Zinc-alpha2-glycoprotein, dysglycaemia and insulin resistance: a systematic review and meta-analysis.

To systematically review the current literature investigating associations between zinc-alpha2-glycoprotein (ZAG) and dysglycaemia (including type 2 diabetes (T2DM), poly-cystic-ovary syndrome (PCOS), pre-diabetes or insulin resistance). This included relationships between ZAG and continuous measures of insulin and glucose. Additionally, we performed a meta-analysis to estimate the extent that ZAG differs between individuals with or without dysglycaemia; whilst examining the potential influence of adiposity. A systematic search was performed on four databases for studies on circulating ZAG concentrations in adult human populations, comparing healthy controls to individuals with dysglycaemia. Key characteristics, including the mean ZAG concentrations (mg∙L-1), and any correlational statistics between ZAG and continuous measures of glucose, glycated haemoglobin (HbA1c) or insulin were extracted. Meta-analyses were performed to compare metabolically healthy controls to cases, and on studies that compared controls and cases considered overweight or obese (body mass index (BMI) ≥25 kg.m2). 1575 papers were identified and 14 studies (16 cohorts) were considered eligible for inclusion. Circulating ZAG was lower in individuals with dysglycaemia compared to metabolically healthy controls (-4.14 [-8.17, -0.11] mg.L-1; I2 = 98.5%; p < 0.001). When using data from only studies with overweight or obese groups with or without dysglycaemia (three studies (four cohorts); pooled n = 332), the difference in circulating ZAG was no longer significant (-0.30 [-3.67, 3.07] mg. L-1; I2 = 28.0%; p = 0.225). These data suggest that ZAG may be implicated in dysglycaemia, although there was significant heterogeneity across different studies and the mediating effect of adiposity cannot be excluded. Therefore, more research is needed before robust conclusions can be drawn.

Sedentary Behavior and Chronic Disease: Mechanisms and Future Directions.

BACKGROUND: Recent updates to physical activity guidelines highlight the importance of reducing sedentary time. However, at present, only general recommendations are possible (ie, "Sit less, move more"). There remains a need to investigate the strength, temporality, specificity, and dose-response nature of sedentary behavior associations with chronic disease, along with potential underlying mechanisms. METHODS: Stemming from a recent research workshop organized by the Sedentary Behavior Council themed "Sedentary behaviour mechanisms-biological and behavioural pathways linking sitting to adverse health outcomes," this paper (1) discusses existing challenges and scientific discussions within this advancing area of science, (2) highlights and discusses emerging areas of interest, and (3) points to potential future directions. RESULTS: A brief knowledge update is provided, reflecting upon current and evolving thinking/discussions, and the rapid accumulation of new evidence linking sedentary behavior to chronic disease. Research "action points" are made at the end of each section-spanning from measurement systems and analytic methods, genetic epidemiology, causal mediation, and experimental studies to biological and behavioral determinants and mechanisms. CONCLUSION: A better understanding of whether and how sedentary behavior is causally related to chronic disease will allow for more meaningful conclusions in the future and assist in refining clinical and public health policies/recommendations.

Sitting Less and Moving More: Improved Glycaemic Control for Type 2 Diabetes Prevention and Management.

Epidemiological evidence indicates that excessive time spent in sedentary behaviours (too much sitting) is associated with an increased risk of type 2 diabetes (T2D). Here, we highlight findings of experimental studies corroborating and extending the epidemiological evidence and showing the potential benefits for T2D of reducing and breaking up sitting time across the whole day. We also discuss future research opportunities and consider emerging implications for T2D prevention and management. This new evidence is stimulating an expansion of diabetes-related physical activity guidelines-suggesting that in addition to moderate-vigorous physical activity, reducing and regularly interrupting prolonged sitting time is likely to have important and varied benefits across the spectrum of diabetes risk.