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  • 1
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    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
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  • 3
    ISSN: 1432-0428
    Keywords: Keywords Obesity ; genetic ; body mass index ; neuropeptide Y ; neuropeptide Y receptors ; leptin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Synthesis and release of neuropeptide Y (NPY) are both regulated by leptin binding to its hypothalamic receptor mediating some of the effects of leptin on food intake. Moreover, NPY administration is a powerful stimulant of feeding behaviour. Thus, we investigated the potential implication of NPY, NPY-Y1 and -Y5 subtype receptors [rNPY-Y1/-Y5] in the development of human obesity. Two complementary genetic approaches were used: 1) linkage analyses between obesity and polymorphic markers located nearby NPY and rNPY-Y1/-Y5 genes (respectively on chromosomes 7p15.1 and 4q[31.3–32]) in 93 French Caucasian morbidly obese families; 2) single strand conformation polymorphism (SSCP) scanning of the coding region of the NPY and rNPY-Y1 genes performed in 50 unrelated obese patients ascertained on the basis of a body mass index of 27 kg/m2 or more and a family history of obesity. No evidence of linkage between morbid obesity or obesity-related quantitative traits and NPY and rNPY-Y1/Y5 regions was found in this population. Moreover, SSCP scanning revealed no mutation in the coding region of NPY and rNPY-Y1 genes among obese subjects. These results suggest that NPY and NPY-Y1/Y5 receptors are unlikely to be implicated in the development of human morbid obesity, at least in the French Caucasian population. [Diabetologia (1997) 40: 671–675]
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Keywords Uncoupling protein (UCP), promoter, mutation, polymorphism, obesity, body mass index (BMI).
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. In obese French Caucasian subjects we previously described a silent UCP3 Tyr99Tyr mutation, associated with body mass index. We hypothesised that an unknown polymorphism in the vicinity of the gene could contribute to obesity.¶Methods. Morbidly obese subjects were screened for mutations in 1 kb upstream from the UCP3 gene. Association studies were done between a variant and obesity in 401 morbidly obese and 231 control subjects.¶Results. We detected three rare genetic variants and one polymorphism: a + 5 G→A in exon 1, a –155 C→T, a –439 A insertion and a –55 C→T located 6 bp from the putative TATA box. This variant was in linkage disequilibrium with the Tyr99Tyr polymorphism. Frequencies of the variant allele at the –55 locus were similar in the obese and control groups (0.23 vs 0.21). The –55 polymorphism was associated with BMI in the obese group (p = 0.0031): BMI was higher in TT than in CC or CT patients. Likewise control subjects with a TT genotype had a higher BMI (p = 0.03). In the obese group, homozygocity for this variant is a risk factor for high BMI (odds ratio: 1:75, p = 0.02). Obese patients were divided into tertiles according to physical activity. In the group with a wild C/C genotype, BMI was negatively associated with physical activity (p = 0.015).¶Conclusion/interpretation. The C→T polymorphism in the 5 ′ sequences of the UCP3 gene might contribute to the corpulence in obese and normal weight subjects and alter the benefit of physical activity. The UCP3 gene can be considered as a gene modifying corpulence. [Diabetologia (2000) 43: 245–249]
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: KeywordsPOMC ; Proopiomelanocortin ; obesity ; leptin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The region 2p21–23, containing the proopiomelanocortin gene (POMC), was reported to be linked to leptin concentrations in Mexican-American, French and African-American cohorts. A polyhormone peptide, POMC is expressed in brain, gut, placenta and pancreas. The POMC mutations are responsible for rare cases of early-onset obesity. Thus we examined the contribution of the POMC locus to obesity in French families. Methods. Single and multipoint linkage studies were done between obesity, obesity associated-phenotypes (leptin values and z-score of the body mass index) and three newly mapped markers surrounding POMC in 264 affected sib-pairs from French obese families. Mutation screening of the exons and intron/exon junctions of the POMC gene was realised by direct sequencing. Association studies were done in 379 unrelated obese patients and 370 non-obese non-diabetic subjects. Results. Linkage analysis confirmed the trend towards linkage between polymorphic markers around POMC and variations of leptin concentrations and z-score (maximum lod score at D2S2337 = 2.03). Mutation screening of the POMC gene in the French Caucasian cohort identified two previously reported polymorphisms. None of these variants was associated with obesity, diabetes or serum leptin and lipid concentrations. Conclusion/interpretation. Our results indicate that mutations in the POMC gene do not contribute to the variance of obesity associated phenotypes, at least in French Caucasians. Given the replicated evidence of linkage between leptin values and the chromosome 2p21–23 region in different populations, it is likely that functional variant(s) in the POMC regulating sequences or in an unknown gene in this region explains this linkage. [Diabetologia (2000) 43: 1554–1557]
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of organic chemistry 55 (1990), S. 4403-4410 
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford BSL : Blackwell Science Ltd
    International journal of food science & technology 31 (1996), S. 0 
    ISSN: 1365-2621
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Notes: Ripe banana, cut to 10mm thick slabs were osmotically treated in sugar solutions of 35, 50 and 65° Brix for 36h. The initial moisture content fell from a value of 3.13kg H2O DM to 2.19, 1.63 and 1.16kg H2O kg−1 for treatment in the three solutions, respectively. These slabs, with Total Soluble Solids (TSS) contents of 26, 34 and 39° Brix, respectively, as well as freshly cut but untreated slabs (15° Brix) were air dried in a cabinet type tray drier to near equilibrium conditions at fixed temperatures from 40 to 80°C and at a constant air speed of 0.62m s−1. Drying was found to occur in the falling rate period only for both banana types and two drying constants K1 and K2 were established for a first and second falling rate period of drying. Increasing the drying air temperature significantly enhanced the drying rate and the K-values, except at 80°C when the rates fell, possibly because of case hardening of the slabs. Reducing the slab thickness also improved the drying rate, but increasing the air speed to 1.03m s−1 did not have any profound effect. As the sugar content of the banana slabs increased through the osmotic treatment, drying rates fell. Calculated apparent moisture diffusivities at 60°C ranged from 34.8× 10−10 m2 s−1 (fresh slab) to 8.8×10−10 m2 s−1 for dried (39° Brix) slabs. The moisture diffusivity was significantly lowered as the moisture content dropped in drying and with increased levels of sugar. Previously osmosed and then air dried banana slabs showed appealing colour and texture compared to the fresh banana.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 12 (1920), S. 173-174 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 16 (1924), S. 580-582 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Industrial & engineering chemistry 17 (1925), S. 830-831 
    ISSN: 1520-5045
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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