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  • 1
    Electronic Resource
    Electronic Resource
    Non-esterified fatty acids do not contribute to insulin resistance in persons at increased risk of developing Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 192-197 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes mellitus ; insulin sensitivity ; peripheral glucose utilisation ; non-esterified fatty acids ; risk group
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanisms underlying insulin resistance in Type 2 (non-insulin-dependent) diabetes mellitus are not fully understood. An enhanced lipid/non-esterified fatty acid oxidation could provide an explanation. To test this hypothesis we examined the relationship between glucose and lipid metabolism in 44 first-degree relatives (28 glucose-tolerant and 16 glucose-intolerant) of Type 2 diabetic patients and in 18 healthy control subjects. Total body glucose disposal was impaired among both glucose-tolerant and glucose-intolerant relatives compared with control subjects (36.3±3.8 and 30.4±2.7 vs 47.7±3.4 μmol · kgLBM/s-1· min−1; p 〈 0.05). The impairment in glucose disposal among the relatives was primarily accounted for by impaired non-oxidative glucose metabolism (14.8±3.0 and 12.5±1.8 vs 25.3±3.1 μmol · kgLBM−1 · min−1; p 〈0.05). Plasma non-esterified fatty acid concentrations were similar in both glucose-tolerant and glucose-intolerant relatives and control subjects (646±36,649±43 and 615±41 μmol/l) and showed the same degree of suppression by insulin (99±8, 86±7 and 84±9 μmol/l). Basal lipid oxidation was similar in all groups (1.29±0.09, 1.52±0.13 and 1.49±0.21 μmol · kgLBM−1· min−1). Furthermore, insulin suppressed lipid oxidation to the same degree in glucose-tolerant, glucose-intolerant relatives and control subjects (0.65±0.13, 0.88±0.15 and 0.59±0.09μmol · kgLBM−1 · min−1). An inverse correlation between plasma non-esterified fatty acid concentration and total body glucose disposal was observed in the group of control subjects (r=−0.540; p〈0.05), but not among the relatives (r=0.002; p=N.S.). In conclusion the present data challenge the view that the “glucose-fatty acid cycle” contributes to the insulin resistance seen in first-degree relatives of patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418275
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 363-369 
    Details
    ISSN: 1432-0428
    Keywords: Microalbuminuria ; insulin resistance syndrome ; insulin sensitivity ; euglycaemic hyperinsulinaemic clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microalbuminuria has recently been associated with insulin resistance in both insulin-dependent and non-insulin-dependent (NIDDM) diabetes mellitus. To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. In addition, insulin sensitivity was assessed in 20 of these subjects with the euglycaemic hyperinsulinaemic clamp technique. Abnormal albumin excretion rate (AER), defined as AER 15–200 Μg/min, was associated with higher systolic blood pressure (p〈0.05), higher fasting glucose values (p〈0.05), lower HDL-cholesterol (p〈0.05) and lower apolipoprotein A-I (p〈0.05) concentrations than observed in subjects with normal AER. The rate of glucose metabolism was lower in subjects with abnormal compared to subjects with normal albumin excretion rate (38.0±2.8 vs 47.3±2.4 Μmol·kg lean body mass−1. min−1; p=0.028). This difference was almost completely accounted for by a reduction in non-oxidative glucose metabolism (17.7±1.9 vs 27.4±2.7 Μmol·kg lean body mass−1. min−1; p = 0.010), which correlated inversely with the AER (r=−0.543; p=0.013). These results suggest that in non-diabetic individuals genetically predisposed to NIDDM, abnormal AER is associated with insulin resistance and abnormalities in glucose and lipid metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400643
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  • 3
    Electronic Resource
    Electronic Resource
    Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 363-369 
    Details
    ISSN: 1432-0428
    Keywords: Key words Microalbuminuria ; insulin resistance syndrome ; insulin sensitivity ; euglycaemic hyperinsulinaemic clamp.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microalbuminuria has recently been associated with insulin resistance in both insulin-dependent and non-insulin-dependent (NIDDM) diabetes mellitus. To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. In addition, insulin sensitivity was assessed in 20 of these subjects with the euglycaemic hyperinsulinaemic clamp technique. Abnormal albumin excretion rate (AER), defined as AER 15–200 μg/min, was associated with higher systolic blood pressure (p 〈 0.05), higher fasting glucose values (p 〈 0.05), lower HDL-cholesterol (p 〈 0.05) and lower apolipoprotein A-I (p 〈 0.05) concentrations than observed in subjects with normal AER. The rate of glucose metabolism was lower in subjects with abnormal compared to subjects with normal albumin excretion rate (38.0 ± 2.8 vs 47.3 ± 2.4 μmol · kg lean body mass–1· min–1; p = 0.028). This difference was almost completely accounted for by a reduction in non-oxidative glucose metabolism (17.7 ± 1.9 vs 27.4 ± 2.7 μmol · kg lean body mass–1· min–1; p = 0.010), which correlated inversely with the AER (r = –0.543; p = 0.013). These results suggest that in non-diabetic individuals genetically predisposed to NIDDM, abnormal AER is associated with insulin resistance and abnormalities in glucose and lipid metabolism. [Diabetologia (1995) 38: 363 –369]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400643
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  • 4
    Electronic Resource
    Electronic Resource
    Insulin secretion and insulin sensitivity in diabetic subgroups: studies in the prediabetic and diabetic state (2000)
    Springer
    Diabetologia 43 (2000), S. 1476-1483 
    Details
    ISSN: 1432-0428
    Keywords: Keywords LADA ; MODY ; Type II diabetes ; IGT ; insulin secretion ; insulin sensitivity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To evaluate insulin sensitivity and insulin secretion in prediabetic and diabetic subjects with mutations in MODY1 (HNF-4α) and MODY3 (HNF-1α) genes, in subjects with GAD antibodies, latent autoimmune diabetes in adults and in subjects with the common form of Type II (non-insulin-dependent) diabetes mellitus. Methods. Insulin secretion was measured as the incremental 30-min insulin (I30) and insulin glucose ratio (I:G30) during OGTT whereas insulin sensitivity was measured as the insulin sensitivity index during OGTT in 131 carriers of MODY mutations [NGT = 38, IFG/IGT = 21, diabetes mellitus (DM) = 72], in 293 subjects with GADA (NGT = 47, IFG/IGT = 29, DM = 217) and in 2961 subjects with a family history of the common form of Type II diabetes but without MODY mutations or GADA (NGT = 1360, IFG/IGT = 857, DM = 744). A subgroup of the subjects underwent a euglycaemic clamp (n = 210) and intravenous glucose tolerance test (n = 337) for the estimation of insulin sensitivity and first-phase insulin secretion. Results. Non-diabetic subjects with MODY mutations had pronounced impaired insulin secretion (I30, I:G30) compared with the two other groups (p = 0.005). Normal or non-diabetic glucose tolerance was maintained by enhanced insulin sensitivity compared with the other two groups (p 〈 0.05 and p 〈 0.005). In contrast to patients with Type II diabetes and with adult latent autoimmune diabetes, MODY patients showed only a modest deterioration in insulin sensitivity at onset of diabetes. The 2-h glucose values inversely correlated with insulin sensitivity in subjects with GADA (r = –0.447, p 〈 0.001) and subjects from Type II diabetic families (r = –0.426, p 〈 0.001), whereas no such relation was observed in subjects with MODY mutations (r = 0.151, p = NS). There were no statistically significant differences in insulin secretion or insulin sensitivity between subjects with GADA or subjects with a family history of Type II diabetes, either at the NGT or the IFG/IGT stage. Conclusion/interpretation. Glucose-tolerant carriers of MODY mutations are characterised by a severe impairment in insulin secretion. Enhanced insulin sensitivity is the most likely explanation for the normal glucose tolerance. Whereas subjects with positive GADA or Type II diabetes have impaired insulin sensitivity with increasing glucose concentrations, MODY mutation carriers seem to be protected from the effect of glucose toxicity. [Diabetologia (2000) 43: 1476–1483]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051558
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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    High frequency of mutations in MODY and mitochondrial genes in Scandinavian patients with familial early-onset diabetes (1999)
    Springer
    Diabetologia 42 (1999), S. 1131-1137 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Glucokinase ; HNF-1 ; HNF-4 ; MODY ; MIDD ; genetics.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To investigate the contribution of mutations in maturity-onset diabetes of the young (MODY) and mitochondrial genes to early-onset diabetes with a strong family history of diabetes in a cohort with a high prevalence of Type I (insulin-dependent) diabetes mellitus. Methods. Screening for sequence variants in the hepatocyte nuclear factor (HNF)–4 α (MODY1), glucokinase (MODY2), HNF-1 α (MODY3) genes and mitochondrial DNA was carried out in 115 Finnish and Swedish patients with early-onset ( ≤ 40 years) diabetes using the single strand conformation polymorphism (SSCP) technique and direct sequencing. Allele frequencies were compared with 118 patients with onset of diabetes Type II (non-insulin-dependent) diabetes mellitus after the age of 40 and 92 non–diabetic control subjects without a family history of diabetes. Results. In total 52 sequence variants were found in the HNF-1α, HNF-4α and glucokinase genes, 12 of which were considered as MODY mutations. Three families had the A3243G mutation in the mitochondrial tRNA Leu gene, which resulted in an overall prevalence of these mutations of 13 %. Conclusion/interpretation. Among 115 Scandinavian families, mutations in the HNF-1α gene represented the most common cause of familial early-onset ( ≤ 40 years) diabetes: MODY3 (5.2 %) more than MODY2 (3.5 %) more than MIDD (2.6 %) more than MODY1 (1.7 %). [Diabetologia (1999) 42: 1131–1137]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051281
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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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