J Clin Endocrinol Metab
January 2025
Context: Physical activity, exercise, or both are a staple of lifestyle management approaches both for type 1 diabetes mellitus (T1DM) and type 2 diabetes (T2DM). While the current literature supports both physical activity and exercise for improving glycemic control, reducing cardiovascular risk, maintaining proper weight, and enhancing overall well-being, the optimal prescription regimen remains debated.
Evidence Acquisition: We searched PubMed and Google Scholar databases for relevant studies on exercise, insulin sensitivity, and glycemic control in people with T1DM and T2DM.
Introduction: The New Jersey Kids Study (NJKS) is a transdisciplinary statewide initiative to understand influences on child health, development, and disease. We conducted a mixed-methods study of project planning teams to investigate team effectiveness and relationships between team dynamics and quality of deliverables.
Methods: Ten theme-based working groups (WGs) (e.
Background And Objectives: Statins are used for metabolic dysfunction-associated steatotic liver disease (MASLD) (NAFLD) treatment, but their role in this context is unclear. Genetic variants of patatin-like phospholipase domain containing 3 (PNPLA3) are associated with MASLD susceptibility and statin treatment efficacy. Access to liver biopsies before established MASLD is limited, and statins and PNPLA3 in early liver steatosis are thus difficult to study.
View Article and Find Full Text PDFAdults with prediabetes are at risk for Alzheimer's Disease and Related Dementia (ADRD). While exercise may lower ADRD risk, the exact mechanism is unclear. We tested the hypothesis that short-term exercise would raise neuronal insulin signaling and pro-BDNF in neuronal extracellular vesicles (nEVs) in prediabetes.
View Article and Find Full Text PDFApolipoprotein-B (APOB)-containing lipoproteins cause atherosclerosis. Whether the vasculature is the initially responding site or if atherogenic dyslipidemia affects other organs simultaneously is unknown. Here we show that the liver responds to a dyslipidemic insult based on inducible models of familial hypercholesterolemia and APOB tracing.
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