RESUMEN
OBJECTIVE: Determine if a point-based attendance system combined with longitudinal gamification is feasible and improves didactic session attendance and learner perceptions at our internal medicine residency. METHODS: A prospective before-after cohort study. Weekly attendance was tracked from June 2022 through April 2023 at our university-affiliated internal medicine residency program. We implemented a point-based longitudinal game incentivizing residents to attend didactics with positive reinforcement in July 2022 (C: carrot). We added tiered positive reinforcement and positive punishment to the game in January 2023 (CS: carrot and stick). Attendance during these periods was compared to pre (P) and postintervention (S). Perceptions were assessed during the P, C, and CS periods with Likert scale ratings. RESULTS: CS was associated with higher attendance than other study periods (P = .002). Median attendance was P-51% (IQR 37.5-64.5), C-65% (IQR 50-74), CS-81% (IQR 78-94), and S-66% (IQR 63-71). Perceptions were similar during pre and intervention study periods, including perceptions of camaraderie (P-4.4, C-4.4, CS-4.5; P = .56), interest in attending didactic sessions (P-3.7, C-3.4, CS-3.2; P = .21), and mandate as the primary reason for attending didactics (P-3.1, C-3.1, CS-3.2; P = .96). CONCLUSIONS: A point-based attendance system combined with a longitudinal game that included tiered positive reinforcement and positive punishment was feasible and associated with higher didactic attendance but not associated with changes in resident perceptions.
RESUMEN
OBJECTIVES: Hypertriglyceridaemia enhances cardiovascular disease risk in patients with diabetes. Lipoprotein lipase (LPL) regulates plasma triglyceride levels by hydrolysing chylomicrons and very-low-density lipoprotein (VLDL). Metformin, an antidiabetic drug, improves plasma lipids including triglycerides. We examined metformin's regulation of angiopoietin-like 3 (ANGPTL3), a liver-derived secretory protein with LPL inhibitory property. METHODS: Using HepG2 cells, a human hepatocyte cell line, the effects of metformin on ANGPTL3 gene and protein expression were determined. The role of AMPK-SIRT1 pathway in metformin regulation of ANGPTL3 was determined using pharmacological, RNAi and reporter assays. Metformin regulation of ANGPTL3 expression was also examined in sodium palmitate-induced insulin resistance. KEY FINDINGS: Metformin and pharmacological activators of AMPK and SIRT1 inhibited the expression of ANGPTL3 in HepG2 cells. Pharmacological or RNAi-based antagonism of AMPK or SIRT1 failed to affect metformin inhibition of ANGPTL3. AMPK-SIRT1 activators and metformin exhibited distinct effects on the expression of ANGPTL3 gene luciferase reporter. Sodium palmitate-induced insulin resistance in cells resulted in increased ANGPTL3 gene expression which was suppressed by pretreatment with metformin. CONCLUSIONS: Metformin inhibits ANGPTL3 expression in the liver in an AMPK-SIRT1-independent manner as a potential mechanism to regulate LPL and lower plasma lipids.