Effect of 2011 Accreditation Council for Graduate Medical Education Duty-Hour Regulations on Objective Measures of Surgical Training.

OBJECTIVE: In July 2011, new Accreditation Council for Graduate Medical Education duty-hour regulations were implemented in surgical residency programs. We examined whether differences in objective measures of surgical training exist at our institution since implementation. DESIGN: Retrospective reviews of the American Board of Surgery In-Training Examination performance and surgical case volume were collected for 5 academic years. Data were separated into 2 groups, Period 1: July 2008 through June 2011 and Period 2: July 2011 through June 2013. SETTING: Single-institution study conducted at the Mount Sinai Hospital, New York, NY, a tertiary-care academic center. PARTICIPANTS: All general surgery residents, levels postgraduate year 1 through 5, from July 2008 through June 2013. RESULTS: No significant differences in the American Board of Surgery In-Training Examination total correct score or overall test percentile were noted between periods for any levels. Intern case volume increased significantly in Period 2 (90 vs 77, p = 0.036). For chief residents graduating in Period 2, there was a significant increase in total major cases (1062 vs 945, p = 0.002) and total chief cases (305 vs 267, p = 0.02). CONCLUSIONS: The duty-hour regulations did not negatively affect objective measures of surgical training in our program. Compliance with the Accreditation Council for Graduate Medical Education duty-hour regulations correlated with an increase in case volume. Adaptations made by our institution, such as maximizing daytime duty hours and increasing physician extenders, likely contributed to our findings.

Glucotoxicity targets hepatic glucokinase in Zucker diabetic fatty rats, a model of type 2 diabetes associated with obesity.

A loss of glucose effectiveness to suppress hepatic glucose production as well as increase hepatic glucose uptake and storage as glycogen is associated with a defective increase in glucose phosphorylation catalyzed by glucokinase (GK) in Zucker diabetic fatty (ZDF) rats. We extended these observations by investigating the role of persistent hyperglycemia (glucotoxicity) in the development of impaired hepatic GK activity in ZDF rats. We measured expression and localization of GK and GK regulatory protein (GKRP), translocation of GK, and hepatic glucose flux in response to a gastric mixed meal load (MMT) and hyperglycemic hyperinsulinemic clamp after 1 or 6 wk of treatment with the sodium-glucose transporter 2 inhibitor (canaglifrozin) that was used to correct the persistent hyperglycemia of ZDF rats. Defective augmentation of glucose phosphorylation in response to a rise in plasma glucose in ZDF rats was associated with the coresidency of GKRP with GK in the cytoplasm in the midstage of diabetes, which was followed by a decrease in GK protein levels due to impaired posttranscriptional processing in the late stage of diabetes. Correcting hyperglycemia from the middle diabetic stage normalized the rate of glucose phosphorylation by maintaining GK protein levels, restoring normal nuclear residency of GK and GKRP under basal conditions and normalizing translocation of GK from the nucleus to the cytoplasm, with GKRP remaining in the nucleus in response to a rise in plasma glucose. This improved the liver's metabolic ability to respond to hyperglycemic hyperinsulinemia. Glucotoxicity is responsible for loss of glucose effectiveness and is associated with altered GK regulation in the ZDF rat.