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  • Articles: DFG German National Licenses  (8)
  • insulin resistance  (5)
  • Keywords Twins  (2)
  • Type 2 (non-insulin-dependent) diabetes  (2)
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  • Articles: DFG German National Licenses  (8)
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Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Low birth weight is associated with NIDDM in discordant monozygotic and dizygotic twin pairs (1997)
    Springer
    Diabetologia 40 (1997), S. 439-446 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Twins ; non-insulin-dependent diabetes mellitus ; birth weight ; intrauterine malnutrition.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Previous studies have demonstrated an association between low weight at birth and risk of later development of non-insulin-dependent diabetes mellitus (NIDDM). It is not known whether this association is due to an impact of intrauterine malnutrition per se, or whether it is due to a coincidence between the putative “NIDDM susceptibility genotype” and a genetically determined low weight at birth. It is also unclear whether differences in gestational age, maternal height, birth order and/or sex could explain the association. Twins are born of the same mother and have similar gestational ages. Furthermore, monozygotic (MZ) twins have identical genotypes. Original midwife birth weight record determinations were traced in MZ and dizygotic (DZ) twins discordant for NIDDM. Birth weights were lower in the NIDDM twins (n = 2 × 14) compared with both their identical (MZ; n = 14) and non-identical (DZ; n = 14) non-diabetic co-twins, respectively (MZ: mean ± SEM 2634 ± 135 vs 2829 ± 131 g, p 〈 0.02; DZ: 2509 ± 135 vs 2854 ± 168 g, p 〈 0.02). Using a similar approach in 39 MZ and DZ twin pairs discordant for impaired glucose tolerance (IGT), no significantly lower birth weights were detected in the IGT twins compared with their normal glucose tolerant co-twins. However, when a larger group of twins with different glucose tolerance were considered, birth weights were lower in the twins with abnormal glucose tolerance (NIDDM + IGT; n = 106; 2622 ± 45 g) and IGT (n = 62: 2613 ± 55 g) compared with twins with normal glucose tolerance (n = 112: 2800 ± 51 g; p = 0.01 and p = 0.03, respectively). Furthermore, the twins with the lowest birth weights among the two co-twins had the highest plasma glucose concentrations 120 min after the 75-g oral glucose load (n = 86 pairs: 9.6 ± 0.6 vs 8.0 ± 0.4 mmol/l, p = 0.03). In conclusion, the association between low birth weight and NIDDM in twins is at least partly independent of genotype and may be due to intrauterine malnutrition. IGT was also associated with low birth weight in twins. However, the possibility cannot be excluded that the association between low birth weight and IGT could be due to a coincidence with a certain genotype causing both low birth weight and IGT in some subjects. [Diabetologia (1997) 40: 439–446]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050698
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Risk and mechanism of dexamethasone-induced deterioration of glucose tolerance in non-diabetic first-degree relatives of NIDDM patients (1997)
    Springer
    Diabetologia 40 (1997), S. 1439-1448 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Minimal model analysis ; insulin secretion ; insulin resistance ; relatives of NIDDM patients ; steroids ; glucose intolerance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We tested the hypothesis that glucose intolerance develops in genetically prone subjects when exogenous insulin resistance is induced by dexamethasone (dex) and investigated whether the steroid-induced glucose intolerance is due to impairment of beta-cell function alone and/or insulin resistance. Oral glucose tolerance (OGTT) and intravenous glucose tolerance tests with minimal model analysis were performed before and following 5 days of dex treatment (4 mg/day) in 20 relatives of non-insulin-dependent diabetic (NIDDM) patients and in 20 matched control subjects (age: 29.6 ± 1.7 vs 29.6 ± 1.6 years, BMI: 25.1 ± 1.0 vs 25.1 ± 0.9 kg/m2). Before dex, glucose tolerance was similar in both groups (2-h plasma glucose concentration (PG): 5.5 ± 0.2 [range: 3.2–7.0] vs 5.5 ± 0.2 [3.7–7.4] mmol/l). Although insulin sensitivity (Si) was significantly lower in the relatives before dex, insulin sensitivity was reduced to a similar level during dex in both the relatives and control subjects (0.30 ± 0.04 vs 0.34 ± 0.04 10–4 min–1 per pmol/l, NS). During dex, the variation in the OGTT 2-h PG was greater in the relatives (8.5 ± 0.7 [3.9–17.0] vs 7.5 ± 0.3 [5.7–9.8] mmol/l, F-test p 〈 0.05) which, by inspection of the data, was caused by seven relatives with a higher PG than the maximal value seen in the control subjects (9.8 mmol/l). These “hyperglycaemic” relatives had diminished first phase insulin secretion (Ø1) both before and during dex compared with the “normal” relatives and the control subjects (pre-dex Ø1: 12.6 ± 3.6 vs 26.4 ± 4.2 and 24.6 ± 3.6 (p 〈 0.05), post-dex Ø1: 22.2 ± 6.6 vs 48.0 ± 7.2 and 46.2 ± 6.6 respectively (p 〈 0.05) pmol · l–1· min–1 per mg/dl). However, Si was similar in “hyperglycaemic” and “normal” relatives before dex (0.65 ± 0.10 vs 0.54 ± 0.10 10−4 · min–1 per pmol/l) and suppressed similarly during dex (0.30 ± 0.07 vs 0.30 ± 0.06 10−4 · min–1 per pmol/l). Multiple regression analysis confirmed the unique importance of low pre-dex beta-cell function to subsequent development of high 2-h post-dex OGTT plasma glucose levels (R 2 = 0.56). In conclusion, exogenous induced insulin resistance by dex will induce impaired or diabetic glucose tolerance in those genetic relatives of NIDDM patients who have impaired beta-cell function (retrospectively) prior to dex exposure. These subjects are therefore unable to enhance their beta-cell response in order to match the dex-induced insulin resistant state. [Diabetologia (1997) 40: 1439–1448]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050847
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    On the determination of basal glucose production rate in patients with Type 2 (non-insulin-dependent) diabetes mellitus using primed-continuous 3-3H-glucose infusion (1990)
    Springer
    Diabetologia 33 (1990), S. 603-610 
    Details
    ISSN: 1432-0428
    Keywords: 3-3H-glucose ; primed-continuous tracer technique ; Type 2 (non-insulin-dependent) diabetes ; basal glucose turnover ; glucose appearance ; glucose disappearance ; steady-state conditions ; Steele's equations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using primed-continuous 3-3H-glucose infusion, basal glucose production rate has been reported to be 140% higher than normal or almost normal in hyperglycaemic patients with Type 2 (non-insulin-dependent) diabetes mellitus. To determine whether these markedly different results could be due to the mode of priming: fixed or adjusted, or the mode of calculation: steady state or non-steady state equations, we studied 11 patients with Type 2 diabetes (fasting plasma glucose 8–20 mmol/l). For 6 h 3-3H-glucose (0.40 μCi/min) was infused preceded by a priming dose of 40 μCi (fixed priming), or 40 μCi · plasma glucose (mmol/l)·5−1 (adjusted priming). In diabetic patients the plasma glucose concentration was not constant but declined 0.52±0.07 mmol·l−1· h−1. Furthermore, the rate of fall was correlated to the fasting plasma glucose concentration (r=0.90, p〈0.01). Thus, the fasting state was not a steady state condition. Using adjusted priming a constant tracer steady state level was obtained within 60 min. In contrast, using fixed priming tracer steady state was not reached within 6 h. The initial tracer level was far below, and increased in time towards the steady state level observed after adjusted priming. Consequently, using Steele's equations after fixed priming, glucose production rates calculated after 90–120 min were overestimated in proportion to fasting hyperglycaemia. In conclusion: The fasting state in patients with Type 2 diabetes is not a steady state condition. Adjusted priming seems most appropriate in Type 2 diabetes. By estimating glucose production 2 h after fixed priming or assuming steady state conditions, most previous studies may have overestimated basal glucose production in Type 2 diabetes in proportion to fasting hyperglycaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400204
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Hyperglycaemia compensates for the defects in insulin-mediated glucose metabolism and in the activation of glycogen synthase in the skeletal muscle of patients with Type 2 (non-insulin-dependent) diabetes mellitus (1992)
    Springer
    Diabetologia 35 (1992), S. 80-88 
    Details
    ISSN: 1432-0428
    Keywords: Glycogen synthase ; skeletal muscle ; Type 2 (non-insulin-dependent) diabetes mellitus ; hyperglycaemia ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m−2min−1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p〈0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p〈0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400856
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Decreased skeletal muscle phosphotyrosine phosphatase (PTPase) activity towards insulin receptors in insulin-resistant Zucker rats measured by delayed Europium fluorescence (1996)
    Springer
    Diabetologia 39 (1996), S. 142-148 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptor ; phosphotyrosine phosphatases ; insulin resistance ; skeletal muscle ; Zucker rats ; metformin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to measure the phosphotyrosine phosphatase (PTPase) activity in small muscle biopsies, a sandwich-immunofluorescence assay was developed using the phosphorylated human insulin receptor as a substrate, a C-terminal insulin receptor antibody as catching antibody and Europium-labelled anti-phosphotyrosine as detecting antibody. Soluble and particulate muscle fractions were prepared from soleus muscle of obese, diabetic (fa/fa) Zucker rats and their lean littermates (Fa/-). In the soluble muscle fractions of the obese (fa/fa) rats PTPase activity was significantly reduced compared to control (Fa/-) rats (45.2±2.6% vs 61.3±4.7%, p〈0.02). This reduction was completely prevented by 24 days of metformin treatment which decreased plasma glucose and plasma insulin levels. In particulate muscle fractions, however, no difference in PTPase activity was found among any groups of rats examined. These results show that the alterations in soluble PTPase activity in the insulin-resistant, diabetic Zucker rat vary with the abnormality in glucose homeostasis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403956
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  • 6
    Electronic Resource
    Electronic Resource
    Enhanced hepatic insulin sensitivity, but peripheral insulin resistance in patients with Type 1 (insulin-dependent) diabetes (1987)
    Springer
    Diabetologia 30 (1987), S. 834-840 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes ; insulin sensitivity ; insulin resistance ; glucose utilization ; hepatic glucose production
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sensitivity to insulin in vivo was studied in 8 normal weight C-peptide negative Type 1 (insulin-dependent) diabetic patients (age 23±1 years, diabetes duration 6±2 years), and in 8 age, weight and sex matched healthy subjects, using the euglycaemic clamp and 3-3H-glucose tracer technique. Prior to the study diabetic patients were maintained normoglycaemic overnight by a glucose controlled insulin infusion. Sequential infusions of insulin in 3 periods of 2 h resulted in mean steady state insulin levels of 12±2 versus 11±1, 18±2 versus 18±2 and 28±3 versus 24±2 μU/ml in diabetic patients and control subjects. Corresponding glucose utilization rates were 2.4±0.2 versus 2.4±0.1, 2.4±0.2 versus 3.0±0.3 and 2.9±0.3 versus 4.6±O.6 mg·kg−1·min−1, p〈0.02. Portal insulin values in the three periods were calculated to 12±2 versus 25±3, 18±2 versus 32±3 and 28±3 versus 37±3 μU/ml in the diabetic patients and control subjects using peripheral insulin and C-peptide concentrations and assuming a portal to peripheral insulin concentration gradient of 1 in diabetic patients and of 2.4 in control subjects. Corresponding glucose production rates were 2.5±0.2 versus 2.4±0.1, 1.6±0.1 versus 0.9±0.2 and 0.7±0.1 versus 0.4±0.2 mg·kg−1·min−1. Using this approach the insulin dose-response curve for the peripheral glucose utilization was right-ward shifted, while the dose-response curve for the hepatic glucose production as a function of portal insulin levels was left-ward shifted. We conclude that in vivo insulin action is increased in the liver but decreased in peripheral tissues in insulin treated Type 1 diabetic patients. Presumably these oppositely directed changes in insulin action are acquired defects, secondary to the present mode of peripheral insulin treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00274790
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Reduced glycogen synthase activity in skeletal muscle from obese patients with and without Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 239-245 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 (non-insulin-dependent) diabetes ; obesity ; insulin resistance ; non-oxidative glucose metabolism ; skeletal muscle ; glycogen synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to evaluate the importance of a defect in insulin mediated non-oxidative glucose metabolism and glycogen synthase activity in skeletal muscles in obese subjects with and without Type 2 (non-insulin-dependent) diabetes mellitus we studied: 10 lean and 10 obese control subjects and 12 obese diabetic patients using the euglycaemic hyperinsulinaemic clamp technique (basal, 20 mU · (m2)−1 · min−1, 80mU·(m2)−1·min−1) in combination with indirect calorimetry. Muscle biopsies were taken from m. vastus lateralis at each insulin level. We found that non-oxidative glucose metabolism could be stimulated by insulin in all three groups (p〈0.01). The values obtained at the highest insulin levels (around 140 μU/ml) were lower in both obese groups compared to the lean control subjects (118±21, 185±31, 249±14 mg·(m2)−1·min−1 (p〈 0.01)). Insulin stimulation of the glycogen synthase activity at a glucose-6-phosphate concentration of 0.1 mmol/l was absent in both obese groups, while activities increased significantly in the lean control subjects (19.6±4.2% to 45.6±6.8%, p〈 0.01). Glycogen synthase activities at the highest insulin concentrations only differed significantly between lean control subjects and obese diabetic patients (45±7% and 31±5%, p〈 0.05). We conclude that insulin resistance in peripheral tissues in obese subjects with and without Type 2 diabetes may be partly explained by a reduced insulin mediated non-oxidative glucose metabolism and that this abnormality might be due to an absent insulin stimulation of glycogen synthase in skeletal muscles. This enzyme defect is correlated to obesity itself.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00405082
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  • 8
    Electronic Resource
    Electronic Resource
    Heritability of Type II (non-insulin-dependent) diabetes mellitus and abnormal glucose tolerance – a population-based twin study (1999)
    Springer
    Diabetologia 42 (1999), S. 139-145 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Twins ; Type-II (non-insulin-dependent) diabetes mellitus ; abnormal glucose tolerance ; concordance rates ; heritability.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To elucidate the relative importance of genetic and environmental factors on the development of Type II (non-insulin dependent) diabetes mellitus, we examined a sample of twins (n = 606) ascertained from the population-based Danish Twin Register. Based on a standard 75 g oral glucose tolerance test and current WHO criteria we identified 62 pairs in which one or both had Type II diabetes. The probandwise concordance (monozygotic: 0.50; dizygotic: 0.37) for Type II diabetes per se was not very different. When including the twins with impaired glucose tolerance (IGT), however, the probandwise concordance for abnormal glucose tolerance was significantly different between monozygotic (0.63) and dizygotic (0.43) twin pairs, (p 〈 0.01). These findings were supported by the heritability estimates for Type II diabetes per se (26 %) and for abnormal glucose tolerance (61 %). The metabolic variables, insulin resistance and insulin secretion, and anthropometric variables, body mass index and waist to hip ratio, known to be associated with the development of glucose intolerance had a heritability of 26, 50, 80 and 6 % respectively. This study confirms the notion of a multifactorial aetiology of Type II diabetes. It supports the contribution of non-genetic aetiological components in the development of Type II diabetes per se. The study also indicates a role for genes in the aetiology of abnormal glucose tolerance. We therefore propose that genetic predisposition is important for the development of abnormal glucose tolerance. Non-genetic factors, however, might play a predominant role in controlling whether a genetically predisposed individual progresses to overt Type II diabetes. [Diabetologia (1999) 42: 139–145]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051131
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