GLUT-4 expression is not consistently higher in type-1 than in type-2 fibres of rat and human vastus lateralis muscles; an immunohistochemical study

2000 ◽  
Vol 441 (2-3) ◽  
pp. 351-358 ◽  
Author(s):  
Lars B. Borghouts ◽  
Gert Schaart ◽  
Matthijs K.C. Hesselink ◽  
Hans A. Keizer
Keyword(s):  
Immunohistochemical Study ◽  
Vastus Lateralis ◽  
Glut 4

Progressive metabolite changes in individual human muscle fibers with increasing work rates

1987 ◽  
Vol 252 (6) ◽  
pp. C630-C639 ◽  
Author(s):  
J. L. Ivy ◽  
M. M. Chi ◽  
C. S. Hintz ◽  
W. M. Sherman ◽  
R. P. Hellendall ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Vastus Lateralis ◽  
Muscle Fibers ◽  
Lactate Concentration ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Almost All ◽  
Fast Twitch

Muscle biopsies were obtained from vastus lateralis muscles of four volunteers exercising at increasing work rates on a bicycle ergometer. Samples were taken at rest (t1), after a work load 23% below the blood lactate threshold (t2), 23% above this threshold (t3), and at exhaustion (t4). Individual muscle fibers were typed by their lactate dehydrogenase and adenylokinase levels and assayed for lactate, glucose-6-phosphate, and malate, (which preliminary data indicated to be the most responsive to increased activity) as well as ATP and phosphocreatine. The results in three of the four cases indicated that by the time of the t2 sample, almost all fibers, regardless of type, had been recruited. Additionally, there were no major differences in lactate concentration between type 1 and 2 fibers from muscle samples taken at t1, t2, and t3. It is concluded that in a muscle with fast-twitch glycolytic and slow-twitch oxidative fibers, all fibers share in the contraction to a substantial degree, even at moderate work loads, and that both the type 1 and 2 fibers contribute significantly to the initial rise in blood lactate during a graded exercise task. Metabolite responses in type 2 fibers differed in certain respects among the four participants. This is attributed to differences in their training backgrounds and consequent differences in type 2 fiber oxidative enzyme levels.

Type 2 Diabetes Overtakes Type 1 in Hispanic Girls

2008 ◽  
Vol 38 (15) ◽  
pp. 18
Author(s):  
SHERRY BOSCHERT
Keyword(s):  
Type 2 Diabetes

Molecular analysis of FVIII gene in severe HA patients of Costa Rica

2010 ◽  
Vol 30 (S 01) ◽  
pp. S150-S152
Author(s):  
G. Jiménez-Cruz ◽  
M. Mendez ◽  
P. Chaverri ◽  
P. Alvarado ◽  
W. Schröder ◽  
...  
Keyword(s):  
Factor Viii ◽  
Coagulation Factor ◽  
Costa Rican ◽  
Factor Viii Gene ◽  
Intron 22 Inversion ◽  
Intron 1 ◽  
Polymerase Chain ◽  
Inversion Analysis

SummaryHaemophilia A (HA) is X-chromosome linked bleeding disorders caused by deficiency of the coagulation factor VIII (FVIII). It is caused by FVIII gene intron 22 inversion (Inv22) in approximately 45% and by intron 1 inversion (Inv1) in 5% of the patients. Both inversions occur as a result of intrachromosomal recombination between homologous regions, in intron 1 or 22 and their extragenic copy located telomeric to the FVIII gene. The aim of this study was to analyze the presence of these mutations in 25 HA Costa Rican families. Patients, methods: We studied 34 HA patients and 110 unrelated obligate members and possible carriers for the presence of Inv22or Inv1. Standard analyses of the factor VIII gene were used incl. Southern blot and long-range polymerase chain reaction for inversion analysis. Results: We found altered Inv22 restriction profiles in 21 patients and 37 carriers. It was found type 1 and type 2 of the inversion of Inv22. During the screening for Inv1 among the HA patient, who were Inv22 negative, we did not found this mutation. Discussion: Our data highlight the importance of the analysis of Inv22 for their association with development of inhibitors in the HA patients and we are continuous searching of Inv1 mutation. This knowledge represents a step for genetic counseling and prevention of the inhibitor development.

Polymorphisms of the Plasminogen Activator Inhibitor- 1 Gene in Type 1 and Type 2 Diabetes, and in Patients with Diabetic Retinopathy

1994 ◽  
Vol 71 (06) ◽  
pp. 731-736 ◽  
Author(s):  
M W Mansfield ◽  
M H Stickland ◽  
A M Carter ◽  
P J Grant
Keyword(s):  
Diabetic Retinopathy ◽  
Plasminogen Activator Inhibitor ◽  
Allelic Frequency ◽  
Repeat Sequence ◽  
Dinucleotide Repeat ◽  
Plasminogen Activator Inhibitor 1 ◽  
The Difference ◽  
Pai 1

SummaryTo identify whether genotype contributes to the difference in PAI-1 levels in type 1 and type 2 diabetic subjects and whether genotype relates to the development of retinopathy, a Hind III restriction fragment length polymorphism and two dinucleotide repeat polymorphisms were studied. In 519 Caucasian diabetic subjects (192 type 1, 327 type 2) and 123 Caucasian control subjects there were no differences in the frequency of the Hind III restriction alleles (type 1 vs type 2 vs control: allele 1 0.397 vs 0.420 vs 0.448; allele 2 0.603 vs 0.580 vs 0.552) nor in the allelic frequency at either dinucleotide repeat sequence. In 86 subjects with no retinopathy at 15 years or more from diagnosis of diabetes and 190 subjects with diabetic retinopathy there was no difference in the frequency of Hind III restriction alleles (retinopathy present vs retinopathy absent: allele 1 0.400 vs 0.467; allele 2 0.600 vs 0.533) nor in the allelic frequencies at either dinucleotide repeat sequence. The results indicate that there is no or minimal influence of the PAI-1 gene on either PAI-1 levels or the development of diabetic retinopathy in patients with diabetes mellitus.

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