Characterizing Short-Term Outcomes Following Surgery for Rectal Cancer: the Role of Race and Insurance Status.

BACKGROUND: There is a paucity of data demonstrating the effect race and insurance status have on postoperative outcomes for patients with rectal cancer. We evaluated factors impacting short-term outcomes following rectal cancer surgery. DESIGN: Patients who underwent surgery for rectal cancer using the University Health System Consortium database from 2011 to 2012 were studied. Univariate and multivariable analyses were used to identify patient related risk factors for 30-day outcomes after proctectomy: complication rate, 30-day readmission, ICU stay, and length of hospital stay (LOS). RESULTS: A total of 9272 proctectomies were identified in this cohort. After adjustment for potential confounders, black patients were more likely to have 30-day readmissions (OR 1.51, 95 % CI 1.26-1.81), ICU stays (OR 1.25, 95 % CI 1.03-1.51), and longer LOS (+1.67 days, 95 % CI 1.21-2.13) when compared to whites. Compared to those with private insurance, patients with public or military insurance or who were self-pay had a higher likelihood of having postoperative complications. CONCLUSIONS: In patients who undergo elective proctectomy for rectal cancer, non-white and non-privately insured status are associated with significantly worse short-term outcomes. Further studies are needed to determine the implications with respect to receipt of adjuvant therapy and survival.

Nutrient stress activates inflammation and reduces glucose metabolism by suppressing AMP-activated protein kinase in the heart.

OBJECTIVE: Heart failure is a major cause of mortality in diabetes and may be causally associated with altered metabolism. Recent reports indicate a role of inflammation in peripheral insulin resistance, but the impact of inflammation on cardiac metabolism is unknown. We investigated the effects of diet-induced obesity on cardiac inflammation and glucose metabolism in mice. RESEARCH DESIGN AND METHODS: Male C57BL/6 mice were fed a high-fat diet (HFD) for 6 weeks, and heart samples were taken to measure insulin sensitivity, glucose metabolism, and inflammation. Heart samples were also examined following acute interleukin (IL)-6 or lipid infusion in C57BL/6 mice and in IL-6 knockout mice following an HFD. RESULTS: Diet-induced obesity reduced cardiac glucose metabolism, GLUT, and AMP-activated protein kinase (AMPK) levels, and this was associated with increased levels of macrophages, toll-like receptor 4, suppressor of cytokine signaling 3 (SOCS3), and cytokines in heart. Acute physiological elevation of IL-6 suppressed glucose metabolism and caused insulin resistance by increasing SOCS3 and via SOCS3-mediated inhibition of insulin receptor substrate (IRS)-1 and possibly AMPK in heart. Diet-induced inflammation and defects in glucose metabolism were attenuated in IL-6 knockout mice, implicating the role of IL-6 in obesity-associated cardiac inflammation. Acute lipid infusion caused inflammation and raised local levels of macrophages, C-C motif chemokine receptor 2, SOCS3, and cytokines in heart. Lipid-induced cardiac inflammation suppressed AMPK, suggesting the role of lipid as a nutrient stress triggering inflammation. CONCLUSIONS: Our findings that nutrient stress activates cardiac inflammation and that IL-6 suppresses myocardial glucose metabolism via inhibition of AMPK and IRS-1 underscore the important role of inflammation in the pathogenesis of diabetic heart.