Insulin sensitivity and glucose disposal -
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Magnesium for ADHD you Elite athletic performance visiting nature. You are Insluin a browser version densitivity limited hlucose for CSS. To obtain the Inulin experience, we recommend you Insulin sensitivity and glucose disposal a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. β 2 -agonist treatment improves skeletal muscle glucose uptake and whole-body glucose homeostasis in rodents, likely via mTORC2-mediated signalling. However, human data on this topic is virtually absent. Cardiovascular Sensitiivity volume 22 Elite athletic performance, Article Elite athletic performance Cite this article. Metrics details. Estimated Insupin disposal rate eGDRa simple Coping with work-related stress noninvasive measure Ineulin insulin resistance, has been sensitiviyt to be an independent risk glucosw for first-time stroke and all-cause mortality. In this study, we aimed to investigate the associations between eGDR and the stroke outcome in patients with first-time acute ischemic stroke AIS. The primary outcome was excellent functional outcome modified Rankin Scale score 0—1 at 3 months. Secondary outcomes included stroke recurrence and favorable functional outcome modified Rankin Scale score 0—2 at 3 months, and functional outcome and combined vascular event at one year.Insulin sensitivity and glucose disposal -
Sano H, Kane S, Sano E et al Insulin-stimulated phosphorylation of a Rab GTPase-activating protein regulates GLUT4 translocation.
Miinea CP, Sano H, Kane S et al AS, the Akt substrate regulating GLUT4 translocation, has a functional Rab GTPase activating protein domain. Biochem J — Larance M, Ramm G, Stockli J et al Characterization of the role of the Rab GTPase-activating protein AS in insulin-regulated GLUT4 trafficking.
Zeigerer A, McBrayer MK, McGraw TE Insulin stimulation of GLUT4 exocytosis, but not its inhibition of endocytosis, is dependent on RabGAP AS Mol Biol Cell — Bruss MD, Arias EB, Lienhard GE, Cartee GD Increased phosphorylation of Akt substrate of kDa AS in rat skeletal muscle in response to insulin or contractile activity.
Bogardus C, Thuillez P, Ravussin E, Vasquez B, Narimiga M, Azhar S Effect of muscle glycogen depletion on in vivo insulin action in man. Kennedy JW, Hirshman MF, Gervino EV et al Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes.
Price TB, Rothman DL, Taylor R, Avison MJ, Shulman GI, Shulman RG Human muscle glycogen resynthesis after exercise: insulin-dependent and -independent phases.
Devlin JT, Horton ES Effects of prior high intensity exercise on glucose metabolism in normal and insulin-resistant men. Perseghin G, Price TB, Petersen KF et al Increased glucose transport-phosphorylation and muscle glycogen synthesis after exercise training in insulin-resistant subjects.
Ross R, Janssen I, Dawson J et al Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial.
Obes Res — PubMed Google Scholar. Dela F, Mikines KJ, Sonne B, Glabo H Effect of training on interaction between insulin and exercise in human muscle.
Christ-Roberts CY, Pratipanawatr T, Pratipanawatr W et al Exercise training increases glycogen synthase activity and GLUT4 expression but not insulin signalling in overweight nondiabetic and type 2 diabetic subjects. Metabolism — Higaki Y, Wojtaszewski JFP, Hirshman MF et al Insulin receptor substrate-2 is not necessary for insulin- and exercise-stimulated glucose transport in skeletal muscle.
Ahmad F, Azevedo JL, Cortright R, Dohm GL, Goldstein BJ Alterations in skeletal muscle protein-tyrosine phosphatase activity and expression in insulin-resistant human obesity and diabetes.
Google Scholar. Christ CY, Hunt D, Hancock J, Garcia-Macedo R, Mandarino LJ, Ivy JL Exercise training improves muscle insulin resistance but not insulin receptor signalling in obese Zucker rats. Staubs PA, Nelson JG, Reichart DR, Olefsky JM Platelet-derived growth factor inhibits insulin stimulation of insulin receptor substrateassociated phosphatidylinositol 3-kinase in 3T3-L1 adipocytes without affecting glucose transport.
Sharma PM, Egawa K, Gustafson TA, Martin JL, Olefsky JM Adenovirus-mediated overexpression of IRS-1 interacting domains abolishes insulin-stimulated mitogenesis without affecting glucose transport in 3T3-L1 adipocytes.
Mol Cell Biol — Deshmukh A, Coffey VG, Ahong Z, Chibalin AV, Hawley JA, Zierath JR Exercise-induced phosphorylation of the novel Akt substrates AS and Filamin in human skeletal muscle. Treebak JT, Glund S, Deshmukt A et al AMPK-mediated AS phosphorylation in skeletal muscle is dependent on AMPK catalytic and regulatory subunits.
Karlsson HKR, Zierath JR, Kane S, Krook A, Lienhard GE, Wallberg-Henriksson H Insulin-stimulated phosphorylation of the Akt substrate AS is impaired in skeletal muscle of type 2 diabetic subjects. Karlsson HKR, Hallsten K, Bjornholm M et al Effects of metformin and rosiglitazone treatment on insulin signalling and glucose uptake in patients with newly diagnosed type 2 diabetes.
Wadley GD, Tunstall RJ, Sanigorski A, Collier GR, Hargreaves M, Cameron-Smith D Differential effects of exercise on insulin-signalling gene expression in human skeletal muscle.
Koistinen HA, Galuska D, Chibalin AV et al 5-Amino-imidazole carboxamide riboside increases glucose transport and cell-surface GLUT4 content in skeletal muscle from subjects with type 2 diabetes.
Download references. This study was supported by a grant from the Irish Health Research Board, the Swedish Research Council, the Swedish Diabetes Association, the Foundation for Scientific Studies of Diabetology, the Strategic Research Foundation, the Swedish Centre for Sports Research, the Commission of the European Communities Contract No LSHM-CT EXGENESIS and Contract No LSHM-CT EUGENE2.
McQuaid, O. Yousif, Y. Rahman, D. Department of Molecular Medicine and Surgery, Section of Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. Karlsson, S. Glund, A. You can also search for this author in PubMed Google Scholar. Correspondence to J.
Reprints and permissions. et al. Exercise training increases insulin-stimulated glucose disposal and GLUT4 SLC2A4 protein content in patients with type 2 diabetes.
Diabetologia 49 , — Download citation. Received : 26 April Accepted : 08 August Published : 26 September Issue Date : December Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Results Insulin-mediated glucose disposal was unchanged following acute exercise in both groups.
Exercise and Type 2 Diabetes Chapter © High-Protein Plant-Based Diet Versus a Protein-Matched Omnivorous Diet to Support Resistance Training Adaptations: A Comparison Between Habitual Vegans and Omnivores Article 18 February Sarcopenia: no consensus, no diagnostic criteria, and no approved indication—How did we get here?
Article Open access 24 November Use our pre-submission checklist Avoid common mistakes on your manuscript. Introduction Whole-body insulin-stimulated glucose disposal is reduced in obesity and type 2 diabetes [ 1 , 2 ].
Experimental design Baseline insulin sensitivity was determined by a 2-h euglycaemic—hyperinsulinaemic clamp. Euglycaemic—hyperinsulinaemic clamp Dietary advice was provided to the subjects to ensure they consumed a balanced, energy-sufficient diet for 2 days prior to the clamp.
Schematic representation of the study design. Full size image. Table 1 Physical and metabolic descriptive characteristics Full size table.
Table 2 IRS1-, IRS2- and phosphotyrosine-associated PI3K activity before and after insulin infusion at baseline, and following 1 day and 7 days of exercise in obese type 2 diabetic and obese non-diabetic subjects Full size table.
Discussion Exercise is the cornerstone of type 2 diabetes prevention and treatment. Abbreviations AMPK: AMP-activated protein kinase AS substrate of phosphorylated Akt DTT: dithiothreitol GAP: GTPase activating protein GIR: glucose infusion rate PI3K: phosphatidylinositol 3-kinase V O 2peak : peak oxygen uptake.
References Cline GW, Petersen KF, Krssak M et al Impaired glucose transport as a cause of decreased insulin-stimulated muscle glycogen synthesis in Type 2 diabetes. N Engl J Med — Article PubMed CAS Google Scholar Cusi K, Maezonon K, Osman A et al Insulin resistance differentially affects the PI3-kinase- and MAP kinase-mediated signalling in human muscle.
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Diabetologia — Article PubMed CAS Google Scholar Dresner A, Laurent D, Marcucci M et al Effects of free fatty acids on glucose transport and IRSassociated phosphatidylinositol 3-kinase activity. J Clin Invest — PubMed CAS Google Scholar Groop LC, Bonadonna RC, Del Prato S et al Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus.
J Clin Invest — PubMed CAS Google Scholar Bjornholm M, Kawano Y, Lehtihet M, Zierath JR Insulin receptor substrate-1 phosphorylation and phosphatidylinositol 3-kinase activity in skeletal muscle from NIDDM subjects after in vivo insulin stimulation. Diabetes — PubMed CAS Google Scholar Krook A, Björnholm M, Galuska D et al Characterization of signal transduction and glucose transport in skeletal muscle from Type 2 diabetic patients.
J Clin Invest — PubMed CAS Google Scholar Pedersen O, Bak JF, Andersen PH et al Evidence against altered expression of GLUT1 or GLUT4 in skeletal muscle of patients with obesity or NIDDM. Diabetes — PubMed CAS Google Scholar Dela F, Larsen JJ, Mikines KJ, Ploug T, Petersen LN, Galbo H Insulin-stimulated muscle glucose clearance in patients with NIDDM: effects of one-legged physical training.
Diabetes — PubMed CAS Google Scholar Houmard JA, Shaw CD, Hickey MS, Tanner CJ Effect of short-term exercise training on insulin-stimulated PI3-kinase activity in human skeletal muscle.
Am J Physiol E—E PubMed CAS Google Scholar Chibalin AV, Yu M, Ryder JW et al Exercise-induced changes in expression and activity of proteins involved in insulin signal transduction in skeletal muscle: differential effects in insulin-receptor substrates 1 and 2.
J Appl Physiol — PubMed CAS Google Scholar Yu M, Blomstrand E, Chibalin AV, Wallberg-Henriksson H, Zierath JR, Krook A Exercise-associated differences in an array of proteins involved in signal transduction and glucose transport.
J Appl Physiol —34 PubMed CAS Google Scholar Cox JH, Cortright RN, Dohm GL, Houmard JA Effect of aging on response to exercise training in humans: skeletal muscle GLUT-4 and insulin sensitivity. J Appl Physiol — PubMed CAS Google Scholar Gulve EA, Spina RJ Effect of 7—10 days of cycle ergometer exercise on skeletal muscle GLUT-4 protein content.
J Appl Physiol — PubMed CAS Google Scholar Phillips SM, Han X-X, Green HJ, Bonen A Increments in skeletal muscle GLUT-1 and GLUT-4 after endurance training in humans. J Biol Chem — PubMed CAS Google Scholar Dela F, Ploug T, Handberg A et al Physical training increases muscle GLUT4 protein and mRNA in patients with NIDDM.
Diabetes — PubMed CAS Google Scholar Tanner CJ, Koves TR, Cortright RL et al Effect of short-term exercise training on insulin-stimulated PI3-kinase activity in middle aged men. Am J Physiol E—E CAS Google Scholar Sano H, Kane S, Sano E et al Insulin-stimulated phosphorylation of a Rab GTPase-activating protein regulates GLUT4 translocation.
J Biol Chem — Article PubMed CAS Google Scholar Miinea CP, Sano H, Kane S et al AS, the Akt substrate regulating GLUT4 translocation, has a functional Rab GTPase activating protein domain. Biochem J —93 Article PubMed CAS Google Scholar Larance M, Ramm G, Stockli J et al Characterization of the role of the Rab GTPase-activating protein AS in insulin-regulated GLUT4 trafficking.
J Biol Chem — Article PubMed CAS Google Scholar Zeigerer A, McBrayer MK, McGraw TE Insulin stimulation of GLUT4 exocytosis, but not its inhibition of endocytosis, is dependent on RabGAP AS Mol Biol Cell — Article PubMed CAS Google Scholar Bruss MD, Arias EB, Lienhard GE, Cartee GD Increased phosphorylation of Akt substrate of kDa AS in rat skeletal muscle in response to insulin or contractile activity.
Diabetes —50 PubMed CAS Google Scholar Bogardus C, Thuillez P, Ravussin E, Vasquez B, Narimiga M, Azhar S Effect of muscle glycogen depletion on in vivo insulin action in man.
J Appl Physiol — PubMed CAS Google Scholar Kennedy JW, Hirshman MF, Gervino EV et al Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Diabetes — PubMed CAS Google Scholar Price TB, Rothman DL, Taylor R, Avison MJ, Shulman GI, Shulman RG Human muscle glycogen resynthesis after exercise: insulin-dependent and -independent phases.
J Appl Physiol — Article PubMed CAS Google Scholar Devlin JT, Horton ES Effects of prior high intensity exercise on glucose metabolism in normal and insulin-resistant men.
Diabetes — PubMed CAS Google Scholar Perseghin G, Price TB, Petersen KF et al Increased glucose transport-phosphorylation and muscle glycogen synthesis after exercise training in insulin-resistant subjects.
N Engl J Med — Article PubMed CAS Google Scholar Ross R, Janssen I, Dawson J et al Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial.
Obes Res — PubMed Google Scholar Dela F, Mikines KJ, Sonne B, Glabo H Effect of training on interaction between insulin and exercise in human muscle. J Appl Physiol — PubMed CAS Google Scholar Christ-Roberts CY, Pratipanawatr T, Pratipanawatr W et al Exercise training increases glycogen synthase activity and GLUT4 expression but not insulin signalling in overweight nondiabetic and type 2 diabetic subjects.
Metabolism — Article PubMed CAS Google Scholar Higaki Y, Wojtaszewski JFP, Hirshman MF et al Insulin receptor substrate-2 is not necessary for insulin- and exercise-stimulated glucose transport in skeletal muscle. J Biol Chem — Article PubMed CAS Google Scholar Ahmad F, Azevedo JL, Cortright R, Dohm GL, Goldstein BJ Alterations in skeletal muscle protein-tyrosine phosphatase activity and expression in insulin-resistant human obesity and diabetes.
J Biol Chem — Google Scholar Christ CY, Hunt D, Hancock J, Garcia-Macedo R, Mandarino LJ, Ivy JL Exercise training improves muscle insulin resistance but not insulin receptor signalling in obese Zucker rats. J Appl Physiol — Article PubMed CAS Google Scholar Staubs PA, Nelson JG, Reichart DR, Olefsky JM Platelet-derived growth factor inhibits insulin stimulation of insulin receptor substrateassociated phosphatidylinositol 3-kinase in 3T3-L1 adipocytes without affecting glucose transport.
When SSPG was paired with each of the other variables in a series of multiple regression models, only SSPG, or insulin response, were independent predictors of CVD events.
In conclusion, approximately one of every five healthy, nonobese subjects in the most insulin-resistant tertile, followed for approximately 5 yr, had a serious clinical event.
These data highlight the importance of insulin resistance as a predictor of CVD. THE ability of insulin to stimulate glucose disposal varies widely in a healthy, nondiabetic population, and a substantial number of such individuals are as approximately insulin resistant as are glucose-intolerant subjects 1 , 2.
What apparently permits insulin-resistant individuals to remain glucose tolerant is their ability to sustain the degree of compensatory hyperinsulinemia needed to overcome the defect in insulin action. Unfortunately, the hyperinsulinemia required to maintain glucose homeostasis has been implicated as a predictor of cardiovascular disease CVD in a number of prospective epidemiological studies 3 — 6.
On the other hand, controversy continues as to the status of hyperinsulinemia as a risk factor for CVD 7 , 8. One possible explanation for the lack of consensus may be because of the fact that hyperinsulinemia is only a surrogate measure of insulin resistance and only one of the consequences of this defect 9 — Indeed, results of several recent cross-sectional studies have suggested that insulin resistance per se is a more powerful predictor of CVD 12 — However, we are unaware of any prospective assessment of the role that differences in insulin-mediated glucose disposal might play as a predictor of CVD events.
The study to be presented was initiated to address this issue, and involved the examination of the interaction between insulin resistance, and associated atherosclerotic risk factors, in the development of CVD in healthy, nonobese male and female volunteers followed for a minimum of 4 yr.
Baseline evaluation included a physical examination, an electrocardiogram, and a complete blood count, and blood chemistry panel to ensure good general health. All subjects with a past history of CVD or hypertension were excluded, as were individuals with an abnormal electrocardiogram.
Baseline measurements included weight, height, sitting BP, and fasting lipid and lipoproteins A g oral glucose tolerance test was done with blood samples for glucose 17 and insulin 18 drawn at 0, 30, 60, , and min.
The area under the curve was calculated by the trapezoidal formula to estimate the postload glucose and insulin areas. Any subject who was found to be diabetic by oral glucose tolerance according to the WHO criteria was eliminated from the study. Insulin resistance was measured by insulin suppression test as previously described Information on smoking history was obtained.
Smokers were those who were currently smoking cigarettes or had done so within the last 5 yr; all others were classified as nonsmokers. Physical activity was measured by the number of physical activities per week that were associated with sweating At follow-up, each subject was asked about current medication use and history of neurological deficits and asked to complete a screening questionnaire on chest pain and intermittent claudication For those who could not be reached and failed to return the questionnaire, it was assumed that either they had moved away without leaving a forwarding address or had died.
The names of these individuals were submitted to the Office of State Registrar in California for search against the death registry and the examination of the death certificate.
The study end points were the development of hypertension or CVD; the latter category included fatal or nonfatal coronary artery disease, fatal or nonfatal cerebral vascular accident, or peripheral vascular disease.
Hypertension was defined by the use of antihypertensive medication. Coronary artery disease included chest pain with positive stress test, percutaneous transluminal angioplasty, coronary bypass surgery, or documented myocardial infarction. Cerebral vascular accident included documented clinical neurological deficit, lasting over 24 h, with or without radiographic evidence.
The diagnosis of peripheral vascular disease was made clinically by history and examination, which demonstrated diminished pedal pulses with poor capillary return or arterial ulceration. All results are expressed as arithmetic or geometric mean ± se. Results were analyzed by ANOVA and contingency table as appropriate.
Nonparametric variables: triglycerides, postload insulin area, and steady state plasma glucose concentration were log-transformed before analysis. Univariate and multivariate logistic regression analyses were used to assess the relationship and interaction of baseline variables and the presence of cardiovascular disease as a categorical outcome.
The baseline clinical characteristics between those who participated and those lost to follow-up were similar in terms of age 50 ± 1 vs. A diagnosable disease developed in 13 subjects 6 males, 7 females during the follow-up period: hypertension in 5, coronary artery disease in 4, cerebral vascular accident in 3, and 1 with peripheral vascular disease.
There was one noncardiovascular death reported. The search through the State of California Death Registry between and the end of was negative for those individuals who were lost to follow-up.
The relationship between the development of disease, hypertension plus CVD, as a function of tertiles of baseline SSPG, is shown in the top half of Fig. It is clear from these data that neither hypertension nor CVD developed in the one third of the population that was most insulin sensitive tertile I.
In contrast, almost one of every five individuals in the most insulin-resistant tertile tertile III developed hypertension or CVD during the period of observation. Relationship between tertile of SSPG from lowest tertile I to highest tertile III and incidence of hypertension plus CVD top and only CVD bottom.
The bottom half of Fig. As in the case of the combined events shown above, CVD did not develop in the most insulin-sensitive tertile. In marked contrast, seven of the eight subjects in whom CVD was documented came from the most insulin-resistant tertile.
The baseline characteristics of the three tertiles are seen in Table 1. When subjects in the highest tertile highest SSPG values were compared with those in the lowest tertile, it can be seen that they differed in multiple variables.
To evaluate the link between SSPG and CVD events, it seemed necessary at first to define the relationship between SSPG and its related variables, adjusting for difference in age, gender, BMI, smoking, and estimates of physical activity. The results of this analysis are given in Table 2 , and it is apparent that SSPG was significantly related to diastolic blood pressure, plasma triglyceride concentration, low-density lipoprotein LDL and high-density lipoprotein HDL cholesterol concentrations, and the glucose and insulin responses to oral glucose.
Characteristics of subjects divided into tertiles according to baseline steady state plasma glucose concentration. Relationship between SSPG and other CVD risk factors—adjusting for age, gender, BMI, exercise, and smoking. Based on the relationships shown in Table 2 , it was not possible to determine whether insulin resistance SSPG , or some variable related to SSPG, was linked to CVD.
Consequently, we ascertained the relationship between SSPG, the variables related to it as seen in Table 2 , and CVD.
The results of this analyses are seen in Table 3 , and demonstrate the presence of a significant univariate relationship between CVD and diastolic blood pressure, triglyceride and HDL cholesterol concentrations, SSPG, and the plasma glucose and insulin responses to the glucose challenge.
Having established the existence of significant relationships between SSPG, as well as other factors related to SSPG, and CVD risk, multiple logistic regression analysis was used in an attempt to estimate the likelihood that the univariate relationship between SSPG and CVD shown in Table 3 was attributable to insulin resistance, as differentiated from the metabolic abnormalities shown in Table 2 to be linked to this defect.
This was done by comparing the degree to which SSPG and each of the relevant individual variables defined in Table 3 predicted CVD. These results are shown in Table 4 , and it is apparent that SSPG remained significantly related to CVD when compared with any of the other individual CVD risk factors.
Furthermore, it can be seen that SSPG was the only variable that remained significantly related to CVD when all of the significant factors from Table 3 were entered into the model. However, essentially similar results were seen when SSPG was replaced by insulin response.
Multiple logistic regression analysis of relationship between SSPG, its associated variables, and CVD. The concept that resistance to insulin-mediated glucose uptake represented a fundamental abnormality that predisposed otherwise healthy individuals to develop a cluster of risk factors for CVD was first clearly articulated in 9.
However, acceptance of the causal relationship between insulin resistance and CVD has been tempered by conflicting results 3 — 8 as to the association between hyperinsulinemia a surrogate measure of insulin resistance and CVD. One way out of this quandary is to suggest that insulin resistance, not hyperinsulinemia, increases risk of CVD: a conclusion reached in several cross-sectional studies 12 — On the other hand, it is not a simple task to differentiate between the role of insulin resistance increasing risk of CVD, as distinguished from any of its consequences.
At the least, it should be possible to demonstrate in a prospective study that differences in insulin-mediated glucose disposal predict risk of CVD. As of now, we are unaware of any such study showing that insulin resistance, per se , can predict CVD events.
We believe that the results presented provide evidence for the first time that this is the case. The results shown in Fig. Focusing on CVD alone, it is apparent that seven of the eight subjects who developed CVD during the period of observation were in the most insulin-resistant tertile.
These data provide substantial support for the view that the presence of insulin resistance identifies a subset of the population who will develop CVD over a relatively short time period. On the other hand, the data in Table 1 clearly demonstrate that the tertile of the most insulin-resistant subjects share a variety of known risk factors for CVD.
Consequently, any effort to identify insulin resistance as the predictor of the observed CVD events must take these other factors into account. This analysis was performed, and results from Table 2 identify six CVD risk factors that were independently related to SSPG adjusting for differences in age, gender, BMI and history of smoking and activity level : diastolic blood pressure, triglyceride and LDL and HDL cholesterol concentrations, and the plasma glucose and insulin responses to oral glucose.
Furthermore, the results in Table 3 show that SSPG, as well as all of the above variables with the exception of LDL cholesterol were significantly correlated with a CVD event.
The information in Tables 2 and 3 were then used in multiple logistic regression analysis with CVD as the outcome, in which SSPG was paired with each of the other variables significantly related to CVD. This output contributes to the following UN Sustainable Development Goals SDGs.
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Exercise enhances insulin-stimulated Minerals for cardiovascular health transport cisposal skeletal muscle through changes in signal transduction and gene Elite athletic performance. The Nutrition for chronic injury prevention of this Elite athletic performance was to assess the impact of acute and short-term dsiposal training on Insulin sensitivity and glucose disposal glucoze glucose disposal and signal transduction sensitivitty the canonical insulin signalling cascade. Insulin-mediated glucose disposal was unchanged following acute exercise in both groups. Insulin activation of 1 IRS1, 2 IRS2, 3 phosphotyrosine-associated phosphatidylinositol-3 kinase activity and 4 the substrate of phosphorylated Akt, AS, a functional Rab GTPase activating protein important for GLUT4 now known as solute carrier family 2 [facilitated glucose transporter], member 4 [SLC2A4] translocation, was unchanged after acute or chronic exercise in either group. Exercise training increased whole-body insulin-mediated glucose disposal in obese type 2 diabetic patients.
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