Partnering for impact: best practices for planning in-person academic events with Patient Partners involvement- Lessons learned from Diabetes Action Canada.

Health-related academic events that focus on patient-oriented research should prioritize the needs and interests of those most affected by their outcomes. Diabetes Action Canada (DAC) has hosted six in-person workshops over eight years, bringing together over 100 participants from research, healthcare delivery, government, non-profit organizations, and communities with lived experience of diabetes. This paper outlines key lessons and best practices from Diabetes Action Canada's collaborative approach to workshop co-design with Patient Partners.

Developing a Quality Improvement Framework to Enhance the Health System User Experience for Individuals Living With Type 1 Diabetes: The Reshape T1D Study.

Introduction: User experience design aims to create products and services that are accessible, usable, and enjoyable. The Reshape T1D study aims to apply these principles to understand how individuals living with T1D interact with and experience healthcare to inform T1D clinical quality improvement.

Methods: Using a community-based participatory research design, we involved four patients and four clinicians as co-researchers throughout the research.

Identifying Sex-Specific Differences in Young-Onset Metabolic Syndrome Using Primary Care Electronic Medical Record.

To apply a case definition to a Northern Alberta-based primary care practice population and to assess the sex-specific characteristics of young-onset metabolic syndrome (MetS). We carried out a cross-sectional study to identify and estimate the prevalence of MetS using electronic medical record (EMR) data and perform descriptive comparative analyses of demographic and clinical characteristics between males and females. Northern Alberta Primary Care Research Network (NAPCReN) consists of EMR patient data from 77 physicians among 18 clinics.

Impaired branched chain amino acid oxidation contributes to cardiac insulin resistance in heart failure.

Background: Branched chain amino acids (BCAA) can impair insulin signaling, and cardiac insulin resistance can occur in the failing heart. We, therefore, determined if cardiac BCAA accumulation occurs in patients with dilated cardiomyopathy (DCM), due to an impaired catabolism of BCAA, and if stimulating cardiac BCAA oxidation can improve cardiac function in mice with heart failure.

Method: For human cohorts of DCM and control, both male and female patients of ages between 22 and 66 years were recruited with informed consent from University of Alberta hospital.

Empagliflozin Prevents Worsening of Cardiac Function in an Experimental Model of Pressure Overload-Induced Heart Failure.

This study sought to determine whether the sodium/glucose cotransporter 2 (SGLT2) inhibitor empagliflozin improved heart failure (HF) outcomes in nondiabetic mice. The EMPA-REG OUTCOME (Empagliflozin, Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients) trial demonstrated that empagliflozin markedly prevented HF and cardiovascular death in subjects with diabetes. However, despite ongoing clinical trials in HF patients without type 2 diabetes, there are no objective and translational data to support an effect of SGLT2 inhibitors on cardiac structure and function, particularly in the absence of diabetes and in the setting of established HF.

Cardiomyocyte-specific ablation of CD36 accelerates the progression from compensated cardiac hypertrophy to heart failure.

Previous studies have shown that loss of CD36 protects the heart from dysfunction induced by pressure overload in the presence of diet-induced insulin resistance and/or obesity. The beneficial effects of CD36 ablation in this context are mediated by preventing excessive cardiac fatty acid (FA) entry and reducing lipotoxic injury. However, whether or not the loss of CD36 can prevent pressure overload-induced cardiac dysfunction in the absence of chronic exposure to high circulating FAs is presently unknown.

Normalization of cardiac substrate utilization and left ventricular hypertrophy precede functional recovery in heart failure regression.

Aims: Impaired cardiac substrate metabolism plays an important role in heart failure (HF) pathogenesis. Since many of these metabolic changes occur at the transcriptional level of metabolic enzymes, it is possible that this loss of metabolic flexibility is permanent and thus contributes to worsening cardiac function and/or prevents the full regression of HF upon treatment. However, despite the importance of cardiac energetics in HF, it remains unclear whether these metabolic changes can be normalized.

Resveratrol treatment of mice with pressure-overload-induced heart failure improves diastolic function and cardiac energy metabolism.

Background: Although resveratrol has multiple beneficial cardiovascular effects, whether resveratrol can be used for the treatment and management of heart failure (HF) remains unclear. In the current study, we determined whether resveratrol treatment of mice with established HF could lessen the detrimental phenotype associated with pressure-overload-induced HF and identified physiological and molecular mechanisms contributing to this.

Methods And Results: C57Bl/6 mice were subjected to either sham or transverse aortic constriction surgery to induce HF.

Improved cardiac metabolism and activation of the RISK pathway contributes to improved post-ischemic recovery in calorie restricted mice.

Recent evidence has suggested that activation of AMP-activated protein kinase (AMPK) induced by short-term caloric restriction (CR) protects against myocardial ischemia-reperfusion (I/R) injury. Because AMPK plays a central role in regulating energy metabolism, we investigated whether alterations in cardiac energy metabolism contribute to the cardioprotective effects induced by CR. Hearts from control or short-term CR mice were subjected to ex vivo I/R and metabolism, as well as post-ischemic functional recovery was measured.