4 resultados para 616.042

em WestminsterResearch - UK


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Aims/hypothesis - It is not known whether the beneficial effects of exercise training on insulin sensitivity are due to changes in hepatic and peripheral insulin sensitivity or whether the changes in insulin sensitivity can be explained by adaptive changes in fatty acid metabolism, changes in visceral fat or changes in liver and muscle triacylglycerol content. We investigated the effects of 6 weeks of supervised exercise in sedentary men on these variables. Subjects and methods - We randomised 17 sedentary overweight male subjects (age 50 ± 2.6 years, BMI 27.6 ± 0.5 kg/m2) to a 6-week exercise programme (n = 10) or control group (n = 7). The insulin sensitivity of palmitic acid production rate (Ra), glycerol Ra, endogenous glucose Ra (EGP), glucose uptake and glucose metabolic clearance rate were measured at 0 and 6 weeks with a two-step hyperinsulinaemic–euglycaemic clamp [step 1, 0.3 (low dose); step 2, 1.5 (high dose) mU kg−1 min−1]. In the exercise group subjects were studied >72 h after the last training session. Liver and skeletal muscle triacylglycerol content was measured by magnetic resonance spectroscopy and visceral adipose tissue by cross-sectional computer tomography scanning. Results - After 6 weeks, fasting glycerol, palmitic acid Ra (p = 0.003, p = 0.042) and NEFA concentration (p = 0.005) were decreased in the exercise group with no change in the control group. The effects of low-dose insulin on EGP and of high-dose insulin on glucose uptake and metabolic clearance rate were enhanced in the exercise group but not in the control group (p = 0.026; p = 0.007 and p = 0.04). There was no change in muscle triacylglycerol and liver fat in either group. Conclusions/interpretation - Decreased availability of circulating NEFA may contribute to the observed improvement in the insulin sensitivity of EGP and glucose uptake following 6 weeks of moderate exercise.

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School playtime provides daily opportunities for children to be active outdoors, but only makes small contributions to physical activity (PA) requirements. Natural environments facilitate unstructured PA and children report a preference for play in nature. Thus, play on the school field might encourage children to be more active during playtime. The primary aim of this study was to examine the impact of the school playing environment on children's PA. Descriptive data and fitness were assessed in 25 children aged 8–9 years from a single primary school. Over two consecutive weeks participants were allocated to either play on the school field or playground during playtime. The order of play in the two areas was randomised and counterbalanced. Moderate to vigorous PA (MVPA) was assessed during playtime on the last two days of each week using accelerometers. There was a significant interaction of environment and sex on MVPA during morning play (F(1,22) = 6.27; P<0.05; np2 = 0.222), but not during lunch (P>0.05; np2 = 0.060) or all of playtime combined (P>0.05; np2 = 0.140). During morning play boys were significantly more active than girls on the playground (t(23) = 1.32; P<0.01; n2 = 0.291), but not on the field (P>0.05; n2 = 0.071). For lunch (F(1,22) = 24,11; P<0.001; np2 = 0.523) and all of playtime combined (F(1,22) = 33.67; P<0.001; np2 = 0.616) there was a significant effect of environment. There was also a significant main effect of sex during lunch (F(1,22) = 11.56; P<0.01; np2 = 0.344) and all of playtime combined (F(1,22) = 12.37; P<0.01; np2 = 0.371). MVPA was higher on the field and boys were more active than girls. Play on the field leads to increases in MVPA, particularly in girls. The promising trend for the effect of the natural environment on MVPA indicates that interventions aimed at increasing MVPA should use the natural environment and that schools should encourage greater use of their natural areas to increase PA.

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OBJECTIVE: To provide a detailed phenotype/genotype characterization of Bietti crystalline dystrophy (BCD). DESIGN: Observational case series. PARTICIPANTS: Twenty patients from 17 families recruited from a multiethnic British population. METHODS: Patients underwent color fundus photography, near-infrared (NIR) imaging, fundus autofluorescence (FAF) imaging, spectral domain optical coherence tomography (SD-OCT), and electroretinogram (ERG) assessment. The gene CYP4V2 was sequenced. MAIN OUTCOME MEASURES: Clinical, imaging, electrophysiologic, and molecular genetics findings. RESULTS: Patients ranged in age from 19 to 72 years (median, 40 years), with a visual acuity of 6/5 to perception of light (median, 6/12). There was wide intrafamilial and interfamilial variability in clinical severity. The FAF imaging showed well-defined areas of retinal pigment epithelium (RPE) loss that corresponded on SD-OCT to well-demarcated areas of outer retinal atrophy. Retinal crystals were not evident on FAF imaging and were best visualized with NIR imaging. Spectral domain OCT showed them to be principally located on or in the RPE/Bruch's membrane complex. Disappearance of the crystals, revealed by serial recording, was associated with severe disruption and thinning of the RPE/Bruch's membrane complex. Cases with extensive RPE degeneration (N = 5) had ERGs consistent with generalized rod and cone dysfunction, but those with more focal RPE atrophy showed amplitude reduction without delay (N = 3), consistent with restricted loss of function, or that was normal (N = 2). Likely disease-causing variants were identified in 34 chromosomes from 17 families. Seven were novel, including p.Met66Arg, found in all 11 patients from 8 families of South Asian descent. This mutation appears to be associated with earlier onset (median age, 30 years) compared with other substitutions (median age, 41 years). Deletions of exon 7 were associated with more severe disease. CONCLUSIONS: The phenotype is highly variable. Several novel variants are reported, including a highly prevalent substitution in patients of South Asian descent that is associated with earlier-onset disease. Autofluorescence showed sharply demarcated areas of RPE loss that coincided with abrupt edges of outer retinal atrophy on SD-OCT; crystals were generally situated on or in the RPE/Bruch's complex but could disappear over time with associated RPE disruption. These results support a role for the RPE in disease pathogenesis.