibenclamide improved insulin sensitivity and was slightly more active than glipizide on fasting blood glucose levels. The differences may be consequences of the pharmacokinetics, but differences in pharmacodynamics cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00607919
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  • 8
    Electronic Resource
    Electronic Resource
    Effect of beta-blocking drugs on beta-cell function and insulin sensitivity in hypertensive non-diabetic patients (1984)
    Springer
    European journal of clinical pharmacology 26 (1984), S. 13-17 
    Details
    ISSN: 1432-1041
    Keywords: beta-blocking drugs ; insulin sensitivity ; pancreatic beta-cell function ; hypertension ; propranolol ; atenolol ; insulin secretion ; plasma GIP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of two beta-blocking drugs on endogenous insulin secretion and insulin sensitivity were investigated in a double blind cross-over study in 13 hypertensive patients. The patients were randomly allocated to each of three 2-week treatment periods with propranolol 80 mg b.i.d., atenolol 50 mg b.i.d. and placebo b.i.d. Endogenous insulin secretion was assessed by measuring serum insulin and C-peptide before and 6 min after iv administration of glucagon; insulin sensitivity was determined by measuring insulin binding to erythrocytes, and as the glucose disappearance rate (KITT) after i.v. insulin. Fasting concentrations of serum free fatty acids (S-FFA) and plasma gastric inhibitory polypeptide (P-GIP) were also recorded during the three study periods. Both propranolol and atenolol reduced blood pressure, heart rate and S-FFA concentrations compared to placebo, and all patients showed measurable plasma concentrations of propranolol and atenolol. The results can be considered representative, therefore, of clinical beta-blockade. The two drugs did not significantly influence the fasting blood glucose level. There was an increase in fasting and glucagon-stimulated serum C-peptide concentration during propranolol therapy compared with placebo (p=0.037 and p=0.030, respectively), although this was not reflected by a significant change in serum insulin. Propranolol and atenolol did not significantly influence insulin binding to erythrocytes, but they clearly reduced the glucose disappearance rate KITT was compared to placebo (p=0.0036 and p=0.0003, respectively). The findings support the view that beta-blocking drugs can influence glucose metabolism by mechanisms other than inhibition of endogenous insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00546701
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of the combination of insulin and glibenclamide in Type 2 (non-insulin-dependent) diabetic patients with secondary failure to oral hypoglycaemic agents (1988)
    Springer
    Diabetologia 31 (1988), S. 206-213 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes ; insulin treatment ; sulfonylurea ; secondary failure ; glibenclamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of combined insulin and sulfonylurea therapy on glycaemic control and B-cell function was studied in 15 Type 2 (non-insulin-dependent) diabetic patients who had failed on treatment with oral hypoglycaemic agents. The patients were first treated with insulin alone for four months. Five patients were given two daily insulin doses and ten patients one dose. During insulin treatment the fasting plasma glucose fell from 14.5±0.8 to 8.8±0.4 mmol/l and the HbA1 concentration from 12.6±0.4 to 9.2±0.2%. This improvement of glycaemic control was associated with a suppression of basal (from 0.31±0.04 to 0.10±0.02 nmol/l) and glucagon-stimulated (from 0.50±0.08 to 0.19±0.04 nmol/l) C-peptide concentrations. Four months after starting insulin therapy the patients were randomised to a four-month double-blind cross-over treatment with insulin combined with either 15 mg glibenclamide per day or with placebo. Addition of glibenclamide to insulin resulted in a further reduction of the fasting plasma glucose (7.9±0.5 mmol/l) and HbA1 (8.3±0.2%) concentration whereas the basal (0.21±0.03 nmol/l) and glucagon-stimulated C-peptide concentrations (0.34±0.06 nmol/l) increased again. Addition of placebo to insulin had no effect. The daily insulin dose could be reduced by 25% after addition of glibenclamide to insulin, while it remained unchanged when insulin was combined with placebo. The fasting free insulin concentration did not differ between the glibenclamide and placebo periods (28±6 vs 30±5 mmol/l). The fasting free insulin concentration correlated, however, positively with the insulin dose (r=0.76, p〈0.01) indicating that the insulin dose was the main determinant of the free insulin concentration. In contrast, the basal C-peptide concentration was higher during the insulin plus glibenclamide than during the insulin plus placebo period (0.21±0.03 vs 0.16±0.03 nmol/l; p〈0.05). Addition of glibenclamide to insulin therapy increased the treatment cost by 30–50%, was associated with increased frequency of mild hypoglycaemic reactions and with a slight, but significant fall in HDL cholesterol concentration (from 1.40±0.07 to 1.29±0.06; p〈0.05) compared with insulin plus placebo. We conclude that in Type 2 diabetic patients, who have failed on treatment with oral hypoglycaemic agents, the combination of insulin and glibenclamide resulted in slightly improved glycaemic control and allowed reduction of the insulin dose. The price for this improvement was higher treatment costs, more (mild) hypoglycaemic reactions and a marginal fall in the HDL cholesterol concentration. Whether the same effect could have been achieved with divided insulin doses in all patients is not known.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290586
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  • 10
    Electronic Resource
    Electronic Resource
    Treatment failures in patients with Type 2 (non-insulin-dependent) diabetes (1988)
    Springer
    Diabetologia 31 (1988), S. 186-187 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276855
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