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Background: The relationship between physical fitness and risk markers for type 2 diabetes (T2D) in children and the contribution to ethnic differences in these risk markers have been little studied. We examined associations between physical fitness and early risk markers for T2D and cardiovascular disease in 9‐ to 10‐year‐old UK children. Methods: Cross‐sectional study of 1445 9‐ to 10‐year‐old UK children of South Asian, black African‐Caribbean and white European origin. A fasting blood sample was used for measurement of insulin, glucose (from which homeostasis model assessment [HOMA]‐insulin resistance [IR] was derived), glycated hemoglobin (HbA1c), urate, C‐reactive protein (CRP), and lipids. Measurements of blood pressure (BP) and fat mass index (FMI) were made; physical activity was measured by accelerometry. Estimated VO2 max was derived from a submaximal fitness step test. Associations were estimated using multilevel linear regression. Results: Higher VO2 max was associated with lower FMI, insulin, HOMA‐IR, HbA1c, glucose, urate, CRP, triglycerides, LDL‐cholesterol, BP and higher HDL‐cholesterol. Associations were reduced by adjustment for FMI, but those for insulin, HOMA‐IR, glucose, urate, CRP, triglycerides and BP remained statistically significant. Higher levels of insulin and HOMA‐IR in South Asian children were partially explained by lower levels of VO2max compared to white Europeans, accounting for 11% of the difference. Conclusions: Physical fitness is associated with risk markers for T2D and CVD in children, which persist after adjustment for adiposity. Higher levels of IR in South Asians are partially explained by lower physical fitness levels compared to white Europeans. Improving physical fitness may provide scope for reducing risks of T2D. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D) is a complex disorder characterized by high blood sugar, insulin resistance, and relative lack of insulin. The collective effects of genome wide minor alleles of common SNPs, or the minor allele content (MAC) in an individual, have been linked with quantitative variations of complex traits and diseases. Here we studied MAC in T2D using previously published SNP datasets and found higher MAC in cases relative to matched controls. A set of 357 SNPs was found to have the best predictive accuracy in a British population. A weighted risk score calculated by using this set produced an area under the curve (AUC) score of 0.86, which is comparable to risk models built by phenotypic markers. These results identify a novel genetic risk element in T2D susceptibility and provide a potentially useful genetic method to identify individuals with high risk of T2D. [ABSTRACT FROM AUTHOR]

Aims To establish whether an 8-week very-low-calorie diet could improve glycaemic control in Type 2 diabetes of long duration. Methods A total of 29 people with Type 2 diabetes [short-duration group (diabetes duration < 4 years), n = 15; long-duration group (diabetes duration > 8 years), n = 14] completed an 8-week very-low-calorie diet, with assessments of fasting anthropometry, blood tests and blood pressure at baseline and weeks 1, 4 and 8 of the diet. Results Similar weight loss was achieved in the short- and long-duration groups (14.8 ± 0.8% and 14.4 ± 0.7% respectively; P = 0.662). The glucose response to acute calorie restriction was heterogeneous in the long-duration group with some responding similarly to those in the short-duration group, some responding, but only slowly, and others not responding at all. Overall, HbA1c concentration in the short- vs. long-duration groups fell to 44 ± 2 vs. 64 ± 6 mmol/l (6.2 ± 0.2 vs. 8.0 ± 0.5%; P = 0.002). Fasting plasma glucose levels decreased to 5.8 ± 0.2 vs. 8.4 ± 1.1 mmol/l ( P = 0.024) respectively. A total of 87% of the short-duration group and 50% of the long-duration group achieved non-diabetic fasting plasma glucose levels at week 8. Clinically significant improvements in blood pressure and lipid profile were seen regardless of diabetes duration. Conclusion In people with Type 2 diabetes of > 8 years' duration, a therapeutic trial of a very-low-calorie diet may be undertaken with a 50% chance of achieving non-diabetic fasting glucose levels off all antidiabetic therapies. [ABSTRACT FROM AUTHOR]

Aims In the UK, lifestyle intervention is first-line management in Type 2 diabetes. It is unclear what type of diet is most efficacious for improving glycaemic control. This study investigated the effects of an oat-enriched diet on glycaemic control, postprandial glycaemia, inflammation and oxidative stress compared with standard dietary advice. Methods In a randomized crossover design, 27 volunteers with Type 2 diabetes, managed on diet and lifestyle only, were observed for two consecutive 8-week periods following either the oat-enriched diet or re-enforced standard dietary advice. Volunteers attended at baseline (habitual intake) and 8 and 16 weeks. Measurements included basic clinical measurements and fasted and postprandial (3-h) glucose and insulin in response to a healthy test meal. Markers of inflammation and oxidative stress, including high-sensitivity C-reactive protein, interleukin 6, interleukin 18, tumour necrosis factor-alpha, adiponectin, thiobarbituric acid reactive substances, oxygen radical antioxidant capacity, oxidized LDL and urinary isoprostanes, were also measured at fasting and in the postprandial period. Results There were no diet-related effects on glycaemic control or glycaemic or insulinaemic responses to the test meal. Total cholesterol (5.1 ± 1.0 vs. 4.9 ± 0.8 mmol/l, P = 0.019) concentrations declined following the oat-enriched diet compared with standard dietary advice. There was a postprandial decline in adiponectin concentration ( P = 0.009), but no effect of dietary intervention. None of the measures of oxidative stress or inflammation were altered by the oat-enriched diet compared with standard dietary advice. Conclusion The oat-enriched diet had a modest impact on lipid lowering, but did not impact on oxidative stress or inflammation in these volunteers with Type 2 diabetes. [ABSTRACT FROM AUTHOR]