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  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Changes of lipolytic enzymes cluster with insulin resistance syndrome (1995)
    Springer
    Diabetologia 38 (1995), S. 344-350 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; lipase activities ; lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The activities of hepatic and lipoprotein lipase and the levels of lipo- and apoproteins were compared in two groups of normoglycaemic men representing the highest (n=18) and lowest (n=15) fasting insulin quintiles of first degree male relatives of non-insulin-dependent diabetic patients. The high insulin group representing insulin-resistant individuals had significantly lower post-heparin plasma lipoprotein lipase activity than the low insulin group (14.2±4.0 vs 20±5.8 Μmol NEFA·ml−1·h−1, p〈0.001); hepatic lipase activity did not differ between the two groups (24.2±11 vs 18.0±5.3 Μmol NEFA·ml−1·h−1, NS). The lipoprotein lipase/hepatic lipase ratio in the high insulin group was decreased by 66% as compared to the low insulin group (0.75±0.57 vs 1.25±0.65, p〈0.01). In the high insulin group both total and VLDL triglycerides were higher than in the low insulin group (1.61±0.57 vs 0.86±0.26 mmol/l, p〈 0.001 and 1.00±0.47 vs 0.36±0.16 mmol/l, p〈0.001, respectively) whereas HDL cholesterol and HDL2 cholesterol were lower (1.20±0.30 vs 1.43±0.22 mmol/l, p〈0.05 and 0.49±0.21 vs 0.71±0.17 mmol/l, p〈0.05, respectively). Total cholesterol, LDL cholesterol or HDL3 cholesterol did not differ between the two groups. The mean particle size of LDL was smaller in the high insulin group than in the low insulin group (258±7 vs 265±6 å, p〈0.05). We propose that the changes of lipoprotein lipase and lipoprotein lipase/hepatic lipase ratio cluster with insulin resistance and provide a possible mechanism to explain the lowering of HDL cholesterol and elevation of triglyceride concentrations observed in insulin-resistant subjects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400640
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  • 5
    Electronic Resource
    Electronic Resource
    A paired-sibling analysis of the XbaI polymorphism in the muscle glycogen synthase gene (1999)
    Springer
    Diabetologia 42 (1999), S. 1138-1145 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Muscle glycogen synthase gene ; GYS1 ; paired-sibling analysis ; Type II diabetes ; hypertension ; metabolic syndrome ; chromosome 19 ; candidate gene ; myocardial infarction ; microalbuminuria.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. We have previously shown an association between a XbaI polymorphism in the muscle glycogen synthase gene (GYS1) and both Type II (non–insulin–dependent) diabetes mellitus and hypertension. Association studies are, however, hampered by the selection of the control group. To circumvent these problems we addressed the same question using a novel genotype discordant paired-sibling approach. Methods. We identified 122 sex-matched sib-pairs discordant for the Xba1 polymorphism among a new set of 743 Finnish subjects from 227 families with Type II diabetes and paired analyses were done by McNemar test of symmetry and by permutation tests. Results. Paired analysis showed that siblings with the A2 variant had more hypertension (p = 0.0067), obesity (p = 0.033) and microalbuminuria (p = 0.031) but not significantly more Type II diabetes (p = 0.27) than siblings with the A1 variant. Siblings with the A2 variant were more often treated by insulin (p = 0.050) or anti-hypertensive medication (p = 0.0060) or both. Diabetic A2 variant carriers had higher triglyceride (p = 0.023) and lower HDL cholesterol (p = 0.0059) concentrations and an earlier age at onset of diabetes (p = 0.022) than diabetic siblings with the A1 variant. In non-diabetic sib-pairs the presence of the A2 variant was associated with higher diastolic (p = 0.0014) blood pressure. Finally, the allele frequency of the XbaI polymorphism differed between 216 randomly chosen unrelated Type II diabetic patients and 115 unrelated healthy control spouses without a family history of Type II diabetes (12.7 vs. 6.5 %, p = 0.013). Conclusion/interpretation. The A2 allele of the XbaI polymorphism in the GYS1 confers an increased susceptibility to different features of the metabolic syndrome and Type II diabetes. [Diabetologia (1999) 42: 1138–1145]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051282
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  • 6
    Electronic Resource
    Electronic Resource
    Effect of insulin on GLUT-4 mRNA and protein concentrations in skeletal muscle of patients with NIDDM and their first-degree relatives (1994)
    Springer
    Diabetologia 37 (1994), S. 401-407 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; glucose transport ; muscle ; insulin ; GLUT-4 ; NIDDM
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined whether insulin resistance, i. e. impaired insulin stimulated glucose uptake in NIDDM patients and their first-degree relatives is associated with alterations in the effect of insulin on the expression of the GLUT-4 gene in skeletal muscle in vivo. Levels of GLUT-4 mRNA and protein were measured in muscle biopsies taken before and after a euglycaemic insulin clamp from 14 NIDDM patients, 13 of their first-degree relatives and 17 control subjects. Insulin stimulated glucose uptake was decreased in the diabetic subjects (19.8±3.0 μmol · kg LBM−1 · min−1, both p〈0.001) compared with control subjects (44.1±2.5 μmol · kg LBM−1 · min−1) and relatives (39.9±3.3 μmol · kg LBM−1 · min−1). Basal GLUT-4 mRNA levels were significantly higher in diabetic subjects and relatives compared to control subjects (99±8 and 108±9 pg/μg RNA vs 68±5 pg/μg RNA; both p〈0.01). Insulin increased GLUT-4 mRNA levels in all control subjects (from 68±5 to 92±6 pg/ug RNA; p〈0.0001), but not in the diabetic patients (from 99±8 to 90±8 pg/μg RNA, NS), or their relatives (from 94±9 to 101±11 pg/μg RNA, NS). In the relatives, individual basal GLUT-4 mRNA concentrations varied between 55 and 137 pg/μg RNA. Insulin-resistant (n=6, mean glucose uptake rate=30.6±3.4 μmol · kg LBM−1 · min−1) but not insulin-sensitive relatives (n=7, mean glucose uptake rate=47.4±3.2 μmol · kg LBM−1 · min−1) had higher basal GLUT-4 mRNA concentrations compared to control subjects (108±9 vs 68±5 pg/ug RNA, p〈0.01). GLUT-4 protein content in muscle did not differ between the groups in the basal state and remained unchanged in all groups after insulin infusion. Neither insulin-stimulated GLUT-4 mRNA nor protein concentrations correlated with insulin-stimulated glucose uptake in any of the groups studied. We conclude, that impaired glucose uptake in NIDDM is not related to insulin-stimulated GLUT-4 mRNA or protein concentrations. Acute stimulation of GLUT-4 mRNA by insulin is altered in skeletal muscle of NIDDM patients and their first-degree relatives. This might be a consequence of chronic hyperinsulinaemia elevating basal GLUT-4 mRNA concentrations rather than the cause of insulin resistance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408478
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