Summary Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are metabolically active fat depots implicated in cardiovascular disease, and EAT has potential as a novel cardiac risk factor, suitable as a target for interventions. The objective of this systematic review and meta‐analysis was to investigate the evidence whether EAT and PAT volume can be reduced by weight‐loss interventions (exercise, diet, bariatric surgery or pharmaceutical interventions). A systematic literature search identified 34 studies that were included in the qualitative synthesis (exercise, n = 10, diet, n = 5, bariatric surgery, n = 9 and pharmaceutical interventions, n = 10). Of the 34 studies, 10 reported sufficient data to be included in the meta‐analysis. The meta‐analysis was only conducted for changes in EAT volume, since only few controlled studies reported changes in PAT ( n = 3) or total cardiac adipose tissue volume ( n = 1). A significant pooled effect size (ES) for reduction in EAT volume was observed following weight‐loss interventions as compared with control interventions (ES = −0.89, 95% CI: −1.23 to −0.55, P < 0.001). When comparing the effect of exercise training versus control on EAT volume reduction, there was a significant pooled ES favouring exercise training (ES: −1.11, 95% CI: −1.57 to −0.65, P < 0.001). Similarly, the ES of pharmaceutical versus control interventions on EAT volume reduction was significant, favouring pharmaceutical interventions (ES: −0.79, 95% CI: −1.37 to −0.21, P < 0.0072). In conclusion, this systematic review and meta‐analysis provides evidence that exercise, diet, bariatric surgery and pharmaceutical interventions can reduce cardiac adipose tissue volume.
Abstract Aim Time‐restricted eating (TRE) limits the time for food intake to typically 6–10 h/day without other dietary restrictions. The aim of the RESET2 (the REStricted Eating Time in the treatment of type 2 diabetes) trial is to investigate the effects on glycaemic control (HbA 1c ) and the feasibility of a 1‐year TRE intervention in individuals with overweight/obesity and type 2 diabetes. The aim of the present paper is to describe the protocol for the RESET2 trial. Methods RESET2 is a randomised, controlled, parallel‐group, open‐label trial. One hundred and sixty individuals with type 2 diabetes (HbA 1c >53 mmol/mol (>7.0%)), and Body Mass Index ≥25 kg/m 2 will be randomised to standard care plus TRE, or to standard care and habitual living. Both the intervention and control group will follow standard diabetes care including regular clinical visits 3–4 times/year. The intervention is divided into two periods: (1) a 3‐month TRE period with a fixed eating window with a self‐selected timing to obtain data from the participants' experiences with TRE and (2) a 9‐month individually adjusted TRE period. Participants in the TRE group will be instructed to reduce their eating window by a minimum of 3 h/day compared to the habitual eating window and with an eating window of 8–10 h/day. Test days will be scheduled at baseline, after 3 months and after 1 year. The primary outcome is HbA 1c (evaluated 3 months and 1 year after randomisation) and secondary outcomes are body weight, fat mass, continuous glucose monitoring derived time‐in‐range and use of antidiabetic medicine (evaluated 1 year after randomisation). Additionally, we will conduct a process evaluation to assess whether the TRE intervention functioned as hypothesised.
The assessment of pancreatic beta cell function in humans is challenging because of a complex interplay between insulin secretion, insulin sensitivity and hepatic insulin extraction. Simplified, the relationship between insulin secretion and insulin sensitivity can be described by an approximate hyperbola with the product of the two variables being constant for individuals with the same degree of glucose tolerance (the disposition index). Strengths and limitations of the disposition index have been widely debated in the literature. In this review we will focus on another and until recently unrecognized dimension of the disposition index, namely the issue of adjusting insulin secretion for hepatic versus peripheral insulin sensitivity. An underlying assumption of this issue is that the liver as compared to muscle plays a different role in the regulation of in vivo insulin secretion.
Additional file 7: Table S5. Differentially abundant phyla and families between Indian and Danish samples. Table S5A: Differentially abundant phyla between Indian (IN) and Danish (DK) gut microbiomes identified using a negative binomial Wald test. A positive log2 fold change value indicates higher relative abundance of the OTU in DK subjects and vice-versa. P-values were adjusted for multiple testing using Benjamini-Hochberg correction (padj
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