Elevated blood branched-chain amino acids (BCAA) are often associated with insulin resistance and type 2 diabetes, which might result from a reduced cellular utilization and/or incomplete BCAA oxidation. White adipose tissue (WAT) has become appreciated as a potential player in whole body BCAA metabolism. We tested if expression of the mitochondrial BCAA oxidation checkpoint, branched-chain ␣-ketoacid dehydrogenase (BCKD) complex, is reduced in obese WAT and regulated by metabolic signals. WAT BCKD protein (E1␣ subunit) was significantly reduced by 35-50% in various obesity models (fa/fa rats, db/db mice, diet-induced obese mice), and BCKD component transcripts significantly lower in subcutaneous (SC) adipocytes from obese vs. lean Pima Indians. Treatment of 3T3-L1 adipocytes or mice with peroxisome proliferatoractivated receptor-␥ agonists increased WAT BCAA catabolism enzyme mRNAs, whereas the nonmetabolizable glucose analog 2-deoxy-D-glucose had the opposite effect. The results support the hypothesis that suboptimal insulin action and/or perturbed metabolic signals in WAT, as would be seen with insulin resistance/type 2 diabetes, could impair WAT BCAA utilization. However, cross-tissue flux studies comparing lean vs. insulin-sensitive or insulin-resistant obese subjects revealed an unexpected negligible uptake of BCAA from human abdominal SC WAT. This suggests that SC WAT may not be an important contributor to blood BCAA phenotypes associated with insulin resistance in the overnight-fasted state. mRNA abundances for BCAA catabolic enzymes were markedly reduced in omental (but not SC) WAT of obese persons with metabolic syndrome compared with weight-matched healthy obese subjects, raising the possibility that visceral WAT contributes to the BCAA metabolic phenotype of metabolically compromised individuals. bariatric; diabetes; hyperinsulinemia; mammalian target of rapamycin; protein IN THE SEARCH FOR BIOMARKERS that associate with or predict type 2 diabetes mellitus (T2DM), it has become appreciated that circulating concentrations of the branched-chain amino acids (BCAA; valine, leucine, isoleucine) are often increased in obese, insulin-resistant states and in T2DM. Higher fasting plasma BCAA concentrations were initially reported in obese subjects by Adibi and by Felig et al. (2,12). Recent metabolomic studies found that plasma concentrations of BCAAs and large neutral amino acids are negatively correlated with insulin sensitivity in overweight and obese subjects (24), whereas the principal component that differentiated lean and obese individuals contained BCAA, methionine, phenylalanine, and tyrosine, with a linear relationship between plasma BCAA and homeostasis model assessment of insulin resistance (HOMA-IR) (36). Plasma concentrations of leucine and valine, as well as the leucine metabolite ␣-ketoisocaproate, were increased in obese female African-American T2DM subjects compared with age-and body mass index (BMI)-matched nondiabetic subjects, and plasma leucine significantly correlated with hemoglobin A ...

plays an important role in the maintenance of white adipose tissue (WAT) architecture and function, and proper ECM remodeling is critical to support WAT malleability to accomodate changes in energy storage needs. Obesity and adipocyte hypertrophy place a strain on the ECM remodeling machinery, which may promote disordered ECM and altered tissue integrity and could promote proinflammatory and cell stress signals. To explore these questions, new methods were developed to quantify omental and subcutaneous WAT tensile strength and WAT collagen content by three-dimensional confocal imaging, using collagen VI knockout mice as a methods validation tool. These methods, combined with comprehensive measurement of WAT ECM proteolytic enzymes, transcript, and blood analyte analyses, were used to identify unique pathophenotypes of metabolic syndrome and type 2 diabetes mellitus in obese women, using multivariate statistical modeling and univariate comparisons with weightmatched healthy obese individuals. In addition to the expected differences in inflammation and glycemic control, approximately 20 ECMrelated factors, including omental tensile strength, collagen, and enzyme transcripts, helped discriminate metabolically compromised obesity. This is consistent with the hypothesis that WAT ECM physiology is intimately linked to metabolic health in obese humans, and the studies provide new tools to explore this relationship. matrix metalloproteinase; bariatric surgery; adipose inflammation; type 2 diabetes mellitus; extracellular matrix WHITE ADIPOSE TISSUE (WAT) is the primary site of energy storage in humans and by its nature must be malleable to respond to changes in energy balance through expansion and contraction. Under healthy conditions, changes in WAT architecture and the extracellular matrix (ECM) are coordinated with alterations in adipocyte size to accommodate fat storage needs. In contrast, sustained excessive energy intake with concomitant development of hypertrophic adipocytes creates a strain on ECM adaptation with pathophysiological consequences such as inflammation and insulin resistance.Adipose transcript abundances of several ECM-related genes were increased in obese compared with nonobese human subjects, including cell adhesion molecules and ECM receptor interaction genes, whereas weight loss after gastric bypass surgery led to decreased expression of these genes (18). Collagen VI is enriched in adipose tissue, and visceral WAT mass is related to increased expression of collagen 6␣3 in humans and in genetically obese mice (21, 38). Some studies have indicated that, at least in severe obesity, WAT fibrosis is more prevalent compared with nonobese individuals and that fibrosis decreases with weight loss (13,14), and this is believed to play a role in obesity-associated inflammation. Genetically obese ob/ob mice deficient in collagen VI (and thus lower fibrosis) fed a high-fat diet have improved glucose tolerance, insulin signaling, and triglyceride disposal with greater adipocyte size along with reduced WAT inf...

In this patient group, DM, HTN, and DYS were poorly compensated, even when pharmacotherapy was consistent with published GL. This may be due to disease burden in bariatric surgery candidates or to inadequate medical management prior to presentation.

Laparoscopic liver resection (LLR) for the treatment of benign and malignant liver lesions is often performed at specialized centers. Technological advances, such as laparoscopic ultrasonography and electrosurgical tools, have afforded surgeons simultaneous improvements in surgical technique. The utilization of minimally invasive techniques for liver resection has been reported to reduce operative time, decrease blood loss, and shorten length of hospital stay with equivalent postoperative mortality and morbidity rates compared to open liver resection (OLR). Non-anatomic liver resection and left lateral sectionectomy are now routinely performed laparoscopically at many institutions. Furthermore, major hepatic resections are performed by pure laparoscopy, hand-assisted technique, and the hybrid method. In addition, robotic surgery and single port surgery are revealing early promising results. The consensus recommendation for the treatment of benign liver disease and malignant lesions remains unchanged when considering a laparoscopic approach, except when comorbidities and anatomic limitations of the liver lesion preclude this technique. Disease free and survival rates after LLR for hepatocellular carcinoma and metastatic colon cancer correspond to OLR. Patient selection is a significant factor for these favorable outcomes. The limitations include LLR of superior and posterior liver lesions; however, adjustments in technique may now consider a laparoscopic approach as a viable option. As growing data continue to reveal the feasibility and efficacy of laparoscopic liver surgery, this skill is increasingly being adopted by hepatobiliary surgeons. Although the full scope of laparoscopic liver surgery remains infrequently used by many general surgeons, this technique will become a standard in the treatment of liver diseases as studies continue to show favorable outcomes.

A significant proportion of academic general surgery is composed of bariatric surgery, yet surgical training does not sufficiently emphasize the necessary exposure to technical expertise and clinical management of the patient undergoing bariatric surgery. As the scope of general surgery practice continues to evolve, general surgery residency training will need to better integrate the exposure to bariatric surgery.