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  • 1
    Electronic Resource
    Electronic Resource
    Assessment of insulin sensitivity in glucokinase-deficient subjects (1996)
    Springer
    Diabetologia 39 (1996), S. 82-90 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; glucokinase mutation ; MODY ; glucose clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The chronic hyperglycaemia of glucokinase-deficient diabetes results from a glucose-sensing defect in pancreatic beta cells and abnormal hepatic glucose phosphorylation. We have evaluated the contribution of insulin resistance to this form of chronic hyperglycaemia. Insulin sensitivity, assessed by the homeostasis model assessment (HOMA) method in 35 kindreds with glucokinase mutations, was found to be significantly decreased in 125 glucokinase-deficient subjects as compared to 141 unaffected first-degree relatives. Logistic regression analysis showed that in glucokinase-deficient subjects a decrease in insulin sensitivity was associated with deterioration of the glucose tolerance status. A euglycaemic hyperin-sulinaemic clamp was performed in 14 glucokinase-deficient subjects and 12 unrelated control subjects. In six patients and six control subjects the clamp was coupled to dideutero-glucose infusion to measure glucose turnover. Average glucose infusion rates (GIR) at 1 and 5 mU · kg body weight · min−1 insulin infusion rates were significantly lower in (the glucokinase-deficient) patients than in control subjects. Although heterogeneous results were observed, in 8 out of the 14 patients GIRs throughout the experiment were lower than 1 SD below the mean of the control subjects. Hepatic glucose production at 1 mU · kg body weight−1 · min−1 insulin-infusion rate was significantly higher in patients than in control subjects. In conclusion, insulin resistance correlates with the deterioration of glucose tolerance and contributes to the hyperglycaemia of glucokinase-deficient diabetes. Taken together, our results are most consistent with insulin resistance being considered secondary to the chronic hyperglycaemia and/or hypoinsulinaemia of glucokinase-deficiency. Insulin resistance might also result from interactions between the unbalanced glucose metabolism and susceptibility gene(s) to low insulin sensitivity likely to be present in this population.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400417
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  • 2
    Electronic Resource
    Electronic Resource
    Maternal diabetes alters birth weight in glucokinase-deficient (MODY2) kindred but has no influence on adult weight, height, insulin secretion or insulin sensitivity (2000)
    Springer
    Diabetologia 43 (2000), S. 1060-1063 
    Details
    ISSN: 1432-0428
    Keywords: Keywords MODY ; glucokinase mutations ; low birth weight ; macrosomia ; gestational diabetes ; insulin secretion defect.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Altered fetal insulin secretion caused by fetal or maternal glucokinase mutations influence birth weight. Here, we attempt to answer two additional questions: firstly, whether this variation in birth weight (from low birth weight to macrosomia) has an effect on adult height or weight. Secondly, whether maternal hyperglycaemia during fetal life has an effect on metabolic phenotypes of the adult offspring. Methods. We studied 447 family members from 37 MODY2 kindred, divided into four groups according to the presence or absence of a glucokinase mutation in the subject (S + or S–, respectively) and his/her mother (M + or M–). Birth weight data were obtained from a questionnaire sent to the mothers. Results. Birth weight was reduced in the presence of a fetal mutation (M–S + ) and increased in the presence of a maternal mutation (M + S–). These effects are additive as similar birth weights were observed in M + S + and M–S– offspring. Adult height, weight or body mass index (weight/height2) were, however, similar in the four groups of subjects. Non-diabetic adult offspring, regardless of the glycaemic status of the mothers (M + S– or M–S–), had similar insulin secretion, insulin sensitivity, blood pressures and lipid profiles. These variables as well as the severity of hyperglycaemia were similar in adult M + S + and M–S + MODY2 subjects. Conclusion/Interpretation. Maternal environment and fetal genotypes could alter growth in utero by changing fetal insulin secretion but these effects do not result in a persistent programming in latter life. [Diabetologia (2000) 43: 1060–1063]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051490
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  • 3
    Electronic Resource
    Electronic Resource
    Determination of peritoneal glucose kinetics in rats: implications for the peritoneal implantation of closed-loop insulin delivery systems (1989)
    Springer
    Diabetologia 32 (1989), S. 331-336 
    Details
    ISSN: 1432-0428
    Keywords: Peritoneal ; rat ; glucose kinetics ; closed-loop insulin therapy ; glucose sensor ; bioartificial pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Peritoneal glucose kinetics were evaluated in the anaesthetized rat, to assess whether the peritoneal cavity would be a suitable site for the implantation of membrane-protected islets of Langerhans (bioartificial pancreas) or the glucose sensor of an artificial B cell. Glucose was measured in peritoneal fluid samples aspirated by needle puncture. Basal peritoneal and blood glucose concentrations were identical in 16 h fasted (n=4) and non fasted (n=3) animals. After 10 min of an i.v. glucose infusion (n=15) the increment in peritoneal glucose concentration was 63±3% of the increment in blood glucose concentration and both values were significantly correlated (r=0.92; p〈0.001). After 10 min of glucose clamping (12.6±0.8 mmol/l), the increment in peritoneal glucose concentration was 69±3% (n=5; p〈0.05) of the increment in blood glucose concentration. In three additional experiments it was 93±3% of the increment in blood glucose concentration (NS), after 30 min of glucose clamping (8.0±0.5 mmol/l). Peritoneal glucose concentration monitored by a glucose sensor: (a) followed blood glucose sluggishly during a glucose clamp (n=5), confirming the data shown above, (b) followed blood glucose with a 5 min delay and reached the same plateau after the intravenous injection of 1U insulin (n=3; NS). We conclude that peritoneal glucose reflects blood glucose at basal state and during variations of glycaemia, nevertheless, presenting heterogeneous kinetics. These kinetics might be appropriate for a bioartificial pancreas but not for an in vivo calibration procedure, of a peritoneally implanted glucose sensor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277254
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  • 4
    Electronic Resource
    Electronic Resource
    Strategies for the collection of sibling-pair data for genetic studies in Type 2 (non-insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 685-685 
    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/BF00401001
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  • 5
    Electronic Resource
    Electronic Resource
    Identification of 14 new glucokinase mutations and description of the clinical profile of 42 MODY-2 families (1997)
    Springer
    Diabetologia 40 (1997), S. 217-224 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetes mellitus ; MODY ; glucokinase mutations ; insulin secretion ; genetics.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Mutations in glucokinase are associated with defects in insulin secretion and hepatic glycogen synthesis resulting in mild chronic hyperglycaemia, impaired glucose tolerance or diabetes mellitus. We screened members of 35 families with features of maturity-onset diabetes of the young for mutations in the glucokinase gene and found 16 different mutations. They included 14 new mutations in the glucokinase gene: 9 missense mutations (A53S, G80A, H137R, T168P, M210T, C213R, V226M, S336L and V367M); 2 nonsense mutations (E248X and S360X); a deletion of one nucleotide resulting in a frameshift (V401del1); a substitution of a conserved nucleotide at a splice acceptor site (L122-1G → T); and a 10 base pair deletion that removed the GT of the splice donor site and the following eight nucleotides (K161 + 2del10). In addition, we found two previously identified mutations: R186X and G261R. Study of 260 subjects with glucokinase-deficient hyperglycaemia from 42 families with 36 different GCK mutations made it possible to define the clinical profile of this subtype of non-insulin-dependent diabetes mellitus (NIDDM). Hyperglycaemia due to glucokinase deficiency is often mild (fewer than 50 % of subjects have overt diabetes) and is evident during the early years of life. Despite the long duration of hyperglycaemia, glucokinase-deficient subjects have a low prevalence of micro- and macro-vascular complications of diabetes. Obesity, arterial hypertension and dyslipidaemia are also uncommon in this form of NIDDM. [Diabetologia (1997) 40: 217–224]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050666
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  • 6
    Electronic Resource
    Electronic Resource
    Missense mutations in the pancreatic islet beta cell inwardly rectifying K+ channel gene (KIR6.2/BIR ): a meta-analysis suggests a role in the polygenic basis of Type II diabetes mellitus in Caucasians (1998)
    Springer
    Diabetologia 41 (1998), S. 1511-1515 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type II (non-insulin-dependent) diabetes mellitus ; gene ; inwardly rectifier potassium channel ; mutation.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The K+ inwardly rectifier channel (KIR) is one of the two sub-units of the pancreatic islet ATP-sensitive potassium channel complex (IKATP), which has a key role in glucose-stimulated insulin secretion and thus is a potential candidate for a genetic defect in Type II (non-insulin-dependent) diabetes mellitus. We did a molecular screening of the KIR6.2 gene by single strand conformational polymorphism (SSCP) and direct sequencing in 72 French Caucasian Type II diabetic families. We identified three nucleotide substitutions resulting in three amino acid changes (E23K, L270V and I337V), that have also been identified in other Caucasian Type II diabetic subjects. These variants were genotyped in French cohorts of 191 unrelated Type II diabetic probands and 119 normoglycaemic control subjects and association studies were done. The genotype frequencies of the L270V and I337V variants were not very different between Type II diabetic subjects and control groups. In contrast, analysis of the E23K variant showed that the KK homozygocity was more frequent in Type II diabetic than in control subjects (27 vs 14 %, p = 0.015). Analyses in a recessive model (KK vs EK/EE) tended to show a stronger association of the K allele with diabetes (p = 0.0097, corrected p-value for multiple testing 〈 0.02). The data for the E23K variant obtained here and those obtained from three other Caucasian groups studied so far were combined and investigated by meta-analysis. Overall, the E23K variant was found to be significantly associated with Type II diabetes (0.001 ≤p≤ 0.0016, corrected p-values for multiple testing p≤ 0.01). This study shows that KIR6.2 polymorphisms are frequently associated with Type II diabetes in French Caucasians. Furthermore, a meta-analysis combining different Caucasian groups suggests an significant role of KIR6.2 in the polygenic context of Type II diabetes. [Diabetologia (1998) 41: 1511–1515]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051098
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  • 7
    Electronic Resource
    Electronic Resource
    Mutation screening in 18 Caucasian families suggest the existence of other MODY genes (1998)
    Springer
    Diabetologia 41 (1998), S. 1017-1023 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Genetics ; MODY ; glucokinase gene ; HNF-1α ; HNF-4α ; HNF-1β ; IPF1 ; transcription factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Maturity-onset diabetes of the young (MODY) is a heterogeneous subtype of non-insulin-dependent diabetes mellitus characterised by early onset, autosomal dominant inheritance and a primary defect in insulin secretion. To date five MODY genes have been identified: hepatocyte nuclear factor-4 alpha (HNF-4 α/MODY1/TCF14) on chromosome 20 q, glucokinase (GCK/MODY2) on chromosome 7 p, hepatocyte nuclear factor-1 alpha (HNF-1 α/MODY3/TCF1) on chromosome 12 q, insulin promoter factor-1 (IPF1/MODY4) on chromosome 13 q and hepatocyte nuclear factor-1 beta (HNF-1 β/MODY5/TCF2) on chromosome 17cen-q. We have screened the HNF-4 α, HNF-1 α and HNF-1 β genes in members of 18 MODY kindreds who tested negative for glucokinase mutations. Five missense (G31D, R159W, A161T, R200W, R271W), one substitution at the splice donor site of intron 5 (IVS5nt + 2T→A) and one deletion mutation (P379fsdelT) were found in the HNF-1 α gene, but no MODY-associated mutations were found in the HNF-4 α and HNF-1 β genes. Of 67 French MODY families that we have now studied, 42 (63 %) have mutations in the glucokinase gene, 14 (21 %) have mutations in the HNF-1 α gene, and 11 (16 %) have no mutations in the HNF-4 α, IPF1 and HNF-1 β genes. Eleven families do not have mutations in the five known MODY genes suggesting that there is at least one additionnal locus that can cause MODY. [Diabetologia (1998) 41: 1017–1023]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051025
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  • 8
    Electronic Resource
    Electronic Resource
    Acral necrosis by Stenotrophomonas maltophilia (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of the European Academy of Dermatology and Venereology 15 (2001), S. 0 
    Details
    ISSN: 1468-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Stenotrophomonas maltophilia (SM) has been considered a nosocomial pathogen. Nevertheless, community acquired infection may occur more frequently than usually recognized.〈section xml:id="abs1-3"〉〈title type="main"〉CaseWe describe distal necrosis of the fingers by SM in a farmer, contracted in the community and successfully treated with a combination of cotrimoxazole and ciprofloxacin. The patient was diagnosed with chronic lymphocytic leukaemia 6 months later.〈section xml:id="abs1-4"〉〈title type="main"〉ConclusionsThis unusual presentation shows that infection with SM should be included in the differential diagnosis of the skin and soft tissue infection, even in apparently healthy patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0926-9959.2001.00273.x
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  • 9
    Electronic Resource
    Electronic Resource
    Cutaneous manifestations of familial amyloidotic polyneuropathy (2005)
    Oxford, UK : Blackwell Science Ltd
    Journal of the European Academy of Dermatology and Venereology 19 (2005), S. 0 
    Details
    ISSN: 1468-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Familial amyloidotic polyneuropathy is an autosomal dominant amyloidosis, characterized by the systemic deposition of amyloid with a particular involvement of the peripheral nerves.The disease generally manifests as a severe sensory, motor and autonomic neuropathy. Cardiomyopathy, nephropathy, vitreous opacities and carpal tunnel syndrome may occur in a variable association with the neuropathy. Trophic dermatological lesions are frequent in the more advanced stages of the disease. We examined the skin of 142 patients. The cutaneous manifestations more frequently observed were: xerosis (81.6%), seborrheic dermatitis (21.8%), traumatic and burn lesions (19.7%), acne (18.3%), neurotrophic ulcers (14%) and onychomycosis (10.5%). Among the hepatic transplanted patients (31%), seborrheic dermatitis and acne were the most frequent diagnoses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1468-3083.2005.01222.x
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  • 10
    Electronic Resource
    Electronic Resource
    Evaluating in vitro and in vivo the interference of ascorbate and acetaminophen on glucose detection by a needle-type glucose sensor
    Amsterdam : Elsevier
    Biosensors and Bioelectronics 7 (1992), S. 345-352 
    Details
    ISSN: 0956-5663
    Keywords: acetaminophen ; ascorbate ; glucose sensor ; interference
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Electrical Engineering, Measurement and Control Technology , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0956-5663(92)85030-E
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