Exchange of Metabolites in the Leg of Exercising Juvenile Diabetic Subjects

Lyngsøe, J.; Clausen, Jan; Trap‐Jensen, J.; Sestoft, L; Muckadell, O. Schaffalitzky de; Holst, Jens J.; Nielsen, Søren; Rehfeld, J. F.

doi:10.1042/cs0550073

Cited by 8 publications

(16 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the basal period, we found a net negative glucose balance of 0.30 ,gmol/ min per 100 ml tissue, comparable with those found by Andres et al (15) for forearm and Lyngsoe et al (38) for leg. Extrapolation of these data would indicate that overnight there had been -11 g depletion of body muscle glycogen, a value quite comparable with the overall amount of glucose that we found was stored in muscle (-10 g).…”

Section: Discussionsupporting

confidence: 79%

“…Before ingestion of glucose, the forearm released lactate and alanine at rates of0.38±0.12 and 0.28±0.06 Mmol/min per 100 ml tissues, respectively. After ingestion of (38). After glucose ingestion, the RQ increased to a peak of 1.07±0.05 at 60 min (P < 0.01) and returned to baseline at 240 min.…”

Section: Plasma For Determination Of [3h]-and ['4c]glucose Specific Amentioning

confidence: 93%

See 1 more Smart Citation

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Kelley¹,

Mitrakou²,

Marsh³

et al. 1988

J. Clin. Invest.

287

181

View full text Add to dashboard Cite

Although muscle is considered to be the most important site for postprandial glucose disposal, the metabolic fate of oral glucose taken up by muscle remains unclear. We, therefore, employed the dual isotope technique (intravenous, [6-3HJ-glucose; oral, l1-'4Clglucose), indirect calorimetry, and forearm balance measurements of glucose, lactate, alanine, pyruvate, 02, and CO2 in nine normal volunteers to determine the relative importance of muscle glycogenic, glycolytic, and oxidative pathways in disposal of an oral glucose load. During the 5 h after glucose ingestion (1 g/kg), 37±3% (24.9±2.3 g) of the load was oxidized and 63±3% (42.8±2.7 g) was stored. At least 29% (19.4±1.3 g) was taken up by splanchnic tissues. Muscle took up 26% (17.9±2.9 g) of the oral glucose coincident with a 50% reduction in its oxidation of fat. 15% of the oral glucose taken up by muscle (2.5±0.9 g) was released as lactate, alanine, or pyruvate; 50% (8.9±1.4 g) was oxidized, and 35% (6.4±2.3 g) was available for storage. We conclude that muscle and splanchnic tissues take up a comparable percentage of an oral glucose load and that oxidation is the predominant fate of glucose taken up by muscle, with storage in muscle accounting for < 10% of the oral load. Thus, contrary to the prevailing view, muscle is neither the major site of storage nor the predominant site of disposal of an oral glucose load.

show abstract

Section: Discussionsupporting

confidence: 79%

Section: Plasma For Determination Of [3h]-and ['4c]glucose Specific Amentioning

confidence: 93%

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Kelley¹,

Mitrakou²,

Marsh³

et al. 1988

J. Clin. Invest.

287

181

View full text Add to dashboard Cite

show abstract

“…In the present study, substrate oxidation during a 60-min exercise period at 50% V O max after ingestion of 30 g of glucose was compared in diabetic patients receiving their usual insulin dose and in control subjects. The glucose ingested was artificially labeled with 13 C to compute the oxidation of exogenous glucose, plasma glucose, glucose released from the liver, and muscle glycogen from calorimetry data and 13 CO 2 production at the mouth, and from the 13 C enrichment of plasma glucose (3,5,6,9,20). On the basis of data from Krzentowski et al (11) and Riddell et al (24), we hypothesized that, during exercise, exogenous and endogenous CHO oxidation, respectively, will not be different in the diabetic patients and control subjects.…”

mentioning

confidence: 99%

Substrate source utilization during moderate intensity exercise with glucose ingestion in Type 1 diabetic patients

Robitaille¹,

Dubé²,

Weisnagel³

et al. 2007

Journal of Applied Physiology

View full text Add to dashboard Cite

Substrate oxidation and the respective contributions of exogenous glucose, glucose released from the liver, and muscle glycogen oxidation were measured by indirect respiratory calorimetry combined with tracer technique in eight control subjects and eight diabetic patients (5 men and 3 women in both groups) of similar age, height, body mass, and maximal oxygen uptake, over a 60-min exercise period on cycle ergometer at 50.8% (SD 4.0) maximal oxygen uptake [131.0 W (SD 38.2)]. The subjects and patients ingested a breakfast (containing approximately 80 g of carbohydrates) 3 h before and 30 g of glucose (labeled with 13C) 15 min before the beginning of exercise. The diabetic patients also received their usual insulin dose [Humalog = 9.1 U (SD 0.9); Humulin N = 13.9 U (SD 4.4)] immediately before the breakfast. Over the last 30 min of exercise, the oxidation of carbohydrate [1.32 g/min (SD 0.48) and 1.42 g/min (SD 0.63)] and fat [0.33 g/min (SD 0.10) and 0.30 g/min (SD 0.10)] and their contribution to the energy yield were not significantly different in the control subjects and diabetic patients. Exogenous glucose oxidation was also not significantly different in the control subjects and diabetic patients [6.3 g/30 min (SD 1.3) and 5.2 g/30 min (SD 1.6), respectively]. In contrast, the oxidation of plasma glucose and oxidation of glucose released from the liver were significantly lower in the diabetic patients than in control subjects [14.5 g/30 min (SD 4.3) and 9.3 g/30 min (SD 2.8) vs. 27.9 g/30 min (SD 13.3) and 21.6 g/30 min (SD 12.8), respectively], whereas that of muscle glycogen was significantly higher [28.1 g/30 min (SD 15.5) vs. 11.6 g/30 min (SD 8.1)]. These data indicate that, compared with control subjects, in diabetic patients fed glucose before exercise, substrate oxidation and exogenous glucose oxidation overall are similar but plasma glucose oxidation is lower; this is associated with a compensatory higher utilization of muscle glycogen.

show abstract

“…Ainsi, même si l'insulinémie décroît lors de l'effort musculaire, son efficacité paraît renforcée [20]. La carence insulinique n'empêche pas l'accroissement de consommation musculaire de glucose lors de l'effort [24] . Cependant, la majoration excessive de la néoglucogénèse amène l'aggravation de l'hyperglycémie et de la cétonémie [5].…”

Section: La Fatigue Dans Les Maladies Endocriniennesunclassified

Aspects endocriniens de la fatigue chronique

Mirouze¹,

Renard²

1991

Syndrome De Fatigue Chronique / Chronic Fatigue Syndrome

View full text Add to dashboard Cite

Aspects endocriniens de la fatigue chronique J Mirouze et E RenardLa fatigue, sous ses formes neuropsychique ou neuromusculaire, est une composante sémiologique de nombreuses pathologies. L'expérience clinique des maladies endocriniennes permet de retenir le rôle de perturbations hormonales dans sa constitution. Différents mécanismes physiopathologiques hormonodépendants sont impliqués, tant au niveau musculaire qu'au plan du système nerveux central pour concourir à la fatigue. Inversement, la fatigue chronique de nature endogène telle qu'observée dans les états dépressifs est à l'origine de modifications neuro-endocriniennes, confirmant ainsi l'étroite intrication des processus. La boucle d'interdépendance entre les désordres endocriniens et l'état de fatigue chronique conduit à envisager la possibilité de terrains propices à l'installation d'un tel cercle vicieux. L'approche génétique et l'analyse moléculaire de la biochimie cellulaire peuvent s'avérer des voies nouvelles pour appréhender la fatigue sur un mode uniciste plutôt qu'à travers ses différents aspects sectoriels attachés à un organe ou à un appareil. G. Serratrice et al. (eds.), Syndrome de Fatigue Chronique / Chronic Fatigue Syndrome © Springer-Verlag France, Paris 1991

show abstract

Exchange of Metabolites in the Leg of Exercising Juvenile Diabetic Subjects

Cited by 8 publications

References 9 publications

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Skeletal muscle glycolysis, oxidation, and storage of an oral glucose load.

Substrate source utilization during moderate intensity exercise with glucose ingestion in Type 1 diabetic patients

Aspects endocriniens de la fatigue chronique

Contact Info

Product

Resources

About