Barriers and facilitators to optimal oral anticoagulant management: a scoping review.

Oral anticoagulants (OACs) are high alert medications and require high-quality management to optimize health outcomes. The objective of this scoping review was to identify barriers and facilitators (B&Fs) associated with the quality of OAC management. We searched MEDLINE, EMBASE, and CINAHL databases until July 12, 2018, and cross-referenced the bibliographies of the retrieved studies. We included quantitative and qualitative studies that assessed B&Fs to OAC management. The study selection and data extraction processes were performed in duplicate. Analyses included measuring the prevalence of reported B&Fs from studies reporting quantitative data, identifying B&Fs in narrative analyses, and identifying their impact on important outcomes of OAC management. B&Fs were coded and aggregated to higher-level themes using a consensus approach. Factors were described as "key" if they were statistically associated with important outcomes in a randomized trial or observational study. We included 62 studies-three randomized clinical trials (RCTs), 46 observational studies (cross-sectional studies, cohort studies, and case-control studies), 11 qualitative studies, and two mixed-methods studies. Factors identified could be grouped into four themes-therapy-related, patient-related, healthcare provider-related, and health system-related. Key barriers to optimal OAC management were mostly patient-related, whereas interventions focused on education or implementing protocols were shown through RCTs to be effective at improving knowledge scores of OAC patients. While multiple barriers and some facilitators were identified in this review, none was proven to be associated with clinical outcomes. With this in mind, individual physicians may wish to address the key barriers in their practice as a quality improvement initiative but system-wide or policy changes should await high-quality evidence. Future trials should address these factors.Systematic review registration: PROSPERO CRD42017069043.

Green tea, black tea, and epigallocatechin modify body composition, improve glucose tolerance, and differentially alter metabolic gene expression in rats fed a high-fat diet.

The mechanisms of how tea and epigallocatechin-3-gallate (EGCG) lower body fat are not completely understood. This study investigated long-term administration of green tea (GT), black tea (BT), or isolated EGCG (1 mg/kg per day) on body composition, glucose tolerance, and gene expression related to energy metabolism and lipid homeostasis; it was hypothesized that all treatments would improve the indicators of metabolic syndrome. Rats were fed a 15% fat diet for 6 months from 4 weeks of age and were supplied GT, BT, EGCG, or water. GT and BT reduced body fat, whereas GT and EGCG increased lean mass. At 16 weeks GT, BT, and EGCG improved glucose tolerance. In the liver, GT and BT increased the expression of genes involved in fatty acid synthesis (SREBP-1c, FAS, MCD, ACC) and oxidation (PPAR-alpha, CPT-1, ACO); however, EGCG had no effect. In perirenal fat, genes that mediate adipocyte differentiation were suppressed by GT (Pref-1, C/EBP-beta, and PPAR-gamma) and BT (C/EBP-beta), while decreasing LPL, HSL, and UCP-2 expression; EGCG increased expression of UCP-2 and PPAR-gamma genes. Liver triacylglycerol content was unchanged. The results suggest that GT and BT suppressed adipocyte differentiation and fatty acid uptake into adipose tissue, while increasing fat synthesis and oxidation by the liver, without inducing hepatic fat accumulation. In contrast, EGCG increased markers of thermogenesis and differentiation in adipose tissue, while having no effect on liver or muscle tissues at this dose. These results show novel and separate mechanisms by which tea and EGCG may improve glucose tolerance and support a role for these compounds in obesity prevention.

Does perinatal omega-3 polyunsaturated fatty acid deficiency increase appetite signaling?

OBJECTIVE: To investigate the effect of maternal dietary omega-3 polyunsaturated fatty acid (PUFA) deficiency and repletion on food appetite signaling. RESEARCH METHODS AND PROCEDURES: Sprague-Dawley rat dams were maintained on diets either supplemented with (CON) or deficient in (DEF) omega-3 PUFA. All offspring were raised on the maternal diet until weaning. After weaning, two groups remained on the respective maternal diet (CON and DEF groups), whereas a third group, born of dams fed the DEF diet, were switched to the CON diet (REC). Experiments on food intake began when the male rats reached 16 weeks of age. Food intake was stimulated either by a period of food restriction, by blocking glucose utilization (by 2-deoxyglucose injection), or by blocking beta-oxidation of fatty acids (by beta-mercaptoacetate injection). RESULTS: DEF animals consumed more than CON animals in response to all stimuli, with the greatest difference (1.9-fold) demonstrated following administration of 2-deoxyglucose. REC animals also consumed more than CON animals in response to food restriction and 2-deoxyglucose but not to beta-mercaptoacetate. DISCUSSION: These findings indicate that supply of omega-3 PUFA, particularly during the perinatal period, plays a role in the normal development of mechanisms controlling food intake, especially glucoprivic (i.e. reduced glucose availability) appetite signaling. Dietary repletion of omega-3 PUFA from 3 weeks of age restored intake responses to fatty acid metabolite signaling but did not reverse those in response to food restriction or glucoprivic stimuli.