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  • 1
    Electronic Resource
    Electronic Resource
    Assignment of the Gene Encoding Glycogen Synthase (GYS) to Human Chromosome 19, Band q13.3
    Amsterdam : Elsevier
    Genomics 15 (1993), S. 460-461 
    Details
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/geno.1993.1092
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  • 2
    Electronic Resource
    Electronic Resource
    A novel mechanism of glipizide sulfonylurea action: decreased metabolic clearance rate of insulin (1995)
    Springer
    Acta diabetologica 32 (1995), S. 273-278 
    Details
    ISSN: 1432-5233
    Keywords: Sulfonylurea ; Glipizide ; C-peptide ; Insulin ; Insulin metabolic clearance rate (MCR1)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine whether sulfonylureas inhibit the metabolic clearance rate (MCR) of insulin, 19 healthy young subjects participated in two experiments. In the first protocol (n=10), a 3-h oral glucose load was performed with and without 2 mg of glipizide given 30 min before glucose ingestion. The total insulin response was 60% greater with than without glipizide (5.9±0.6 vs 3.7±0.5 μU/ml;P〈0.001). However, the total C-peptide responses were virtually identical (4.7±0.5 vs 4.8±0.4 nmol/l) in both studies. In the second protocol (n=9), the MCR of insulin was measured during 4-h euglycemic insulin clamps performed with and without glipizide. In the study with glipizide, the subjects ingested 5 mg of glipizide at 120 min. The steady-state plasma insulin concentration during the 4th h, i.e., 1–2 h after glipizide ingestion, was significantly higher than during the 2nd h, i.e., before glipizide ingestion (99±22 vs 78±17 μU/ml;P〈0.01). In addition, glucose uptake during the 4th h was greater (8.0±1.6 vs 6.4±1.5 mg/kg·min) and the MCR of insulin was reduced (503±126 vs 621±176 ml/m2·min;P〈0.01). We conclude that glipizide augments plasma insulin levels both by enhancing its secretion and by decreasing the MCR of insulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00576262
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  • 3
    Electronic Resource
    Electronic Resource
    Proportional proinsulin responses in first-degree relatives of patients with type 2 diabetes mellitus (1993)
    Springer
    Acta diabetologica 30 (1993), S. 132-137 
    Details
    ISSN: 1432-5233
    Keywords: C-peptide ; Diabetes mellitus ; Glucose clamp ; Insulin ; Proinsulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Elevated fasting proinsulin immunoreactive material (PIM) has previously been found in patients with type 2 (non-insulin-dependent) diabetes mellitus. It is not known whether this is a genetic trait or whether it is related to the manifestation of type 2 diabetes. Neither is it clear whether the raised fasting insulin immunoreactivity previously observed in first-degree relatives of patients with type 2 diabetes is due to raised PIM. Furthermore, it has not been investigated whether first-degree relatives have altered PIM responses to different secretagogoues. To study this, PIM, insulin and C-peptide were measured in patients with type 2 diabetes, in their first-degree relatives and in healthy control subjects in the fasting state and in relatives and controls during a hyperglycemic clamp. At the end of the hyperglycemic clamp, 0.5 mg of glucagon was given intravenously to stress the beta cells further. Fasting PIM concentrations were significantly higher in patients with type 2 diabetes (P〈0.05). These patients did not have significantly elevated fasting insulin levels when corrected for PIM. In the relatives, fasting insulin concentrations were elevated but PIM levels were normal suggesting that the increase in fasting insulin concentrations reflected an increase in true insulin. The incremental PIM, insulin and C-peptide responses to glucose and glucagon in the relatives were not different from those in the controls. We conclude that elevated fasting PIM levels in patients with type 2 diabetes seem not to be a genetic trait. First-degree relatives of patients with type 2 diabetes are truly hyperinsulinemic in the fasting state, and they have proportional PIM, insulin and C-peptide responses to glucose and glucagon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00572856
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of an antilipolytic agent (acipimox) on the insulin resistance of lipid and glucose metabolism in hypertriglyceridaemic patients (1994)
    Springer
    Acta diabetologica 31 (1994), S. 6-13 
    Details
    ISSN: 1432-5233
    Keywords: Hypertriglyceridaemia ; Insulin resistance ; Antilipolysis ; Acipimox
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hypertriglyceridaemia is associated with insulin resistance of both lipid and glucose metabolism. It is not known whether the insulin resistance affects both glucose oxidation and glycogen formation. To study the oxidative and non-oxidative pathways of non-esterified fatty acids (NEFA) and glucose metabolism, eight male hypertriglyceridaemic subjects were studied during insulin infusion (75 and 340 pmol/m2 · min) in combination with indirect calorimetry and infusions of [3-3H]glucose and [1-14C]palmitate before and after 4 weeks of treatment with the antilipolytic agent acipimox (250 mg three times daily). Compared with eight healthy subjects the hypertriglyceridaemic subjects were resistant to the antilipolytic effect of insulin, both in the basal state (P〈0.05) and during insulin infusion (P〈0.05). This was associated with impaired insulin-stimulated glucose uptake (P〈0.05), predominantly in the non-oxidative pathway (P〈0.05). Acipimox decreased basal NEFA concentrations (P〈0.01) and reduced lipid oxidation during low-dose insulin infusion (P〈0.05). Glucose uptake, predominantly glycogen formation, was stimulated by acipimox (P〈0.05). In conclusion, the insulin resistance of glucose metabolism associated with hypertriglyceridaemia is largely due to a defect in non-oxidative glucose metabolism. Acipimox improves glucose metabolism both by affecting glucose oxidation (low-dose insulin) and non-oxidative glucose metabolism (high-dose insulin).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580753
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of sulphonylurea on glucose-stimulated insulin secretion in healthy and non-insulin dependent diabetic subjects: a dose-response study (1991)
    Springer
    Acta diabetologica 28 (1991), S. 162-168 
    Details
    ISSN: 1432-5233
    Keywords: Insulin ; C-peptide ; Glucose ; Glipizide ; Non-insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of a rapid-acting sulphonylurea, glipizide, on the dose-response relationship between the β-cell response (insulin and C-peptide secretion) and the ambient plasma glucose concentration was examined in 12 healthy and 6 non-insulin-dependent diabetic subjects. The subjects participated in two sets of experiments which were performed in random order: (A) four hyperglycaemic clamp studies, during which the plasma glucose concentration was raised for 120 min by 1 (only in healthy subjects), 3, 7, and 17 mmol/l; and (B) the same four hyperglycaemic clamp studies preceded by ingestion of 5 mg glipizide. All subjects participated in a further study, in which glipizide was ingested and the plasma glucose concentration was maintained at the basal level. In control subjects in the absence of glipizide, the firstphase plasma insulin response (0–10 min) increased progressively with increasing plasma glucose concentration up to 10 mmol/l, above which it tended to plateau. Glipizide augmented the first-phase insulin response without changing the slope of the regression line relating plasma insulin to glucose concentrations. The second-phase plasma insulin response (20–120 min) increased linearly with increasing hyperglycaemia (r=0.997). Glipizide alone increased the plasma insulin response by 180 pmol/l. A similar increase in plasma insulin response following glipizide was observed at each hyperglycaemic step, indicating that glipizide did not affect the sensitivity of the β-cell to glucose. First-phase insulin secretion was reduced in the type 2 (non-insulin-dependent) diabetic patients, and was not influenced by glipizide. The dose-response curve relating second-phase insulin secretion to the ambient plasma glucose concentration was significantly (P〈0.001) flatter in the diabetic patients than in the control subjects. Glipizide alone increased the plasma insulin response by 60 pmol/l without changing the slope of the dose-response curve. It is concluded that, in both type 2 diabetic patients and healthy subjects: (A) sulphonylurea augments glucose-stimulated second-phase insulin secretion without changing the sensitivity of the β-cell to glucose; (B) first-phase insulin secretion is reduced in non-insulin-dependent diabetic patients with fasting hyperglycaemia and is not influenced by sulphonylurea.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00579720
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  • 6
    Electronic Resource
    Electronic Resource
    Human hexokinase II: localization of the polymorphic gene to chromosome 2 (1993)
    Springer
    Diabetologia 36 (1993), S. 1299-1302 
    Details
    ISSN: 1432-0428
    Keywords: Genetics ; DNA polymorphism ; glucose ; phosphorylation ; glycolysis ; chromosome 2 ; insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Type 2 (non-insulin-dependent) diabetes mellitus is characterized by decreased levels of glucose 6-phosphate in skeletal muscle. It has been suggested that the lower concentrations of glucose 6-phosphate contribute to the defect in glucose metabolism noted in muscle tissue of subjects with Type 2 diabetes or subjects at increased risk of developing Type 2 diabetes. Lower levels of glucose 6-phosphate could be due to a defect in glucose uptake, or phosphorylation, or both. Hexokinase II is the isozyme of hexokinase that is expressed in skeletal muscle and is responsible for catalysing the phosphorylation of glucose in this tissue. The recent demonstration that mutations in another member of this family of glucose phosphorylating enzymes, glucokinase, can lead to the development of Type 2 diabetes prompted us to begin to examine the possible role of hexokinase II in the development of this genetically heterogeneous disorder. As a first step, we have cloned the human hexokinase II gene (HK2) and mapped it to human chromosome 2, band p13.1, by fluorescence in situ hybridization to metaphase chromosomes. In addition, we have identified and characterized a simple tandem repeat DNA polymorphism in HK2 and used this DNA polymorphism to localize this gene within the genetic linkage map of chromosome 2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400809
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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Chronic diabetic complications in patients with MODY3 diabetes (1998)
    Springer
    Diabetologia 41 (1998), S. 467-473 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY3 ; NIDDM ; complications ; retinopathy ; neuropathy ; microalbuminuria ; cardiovascular disease ; hypertension.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary MODY3 diabetes, which is caused by a mutation in the hepatocyte nuclear factor-1α gene (HNF-1α) on chromosome 12, represents a relatively common monogenic form of diabetes in Finland. Age at onset of the disease can vary from 10 to 60 years, but little is known about the natural course of the disease, particularly the development of diabetes-related chronic complications. The availability of genetic markers now allows description of the clinical course of the disease. In order to examine the prevalence of chronic diabetic complications in MODY3, we examined 57 carriers with HNF-1α mutations for the presence of micro- and macrovascular complications. Thirty-four percent of the MODY patients had mild and 13 % had severe non-proliferative or proliferative retinopathy; this figure did not differ from the figures in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) patients matched for duration and glycaemic control but not for age. Neither did the prevalence of microalbuminuria differ between MODY3 and IDDM or NIDDM patients (19 vs 24 and 23 %). Neuropathy was observed with the same frequency as previously reported in IDDM. Hypertension was less frequent in MODY3 and IDDM than in NIDDM (24.5 and 19 vs 53.7 %; p 〈 0.001). Coronary heart disease was more common in MODY3 than in IDDM (16 vs 4.5 %; p 〈 0.02) but less common than in the older NIDDM patients (33.3 %; p 〈 0.02). In a multiple logistic regression analysis, poor glycaemic control was an independent risk factor for retinopathy (p = 0.03), microalbuminuria (p 〈 0.04) and neuropathy (p = 0.03). In conclusion, microangiopathic complications are observed with the same frequency in patients with MODY3 diabetes as in IDDM and NIDDM and are strongly related to poor glycaemic control. [Diabetologia (1998) 41: 467–473]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050931
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  • 9
    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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  • 10
    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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