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28 records – page 1 of 3.

Catalases protect cellular proteins from oxidative modification in Saccharomyces cerevisiae.

https://arctichealth.org/en/permalink/ahliterature9223
Source
Cell Biol Int. 2005 Mar;29(3):187-92
Publication Type
Article
Date
Mar-2005
Author
Volodymyr I Lushchak
Dmytro V Gospodaryov
Author Affiliation
Department of Biochemistry, Vassyl Stefanyk Precarpathian National University, 57 Shevchenko Str., 76025 Ivano-Frankivsk, Ukraine. lushchak@pu.if.ua
Source
Cell Biol Int. 2005 Mar;29(3):187-92
Date
Mar-2005
Language
English
Publication Type
Article
Keywords
Antioxidants - metabolism
Catalase - physiology
Cytosol - drug effects - enzymology
Ethanol - pharmacology
Glucose - pharmacology
Glucosephosphate Dehydrogenase - metabolism
Glutathione Reductase - metabolism
Oxidation-Reduction
Oxidative Stress
Peroxisomes - drug effects - enzymology
Saccharomyces cerevisiae - drug effects - enzymology - growth & development
Superoxide Dismutase - metabolism
Abstract
The yeast Saccharomyces cerevisiae cells had higher antioxidant enzyme activities under growth in ethanol than that in glucose as a carbon and energy source. The correlations between catalase activity and protein carbonyl level (r(2)=0.857), between catalase and glucose-6-phosphate dehydrogenase activities (r(2)=0.924) and between protein carbonyl levels and glucose-6-phosphate dehydrogenase activity (r(2)=0.988) under growth in ethanol were found. Growing in ethanol the strain deficient in cytosolic and peroxisomal catalases had 7.1-fold higher level of carbonyl proteins than that of wild-type strain. Our data suggest that in vivo catalases may protect glucose-6-phosphate dehydrogenase against oxidative inactivation.
PubMed ID
15893481 View in PubMed
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[Changes in activity of the hypothalamic neurons in response to physiological fluctuations of the homeostasis constants]

https://arctichealth.org/en/permalink/ahliterature81094
Source
Fiziol Zh. 2006;52(3):57-63
Publication Type
Article
Date
2006
Author
Natrus L V
Source
Fiziol Zh. 2006;52(3):57-63
Date
2006
Language
Ukrainian
Publication Type
Article
Keywords
Action Potentials - drug effects - physiology
Animals
Cats
Evoked Potentials, Somatosensory - drug effects - physiology
Female
Glucose - pharmacology
Homeostasis - drug effects - physiology
Hypothalamus - drug effects - physiology
Male
Microelectrodes
Neurons - drug effects - physiology
Phenylephrine - pharmacology
Sodium Chloride - pharmacology
Temperature
Abstract
In acute experiments on cats under the combined narcosis (ketamine + N2O) we have investigated impulse activity of the rostral hypothalamic neurons and analyzed its modifications due to visceral stimulation. As stimulation we used warmed up or cooled (on 7 degrees C) a paw of an animals, cooled a body of an animal, we administered solutions into a carotid artery: 5 % of glucose, 0,2 % and 3 % NaCl, phenilephrine. Thus we modeled fluctuation of homeostasis's constants in physiological limits in an animal organism. It is shown that the greatest quantity of investigated neurons--more than 10 % authentically changes a pattern impulse activity when we entered solutions of 5 % of glucose and 0,2 % NaCl into a carotid artery of animals. In other cases the degree of transformation of a pattern was less (6-7 %) and approximately identical. When we entered of a microdose phenilephrine into the v. femoralis in order to modulate press effect we registered minimal quantity of neurons (1,4%). Studing of the parameters of the IA hypothalamic neurons during the homeostatic changes could be a basis for finding of transformation of the functional state of neurons which take part in the regulator mechanisms for maintaining of homeostasis.
PubMed ID
16909757 View in PubMed
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Common single nucleotide polymorphisms in TCF7L2 are reproducibly associated with type 2 diabetes and reduce the insulin response to glucose in nondiabetic individuals.

https://arctichealth.org/en/permalink/ahliterature80499
Source
Diabetes. 2006 Oct;55(10):2890-5
Publication Type
Article
Date
Oct-2006
Author
Saxena Richa
Gianniny Lauren
Burtt Noël P
Lyssenko Valeriya
Giuducci Candace
Sjögren Marketa
Florez Jose C
Almgren Peter
Isomaa Bo
Orho-Melander Marju
Lindblad Ulf
Daly Mark J
Tuomi Tiinamaija
Hirschhorn Joel N
Ardlie Kristin G
Groop Leif C
Altshuler David
Author Affiliation
Program in Medical and Population Genetics, Broad Institute of Harvard and Massachusetts Institute of Technology, MA, USA.
Source
Diabetes. 2006 Oct;55(10):2890-5
Date
Oct-2006
Language
English
Publication Type
Article
Keywords
Case-Control Studies
Diabetes Mellitus, Type 2 - genetics
Glucose - pharmacology
Humans
Insulin - physiology
Insulin Resistance - genetics
Polymorphism, Single Nucleotide
Risk
TCF Transcription Factors - genetics
Abstract
Recently, common noncoding variants in the TCF7L2 gene were strongly associated with increased risk of type 2 diabetes in samples from Iceland, Denmark, and the U.S. We genotyped 13 single nucleotide polymorphisms (SNPs) across TCF7L2 in 8,310 individuals in family-based and case-control designs from Scandinavia, Poland, and the U.S. We convincingly confirmed the previous association of TCF7L2 SNPs with the risk of type 2 diabetes (rs7903146T odds ratio 1.40 [95% CI 1.30-1.50], P = 6.74 x 10(-20)). In nondiabetic individuals, the risk genotypes were associated with a substantial reduction in the insulinogenic index derived from an oral glucose tolerance test (risk allele homozygotes have half the insulin response to glucose of noncarriers, P = 0.003) but not with increased insulin resistance. These results suggest that TCF7L2 variants may act through insulin secretion to increase the risk of type 2 diabetes.
PubMed ID
17003358 View in PubMed
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The effect of estrogen level on glucose-induced changes in serum insulin-like growth factor binding protein-1 concentration.

https://arctichealth.org/en/permalink/ahliterature223222
Source
Fertil Steril. 1992 Sep;58(3):543-6
Publication Type
Article
Date
Sep-1992
Author
H. Martikainen
R. Koistinen
M. Seppälä
Author Affiliation
Department of Obstetrics and Gynecology, University of Oulu, Finland.
Source
Fertil Steril. 1992 Sep;58(3):543-6
Date
Sep-1992
Language
English
Publication Type
Article
Keywords
Adult
Buserelin - diagnostic use
Carrier Proteins - blood
Estradiol - blood
Female
Fertilization in Vitro
Glucose - pharmacology
Glucose Tolerance Test
Humans
Insulin - blood
Insulin-Like Growth Factor Binding Protein 1
Insulin-Like Growth Factor I - metabolism
Menotropins - diagnostic use
Prospective Studies
Sex Hormone-Binding Globulin - metabolism
Abstract
To investigate the regulation of insulin-like growth factor binding protein-1 (IGFBP-1) concentration during ovarian stimulation.
A prospective study of patients undergoing in vitro fertilization treatment.
Infertility unit at the University Central Hospital of Oulu, a tertiary referral center.
Sixteen healthy, regularly menstruating lean tubal infertility patients.
Oral glucose tolerance test was performed first in a hypoestrogenic state after suppression by long-term gonadotropin-releasing hormone (GnRH) agonist and, second, in a hyperestrogenic state after stimulation by human menopausal gonadotropins.
Serum concentrations of IGFBP-1, insulin-like growth factor I (IGF-I), insulin and sex hormone-binding globulin were measured before and 2 hours after glucose administration.
Before and after glucose administration, the serum IGFBP-1 concentrations were significantly higher in the hyperestrogenic state (estradiol [E2] level 3.5 +/- 0.57 nmol/L) after ovarian stimulation than in the GnRH-analogue-induced hypoestrogenic state before the gonadotropin treatment (E2 level 0.10 +/- 0.02 nmol/L). On both occasions glucose-induced hyperinsulinemia caused a significant decrease in the circulating IGFBP-1 levels, whereas the IGF-I levels remained unchanged. There was a significant correlation between E2 and the insulin-suppressed IGFBP-1 level. The sum of follicular diameters correlated positively with the serum IGFBP-1 concentration.
Gonadotropin-induced hyperestrogenism is related to elevated serum IGFBP-1 levels, either via estrogen-stimulated synthesis or via increased contribution from multiple follicles. Glucose-induced hyperinsulinemia suppresses serum IBFBP-1 concentration equally both in the hypoestrogenic and hyperestrogenic states. Because of similar IGF-I levels, it is likely that the biological activity of IGF-I is different before and after gonadotropin stimulations.
PubMed ID
1381688 View in PubMed
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Familiality of quantitative metabolic traits in Finnish families with non-insulin-dependent diabetes mellitus. Finland-United States Investigation of NIDDM Genetics (FUSION) Study investigators.

https://arctichealth.org/en/permalink/ahliterature201829
Source
Hum Hered. 1999 Jun;49(3):159-68
Publication Type
Article
Date
Jun-1999
Author
R M Watanabe
T. Valle
E R Hauser
S. Ghosh
J. Eriksson
K. Kohtamäki
C. Ehnholm
J. Tuomilehto
F S Collins
R N Bergman
M. Boehnke
Author Affiliation
University of Michigan, School of Public Health, Department of Biostatistics, Ann Arbor, Mich. 48109-2029, USA. rwatt@sph.umich.edu
Source
Hum Hered. 1999 Jun;49(3):159-68
Date
Jun-1999
Language
English
Publication Type
Article
Keywords
Adult
Aged
Analysis of Variance
Blood Glucose - drug effects - metabolism
Blood Pressure - drug effects
Body mass index
Diabetes Mellitus, Type 2 - blood - genetics - physiopathology
Family Health
Fasting
Female
Finland
Glucose - pharmacology
Glucose Tolerance Test - methods
Humans
Insulin - blood
Lipids - blood
Male
Middle Aged
Pedigree
Quantitative Trait, Heritable
Tolbutamide - pharmacology
Abstract
Type 2 diabetes mellitus (NIDDM) is a complex disorder encompassing multiple metabolic defects. There exists strong evidence for a genetic component to NIDDM; however, to date there have been few reports of linkage between genetic markers along the genome and NIDDM or NIDDM-related quantitative traits. We sought to determine whether individual quantitative traits which determine glucose tolerance exhibit familiality in Finnish families with at least one NIDDM-affected sibling pair. Tolbutamide-modified frequently sampled intravenous glucose tolerance tests (FSIGT) were performed on unaffected offspring (n = 431) and spouses (n = 154) of affected sibling pairs sampled for the Finland-United States Investigation of NIDDM Genetics (FUSION) study. FSIGT data were analyzed using the Minimal Model to obtain quantitative measures of insulin sensitivity (SI), glucose effectiveness (SG), and insulin secretion assessed as the acute insulin response to glucose (AIR). The disposition index (DI), a measure of insulin resistance-corrected beta-cell function, was also derived as the product of SI and AIR. Variance components analysis was used to determine for each trait, the heritability (h2), the proportion of the total trait variance accounted for by additive genes. After adjustment for age, gender, and body mass index, h2 estimates were: SG: 18 +/- 9%, SI: 28 +/- 8%, AIR: 35 +/- 8%, and DI: 23 +/- 8%. We conclude that there is strong evidence for modest heritability of Minimal-Model-derived NIDDM-related quantitative traits in unaffected spouses and offspring of Finnish affected sibling pairs.
PubMed ID
10364681 View in PubMed
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Functional aspects of mouse islets transplanted to the kidney.

https://arctichealth.org/en/permalink/ahliterature48441
Source
Diabetologia. 1994 Sep;37 Suppl 2:S112-6
Publication Type
Article
Date
Sep-1994
Author
I B Täljedal
C L Shi
P. Rooth
Author Affiliation
Department of Histology and Cell Biology, University of Umeå, Sweden.
Source
Diabetologia. 1994 Sep;37 Suppl 2:S112-6
Date
Sep-1994
Language
English
Publication Type
Article
Keywords
Animals
Awards and Prizes
Cells, Cultured
Cyclosporine - therapeutic use
Diabetes Mellitus - history
Europe
Glucose - pharmacology
Graft Survival - drug effects
History, 20th Century
Insulin - secretion
Islets of Langerhans Transplantation - physiology
Kidney
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred Strains
Portraits
Research Support, Non-U.S. Gov't
Societies, Medical
Sweden
Time Factors
Transplantation, Heterotopic
Transplantation, Isogeneic
Abstract
To test whether the transplantation of pancreatic islets affects their basic functions, collagenase-isolated mouse islets were inserted under the left renal capsule of recipient animals. After various periods of time, grafts were removed from the kidney and examined for insulin content and secretory dynamics in a perifusion system. During syngeneic (C57BL/6, BALB/c) or subsyngeneic (NMRI) intrastrain transplantation, the graft insulin content fell drastically during the first week and stayed low for at least 6 weeks; first-phase secretion in general appeared suppressed. Immunosuppression by cyclosporin A had little effect on (sub)syngeneic grafts but markedly improved the performance of allotransplants. Daily injections of the calcium antagonist, verapamil, enhanced the insulin secretory responses of isolated grafts, whether (sub)syngeneic or allogeneic. In syngeneic and subsyngeneic grafts, the potentiating effect of acetylcholine on glucose-induced insulin release was markedly diminished, whereas that of caffeine was not. Transplanted islets also exhibited a subnormal responsiveness to the inhibiting action of noradrenaline. It is concluded that chronic denervation and transplantation of pancreatic islets may cause fundamental changes in the beta-cell responses to physiological regulators of insulin release.
PubMed ID
7821726 View in PubMed
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G-allele of intronic rs10830963 in MTNR1B confers increased risk of impaired fasting glycemia and type 2 diabetes through an impaired glucose-stimulated insulin release: studies involving 19,605 Europeans.

https://arctichealth.org/en/permalink/ahliterature89521
Source
Diabetes. 2009 Jun;58(6):1450-6
Publication Type
Article
Date
Jun-2009
Author
Sparsø Thomas
Bonnefond Amélie
Andersson Ehm
Bouatia-Naji Nabila
Holmkvist Johan
Wegner Lise
Grarup Niels
Gjesing Anette P
Banasik Karina
Cavalcanti-Proença Christine
Marchand Marion
Vaxillaire Martine
Charpentier Guillaume
Jarvelin Marjo-Riitta
Tichet Jean
Balkau Beverley
Marre Michel
Lévy-Marchal Claire
Faerch Kristine
Borch-Johnsen Knut
Jørgensen Torben
Madsbad Sten
Poulsen Pernille
Vaag Allan
Dina Christian
Hansen Torben
Pedersen Oluf
Froguel Philippe
Author Affiliation
Steno Diabetes Center, Gentofte, Denmark. tspr@steno.dk.
Source
Diabetes. 2009 Jun;58(6):1450-6
Date
Jun-2009
Language
English
Publication Type
Article
Keywords
Adult
Aged
Blood Glucose - genetics - metabolism
Denmark
Diabetes Mellitus, Type 2 - genetics
European Continental Ancestry Group - genetics
Genetic Variation
Glucose - pharmacology
Humans
Insulin - secretion
Insulin Resistance - genetics
Insulin-Secreting Cells - physiology
Introns
Liver - physiopathology
Quantitative Trait Loci
Receptor, Melatonin, MT1 - genetics
Risk factors
Twins
Abstract
OBJECTIVE: Genome-wide association studies have identified several variants within the MTNR1B locus that are associated with fasting plasma glucose (FPG) and type 2 diabetes. We refined the association signal by direct genotyping and examined for associations of the variant displaying the most independent effect on FPG with isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), type 2 diabetes, and measures of insulin release and peripheral and hepatic insulin sensitivity. RESEARCH DESIGN AND METHODS: We examined European-descent participants in the Inter99 study (n = 5,553), in a sample of young healthy Danes (n = 372), in Danish twins (n = 77 elderly and n = 97 young), in additional Danish type 2 diabetic patients (n = 1,626) and control subjects (n = 505), in the Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study (n = 4,656), in the North Finland Birth Cohort 86 (n = 5,258), and in the Haguenau study (n = 1,461). RESULTS: The MTNR1B intronic variant, rs10830963, carried most of the effect on FPG and showed the strongest association with FPG (combined P = 5.3 x 10(-31)) and type 2 diabetes. The rs10830963 G-allele increased the risk of i-IFG (odds ratio [OR] 1.64, P = 5.5 x 10(-11)) but not i-IGT. The G-allele was associated with a decreased insulin release after oral and intravenous glucose challenges (P
PubMed ID
19324940 View in PubMed
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Glucose induces oscillatory Ca2+ signalling and insulin release in human pancreatic beta cells.

https://arctichealth.org/en/permalink/ahliterature48442
Source
Diabetologia. 1994 Sep;37 Suppl 2:S11-20
Publication Type
Article
Date
Sep-1994
Author
B. Hellman
E. Gylfe
P. Bergsten
E. Grapengiesser
P E Lund
A. Berts
A. Tengholm
D G Pipeleers
Z. Ling
Author Affiliation
Department of Medical Cell Biology, University of Uppsala, Sweden.
Source
Diabetologia. 1994 Sep;37 Suppl 2:S11-20
Date
Sep-1994
Language
English
Publication Type
Article
Keywords
Adenosine Triphosphate - pharmacology
Adult
Awards and Prizes
Calcium - metabolism
Carbachol - pharmacology
Cytoplasm - metabolism
Diabetes Mellitus - history
Europe
Glucagon - pharmacology
Glucose - pharmacology
Guanosine 5'-O-(3-Thiotriphosphate) - pharmacology
History, 20th Century
Humans
In Vitro
Insulin - secretion
Islets of Langerhans - drug effects - physiology - secretion
Kinetics
Membrane Potentials - drug effects
Models, Biological
Patch-Clamp Techniques
Portraits
Research Support, Non-U.S. Gov't
Signal Transduction - drug effects
Societies, Medical
Sweden
Abstract
Mechanisms of pulsatile insulin release in man were explored by studying the induction of oscillatory Ca2+ signals in individual beta cells and islets isolated from the human pancreas. Evidence was provided for a glucose-induced closure of ATP-regulated K+ channels, resulting in voltage-dependent entry of Ca2+. The observation of step-wise increases of capacitance in response to depolarizing pulses suggests that an enhanced influx of Ca2+ is an effective means of stimulating the secretory activity of the isolated human beta cell. Activation of muscarinic receptors (1-10 mumol/l carbachol) and of purinergic P2 receptors (0.01-1 mumol/l ATP) resulted in repetitive transients followed by sustained elevation of the cytoplasmic Ca2+ concentration ([Ca2+]i). Periodic mobilisation of intracellular calcium was seen also when injecting 100 mumol/l GTP-gamma-S into beta cells hyperpolarized to -70 mV. Individual beta cells responded to glucose and tolbutamide with increases of [Ca2+]i, manifested either as large amplitude oscillations (frequency 0.1-0.5/min) or as a sustained elevation. Glucose regulation was based on sudden transitions between the basal and the two alternative states of raised [Ca2+]i at threshold concentrations of the sugar characteristic for the individual beta cells. The oscillatory characteristics of coupled cells were determined collectively rather than by particular pacemaker cells. In intact pancreatic islets the glucose induction of well-synchronized [Ca2+]i oscillations had its counterpart in 2-5 min pulses of insulin. Each of these pulses could be resolved into regularly occurring short insulin transients. It is concluded that glucose stimulation of insulin release in man is determined by the number of beta cells entering into a state with Ca(2+)-induced secretory pulses.
PubMed ID
7821725 View in PubMed
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Heritability of model-derived parameters of beta cell secretion during intravenous and oral glucose tolerance tests: a study of twins.

https://arctichealth.org/en/permalink/ahliterature174172
Source
Diabetologia. 2005 Aug;48(8):1604-13
Publication Type
Article
Date
Aug-2005
Author
M. Lehtovirta
J. Kaprio
L. Groop
M. Trombetta
R C Bonadonna
Author Affiliation
Department of Medicine, Helsinki University Central Hospital, University of Helsinki, Finland. mikko.lehtovirta@helsinki.fi
Source
Diabetologia. 2005 Aug;48(8):1604-13
Date
Aug-2005
Language
English
Publication Type
Article
Keywords
Databases, Factual
Female
Finland
Glucose - pharmacology
Glucose Clamp Technique
Glucose Tolerance Test
Humans
Insulin - genetics - metabolism
Islets of Langerhans - metabolism
Male
Models, Statistical
Phenotype
Twins, Dizygotic
Twins, Monozygotic
Abstract
The genetic architecture of model-derived parameters of beta cell function has never been assessed. Therefore, we estimated heritability (h(2)) for model-derived phenotypes of insulin secretion in twins.
Thirty-three monozygotic (MZ) and 23 dizygotic (DZ) twin pairs from the Finnish Twin Cohort Study underwent an OGTT (plasma glucose/C-peptide at 0, 30, 60, 90 and 120 min). A subset of the twin pairs (21 MZ/20 DZ) also underwent an IVGTT (frequent sampling of plasma glucose/insulin from 0 to 60 min) followed by a 160-min euglycaemic-hyperinsulinaemic clamp (45 mU.min(-1).m(-2)). Mathematical modelling was applied to the IVGTT and the OGTT to assess first-phase (readily releasable insulin [RRI]) and second-phase (sigma) secretion (IVGTT), and a global index of beta cell performance (OGTT beta index). Intraclass correlation coefficients and genetic and non-genetic components for trait variances were computed to assess the h(2) of model-derived parameters.
The intraclass correlation coefficients in MZ twins were 0.78 for RRI, 0.67 for sigma and 0.57 for OGTT beta index. In DZ twins the correlation coefficients were 0.23, 0.32 and 0.42, respectively. Using the most parsimonious model for each trait, the h(2)--the proportion of variance accounted for by genetic factors--was 76% (95% CI: 53-88%) for RRI, 28% (34-80%) for sigma and 53% (26-72%) for OGTT beta index.
Our findings demonstrate that model-derived parameters of insulin secretion have a substantial genetic component and may be used in the search for genetic determinants of beta cell function in humans.
PubMed ID
15977011 View in PubMed
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28 records – page 1 of 3.