BACKGROUND GLUT2 is translocated to the apical membrane of enterocytes exposed to glucose concentrations >~50 mM. Mechanisms of GLUT2-mediated glucose uptake in cell culture models of enterocytes have not been studied. AIM To explore mechanism(s) of glucose uptake in three enterocyte-like cell lines. METHODS Glucose uptake was measured in Caco-2, RIE-1, and IEC-6 cell lines using varying concentrations of glucose (0.5–50 mM). Effects of phlorizin (SGLT1 inhibitor), phloretin (GLUT2 inhibitor), nocodazole and cytochalasin B (disrupters of cytoskeleton), calphostin C and chelerythrine (PKC inhibitors), and phorbol 12-myristate 13-acetate (PKC activator) were evaluated. RESULTS Phlorizin inhibited glucose uptake in all three cell lines. Phloretin inhibited glucose uptake in Caco-2 and RIE-1 cells. Starving cells decreased glucose uptake in Caco-2 and RIE-1 cells. Glucose uptake was saturated at ≥10 mM glucose in all three cell lines when exposed briefly (≤ 1 min) to glucose. After exposure for ≥5 min in Caco-2 and RIE-1 cells, glucose uptake did not saturate and Km and Vmax increased. This increase in glucose uptake was inhibited by phloretin, nocodazole, cytochalasin B, calphostin C, and chelerythrine. PMA enhanced glucose uptake by 20%. Inhibitors and PMA had little or no effect in the IEC-6 cells. CONCLUSION Constitutive expression of GLUT2 in the apical membrane along with additional translocation of cytoplasmic GLUT2 to the apical membrane via an intact cytoskeleton and activated PKC appears responsible for enhanced carrier-mediated glucose uptake at greater glucose concentrations (≥20 mM) in Caco-2 and RIE-1 cells. IEC-6 cells do not appear to express functional GLUT2.

Primary angiosarcoma occurs in younger patients than secondary and more frequently presents with a mass. Mastectomy is the mainstay of treatment for breast angiosarcoma. Breast angiosarcoma is a rare malignancy with poor long-term prognosis.

Objective To determine if bacterial colonization of drains can be reduced by local antiseptic interventions. Summary Background Drains are a potential source of bacterial entry into surgical wounds and may contribute to surgical site infection (SSI) after breast surgery. Methods Following IRB approval, patients undergoing total mastectomy and/or axillary lymph node dissection were randomized to standard drain care (control) or drain antisepsis (treated). Standard drain care comprised twice daily cleansing with alcohol swabs. Antisepsis drain care included 1) a chlorhexidine disc at the drain exit site and 2) irrigation of the drain bulb twice daily with dilute sodium hypochlorite (Dakin’s) solution. Cultures results of drain fluid and tubing were compared between control and antisepsis groups. Results Overall, 100 patients with 125 drains completed the study with 48 patients (58 drains) in the control group and 52 patients (67 drains) in the antisepsis group. Cultures of drain bulb fluid at one week were positive (1+ or greater growth) in 66% (38/58) of control drains compared to 21% of antisepsis drains (14/67), (p=0.0001). Drain tubing cultures demonstrated >50 CFU in 19% (8/43) of control drains versus 0% (0/53) of treated drains (p=0.004). SSI was diagnosed in 6 patients (6%) - 5 patients in the control group and 1 patient in the antisepsis group (p=0.06). Conclusions Simple and inexpensive local antiseptic interventions with a chlorhexidine disc and hypochlorite solution reduce bacterial colonization of drains. Based on these data, further study of drain antisepsis and its potential impact on SSI rate is warranted.

Background The aim of this study was to assess national practice patterns regarding use of perioperative antibiotics by surgeons performing breast operations requiring drainage tubes. Methods The members of the American Society of Breast Surgeons (ASBrS) were surveyed regarding use of perioperative antibiotics for breast operations requiring drains, with or without immediate tissue expander or implant reconstruction. Results Of 2857 ASBrS members contacted, 917 (32%) responded and all self-identified as surgeons. Of 905 evaluable respondents, most described themselves as general surgeons (46%) or breast surgeons (46%). For cases in which drains are anticipated, most respondents (86%) reported routine use of preoperative prophylactic antibiotics, 99% selecting cephalosporins. Use of antibiotic >24 hours postoperatively varied by whether or not reconstruction was performed. In non-reconstruction cases, the majority (76%) reported “never/almost never” prescribing antibiotics beyond the 24 hour postoperative period, but 16% reported “always/almost always”. In reconstruction cases, the majority (58%) reported routine antibiotic use beyond 24 hours and the primary driver of the decision to use antibiotics was reported to be the plastic surgeon (83%). Among those reporting use >24 hours, the duration recommended for non-reconstruction cases was “up to one week” in 38% and “until drains removed” in 39%, and this was similar for reconstruction cases. Conclusions Cephalosporins are utilized uniformly as preoperative antibiotic prophylaxis in breast operations requiring drains. However, use of postoperative antibiotic prophylaxis is strongly dependent on the presence of immediate breast reconstruction. Consensus is lacking on the role of postoperative antibiotic prophylaxis in breast operations utilizing drains.

Background Glucose absorption postprandially increases markedly to levels far greater than possible by the classic glucose transporter sodium-glucose cotransporter 1 (SGLT1). Hypothesis Luminal concentrations of glucose >50 mM lead to rapid, phenotypic, non-genomic adaptations by the enterocyte to recruit another transporter, glucose transporter 2 (GLUT2), to the apical membrane to increase glucose absorption. Methods Isolated segments of jejunum were perfused in vivo with glucose-containing solutions in anesthetized rats. Carrier-mediated glucose uptake was measured in 10mM and 100 mM glucose solutions (n=6 rats, each) with and without selective inhibitors of SGLT1 and GLUT2. Results Mean rate of carrier-mediated glucose uptake increased in rats perfused with 100 mM versus 10 mM glucose to 13.9±2.9μmol from 2.1±0.1μmol, respectively (p<0.0001). Using selective inhibitors, the relative contribution of GLUT2 to glucose absorption was 56% in the 100 mM concentration of glucose compared to the 10 mM concentration (27%; p<0.01). Passive absorption accounted for 6% of total glucose absorption at 100 mM glucose. Conclusion A small amount of GLUT2 is active at the lesser luminal concentrations of glucose, but when exposed to concentrations of 100 mM, the enterocyte presumably changes its phenotype be recruiting GLUT2 apically to markedly augment glucose absorption.