Impaired Energy Expenditure Despite Normal Cardiovascular Capacity in Children with Type 1 Diabetes
ABSTRACT Benefit of fitness on children with type 1 diabetes mellitus (T1DM) is still debated. Aim: To evaluate the influence of physical activity on metabolic balance and exercise tolerance in prepubertal children affected by T1DM.
We analyzed 35 pre-/peripubertal T1DM children and 31 matched controls using an activity monitor (SenseWear Armbad) and physical activity questionnaire (PAQ) to assess energy expenditure (EE), total and active, sedentary and physical activities (h/day and Mets = metabolic equivalents). The maximal cardiopulmonary exercise test (CPET) was also performed.
Total physical activities and total and active EE (>3 Mets) resulted higher in controls than in T1DM patients and self-reported perception of physical and sedentary activities was altered in T1DM children as well in controls and were different from the measured data. No differences were found in CPET parameters with the exception of a higher maximal blood pressure in T1DM children. In multivariate analysis HbA1c negatively correlated with VO(2).
Prepubertal T1DM children seem to have a lower level of physical activity and EE and a probable altered feeling of physical and sedentary activities. On the other hand, T1DM children do not show any alteration of cardiovascular performance, although glycemic control (HbA1c) may play a role in cardiovascular performance.
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ABSTRACT: Objective To analyze the expression of phosphatidylinositol 3 kinase (PI3-K), protein kinase B (PKB) and glycogen synthase kinase 3 beta (GSK-3 β) in skeletal muscle tissue of gestational diabetes mellitus (GDM). Methods A total of 90 cases of pregnant women were divided into observation group and control group according to the occurrence of GDM with 45 cases in either, and the expression of PI3-K, PKB, GSK-3 β mRNA expression in skeletal muscle tissue was compared between two groups. Results The total PI3-K p85 protein was significantly higher in the observation group compared with the control group, the activity of PI3-K was lower than that of the latter; The total PKB, GSK-3 β protein in skeletal tissue had no significant difference between two groups, while the serine phosphorylation levels of PKB and GSK-3βwere significantly lower in observation group compared with the control group. Conclusions The downregulation of PI3-K, PKB and GSK-3βin skeletal tissue of GDM caused by phosphorylation dysfunction of signaling molecules is the reason for insulin resistance and transporter function decline which lead to GDM.Asian Pacific Journal of Tropical Medicine 04/2014; 7(4):309–312. DOI:10.1016/S1995-7645(14)60045-6 · 0.93 Impact Factor
- Circulation 08/2014; 130(17). DOI:10.1161/CIR.0000000000000094 · 14.95 Impact Factor
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ABSTRACT: Diabetes is a leading chronic disease of childhood and adolescence. In addition to the well-known auto-immune, insulin-dependent diabetes mellitus (type 1 diabetes (T1D)), the past two decades have witnessed the emergence of type 2 diabetes (T2D) in children and adolescents, which previously was only seen in middle-aged or older adults. One of the key components of diabetes management is physical activity (PA). The beneficial effects of increased PA and decreased sedentary behavior are extremely important in youth with diabetes because of the markedly increased long-term risk of cardiovascular disease in this population compared to persons without diabetes. This review aims to comprehensively summarize the epidemiologic, observational research published and listed in PubMed between 1970 and 2012 on PA and sedentary behaviors, as well as physical fitness in children and adolescents with T1D and T2D. Additionally, we describe briefly the state of knowledge on perceived barriers of PA in persons with diabetes, with a focus on hypoglycemia. Finally, we provide an overview of the epidemiological literature pertaining to health benefits of increased PA in youth with T1D and T2D and briefly discuss the topic of exercise-related hypoglycemia.Journal of Sport and Health Science 03/2013; 2(1):21–38. DOI:10.1016/j.jshs.2012.10.005 · 1.23 Impact Factor