Glut4

[Popa Murph]

An interesting little study.


Titre du document / Document title
Prevention of glycogen supercompensation prolongs the increase in muscle GLUT4 after exercise
Auteur(s) / Author(s)
GARCIA-ROVES Pablo M. (1) ; HAN Dong-Ho (1) ; ZHENG SONG (1) ; JONES Terry E. (1) ; HUCKER Kathleen A. (1) ; HOLLOSZY John O. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, ETATS-UNIS
Résumé / Abstract
June 10, 2003; 10.1152/ajpendo.00216.2003.-Exercise induces an increase in GLUT4 in skeletal muscle with a proportional increase in glucose transport capacity. This adaptation results in enhanced glycogen accumulation, i.e., supercompensation, in response to carbohydrate feeding after glycogen-depleting exercise. The increase in GLUT4 reverses within 40 h after exercise in carbohydrate-fed rats. The purpose of this study was to determine whether prevention of skeletal muscle glycogen supercompensation after exercise results in maintenance of the increases in GLUT4 and the capacity for glycogen supercompensation. Rats were exercised by means of three daily bouts of swimming. GLUT4 mRNA was increased ∼3-fold and GLUT4 protein was increased ∼2-fold 18 h in epitrochlearis muscle after exercise. These increases in GLUT4 mRNA and protein reversed completely within 42 h after exercise in rats fed a high-carbohydrate diet. In contrast, the increases in GLUT4 protein, insulin-stimulated glucose transport, and increased capacity for glycogen supercompensation persisted unchanged for 66 h in rats fed a carbohydrate-free diet that prevented glycogen supercompensation after exercise. GLUT4 mRNA was still elevated at 42 h but had returned to baseline by 66 h after exercise in rats fed the carbohydrate-free diet. Glycogen-depleted rats fed carbohydrate 66 h after exercise underwent muscle glycogen supercompensation with concomitant reversal of the increase in GLUT4. These findings provide evidence that prevention of glycogen supercompensation after exercise results in persistence of exercise-induced increases in GLUT4 protein and enhanced capacity for glycogen supercompensation.
Revue / Journal Title
American journal of physiology. Endocrinology and metabolism (Am. j. physiol., Endocrinol. metab.) ISSN 0193-1849 CODEN AJPMD9
Source / Source
2003, vol. 48, no4, pp. E729-E736 (47 ref.)
Langue / Language
Anglais
Editeur / Publisher
American Physiological Society, Bethesda, MD, ETATS-UNIS (1980) (Revue)
Mots-clés anglais / English Keywords
Pancreatic hormone ; Feeding behavior ; Feeding ; Carbohydrate ; Physical exercise ; Muscle ; Prolonged ; Glycogen ; Prevention ;
Mots-clés français / French Keywords
Hormone pancréatique ; Comportement alimentaire ; Alimentation ; Glucide ; Exercice physique ; Muscle ; Prolongé ; Glycogène ; Prévention ;

002a28 ;
Mots-clés espagnols / Spanish Keywords
Hormona pancreática ; Conducta alimenticia ; Alimentación ; Glúcido ; Ejercicio físico ; Músculo ; Prolongado ; Glicógeno ; Prevención ;
Mots-clés d'auteur / Author Keywords
carbohydrate feeding ; insulin responsiveness ; muscle glucose transport ;
Localisation / Location
INIST-CNRS, Cote INIST : 670 C1, 35400011307247.0070

 

[WSUstudent]

English please

 

[314]

fasting increases insulin sensitivity

 

[jonny21]

fasting increases insulin sensitivity

No, exercise increases glycogen storage potential in rats for 42 hours when fed carbohydrate. For those not fed carbohydrate post exercise remained in a state of increased glycogen storage potential for 66 hours after exercise.

 

[Ziricote]

And what about adipose tissue?

 

[jonny21]

And what about adipose tissue?

From what was originally posted who knows?

This is text from an online source:

"...most of the transport of glucose into muscle is by the insulin-dependent GLUT 4 carrier system. Besides causing increased glucose transport in muscle, insulin activates glycogen synthetase to cause glycogen synthesis and phosphofructokinase that is responsible for glucose use. During exercise, glucose uptake is independent of increased insulin secretion. During rest, muscle burns fatty acids, not glucose, for most of its energy.

In adipose tissue, the GLUT 4 carrier system is used for insulin -stimulated glucose transport. It activates enzymes involved in glucose metabolism (glycolysis). The ultimate conversion of glucose to alpha-glycerophosphate is important in fat storage because glycerophosphate esterifies with fats to form triglycerides..." Invalid Link Removed