Physical activity, sport, and pediatric diabetes

Riddell, M. C.; Iscoe, KE

doi:10.1111/j.1399-543x.2006.00146.x

Cited by 129 publications

(115 citation statements)

References 84 publications

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“…Some evidence suggests that optimal metabolic control maximises physical performance in patients with diabetes, although more studies are needed to confirm this suggestion. With the increasing prevalence of T1DM and T2DM patients, the importance of physical exercise to help prevent T1DM and T2DM in patients is of more recent consideration [1,2].…”

Section: Introductionmentioning

confidence: 99%

“…It is likely that excess caloric intake to prevent or treat hypoglycemia may counter the beneficial effects of exercise on glycemic control in some subjects because standardised carbohydrate and insulin modifications for active patients are not readily available. Nonetheless, the goal of physical exercise should be to increase SI index of the patients with T1DM and T2DM, regardless of any putative benefits to blood glucose management [1,2].…”

Section: Introductionmentioning

confidence: 99%

“…Additional benefits specific to diabetes include improved SI index, a diminished glycemic response to a meal, and a reduction in daily insulin needs [1,3,4].…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Physical Exercise on the Insulin-Dependent Diabetes Mellitus Subjects Using the Modified Minimal Model

Kartono

Irawati

Setiawan

et al. 2017

Int J Pharm Pharm Sci

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Objective: In this paper, the modified minimal model (MM) with a mathematical function for describing the insulin infusion rates was used to study of the effects of physical exercise on the dynamics of glucose and insulin on the insulin dependent diabetes mellitus (IDDM), including type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) subjects. Methods:In an intravenous glucose tolerance test (IVGTT) procedure, a dose of glucose was administered intravenously to overnight-fasted subjects, 20 min after the glucose bolus, insulin was injected over 1-2 min either into the portal vein or into the femoral vein, and subsequently the glucose and insulin concentrations in plasma were frequently sampled (usually 30 times) over a period of 180 min. The dynamic glucose and insulin responses to glucose and insulin injection were analysed using the modified MM without and with physical exercise from IVGTT data. Results:Our simulation results shown physical exercise improved blood glucose control and enhanced insulin sensitivity (SI) index in subjects with T1DM and T2DM. However, the T1DM and T2DM subjects need to be aware of the basic strategies to prevent hypoglycemia and maintain reasonable glucose control. It should be noted that the putative improvement in exercise-induced peripheral SI index in subjects with T1DM and T2DM was not always coincidental with the improvement of the insulin dosage. Conclusion:The feature increased physical exercise, along with knowledge about how to modify daily insulin dosage to prevent hypoglycemia, improved blood glucose control and enhanced SI index.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Effects of Physical Exercise on the Insulin-Dependent Diabetes Mellitus Subjects Using the Modified Minimal Model

Kartono

Irawati

Setiawan

et al. 2017

Int J Pharm Pharm Sci

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“…MUSCLE ATROPHY in poorly controlled diabetes, also called diabetic myopathy, is a clinical condition in which skeletal muscle size and strength/endurance are reduced (21,39). Adequate muscle size and strength capacity enable work at a lower relative submaximal level during normal daily activities.…”

mentioning

confidence: 99%

Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

Hulmi

Silvennoinen

Lehti

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Hulmi JJ, Silvennoinen M, Lehti M, Kivelä R, Kainulainen H. Altered redd1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy. Am J Physiol Endocrinol Metab 302: E307-E315, 2012. First published November 8, 2011 doi:10.1152/ajpendo.00398.2011.-Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven-to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. This result was accompanied by the increased gene expression of DNA damage/repair pathways and decreased expression in ATP production pathways. Concomitantly, increased phosphorylation of AMPK and dephosphorylation of the Akt/mTOR/S6K1/FoxO pathway of proteins were observed together with increased protein ubiquitination. These changes were especially evident during the first 3 wk, along with the strong decrease in muscle mass. Diabetes also induced an increase in myostatin protein and decreased MAPK signaling. These, together with decreased serum insulin and increased serum glucose, remained altered throughout the 5-wk period. In conclusion, diabetic myopathy induced by streptozotocin led to alteration of multiple signaling pathways. Of those, increased REDD1 and myostatin together with decreased Akt/mTOR/FoxO signaling are associated with diabetic muscle atrophy. The increased REDD1 and decreased Akt/mTOR/FoxO signaling followed a similar time course and thus may be explained, in part, by increased expression of genes in DNA damage/repair and possibly also decrease in ATP-production pathways.

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“…Epidemiological evidence also suggests that youth with diabetes are less physically active and less engaged in sporting activities than their nondiabetic peers [27], which may help to explain, at least in part, their reduced physical capacities [28]. Animal models of diabetes confirm impaired muscle growth [8,9] and reduced rates of muscle protein synthesis when compared with healthy control animals, at least in sedentary cage conditions [9,[11][12][13]29].…”

Section: Discussionmentioning

confidence: 99%

Voluntary physical activity and leucine correct impairments in muscle protein synthesis in partially pancreatectomised rats

et al. 2011

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Aims/hypothesis Poorly controlled type 1 diabetes mellitus can cause reduced skeletal muscle mass and weakness during adolescence, which may affect long-term management of the disease. The aim of this study was to determine whether regular voluntary physical activity and leucine feeding restore rates of protein synthesis and deficits in skeletal muscle mass in a young, hypoinsulinaemic/hyperglycaemic rat model of diabetes. Methods Four-week-old male Sprague-Dawley rats were partially pancreatectomised (Px) to induce hypoinsulinaemia/hyperglycaemia and housed with/without access to running wheels for 3 weeks (n=12-14/group). Sham surgery rats (shams) served as sedentary controls (n=18). Protein synthesis and markers of protein anabolism were assessed in the fasted state and following leucine gavage.Fibre type and cross-sectional areas of the gastrocnemius muscle were measured using a metachromatic ATPase stain. Results Compared with sedentary behaviour, regular activity lowered fasting glycaemia and reduced fed hyperglycaemia in Px rats. Active-Px rats, which ran 2.2±0.71 km/night, displayed greater muscle mass and fibre areas similar to shams, while sedentary-Px rats displayed a 20-30% loss in muscle fibre areas. Muscle protein synthesis (basal and in response to leucine gavage) was impaired in sedentary-Px (by~65%), but not in active-Px rats, when compared with shams. Following leucine gavage, the phosphorylation status of eIF4E binding protein 1 (4E-BP1) and ribosomal S6 kinase 1 (S6K1), markers of mammalian target of rapamycin complex 1 (mTORC1) signalling, increased in shams (by two-and ninefold, respectively) and in active-Px (1.5-and fourfold, respectively) rats, but not in sedentary-Px rats. Conclusion/interpretation Moderate physical activity in young Px rats normalises impairments in skeletal muscle growth and protein synthesis. These findings illustrate the critical compensatory role that modest physical activity and targeted nutrition can have on skeletal muscle growth during periods of hypoinsulinaemia in adolescent diabetes.

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Physical activity, sport, and pediatric diabetes

Cited by 129 publications

References 84 publications

The Effects of Physical Exercise on the Insulin-Dependent Diabetes Mellitus Subjects Using the Modified Minimal Model

The Effects of Physical Exercise on the Insulin-Dependent Diabetes Mellitus Subjects Using the Modified Minimal Model

Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

Voluntary physical activity and leucine correct impairments in muscle protein synthesis in partially pancreatectomised rats

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