Laparoscopic conversion of failed gastric banding to Roux-en-Y gastric bypass: short-term follow-up and technical considerations.

BACKGROUND: The most common bariatric procedure in Australia is laparoscopic adjustable gastric banding (LAGB). Although successful, there is a substantial long-term complication and failure rate. Band removal and conversion to Roux-en-Y gastric bypass (RYGB) can be an effective treatment for complicated or failed bands. There is increasing evidence supporting good weight loss and resolution of band-related complications after conversion. METHODS: A prospective database of all bariatric procedures is maintained. Patients having revision of LAGB to RYGB between December 2007 and April 2011 were included in this study. Indications for surgery, operative details, morbidity and mortality, weight loss data, and post-operative symptoms were recorded. RESULTS: Eighty-two patients were included. Indications for surgery were inadequate weight loss (n = 42), adverse symptoms (reflux = 8, dysphagia = 2), and band complications (band erosion = 7, band sepsis = 1, band slip = 11, esophageal dilatation = 11). Seventy-eight percent of procedures were completed in a single stage and 96.3% laparoscopically. There was no 30-day mortality. Total morbidity was 46.3% (minor complications = 32.9%, major complications = 13.4%). Median BMI was 43 kg/m(2) pre-RYGB and 34 kg/m(2) after 12 months. All patients with adverse band-related symptoms had resolution. CONCLUSIONS: LAGB has a considerable complication and failure rate. Conversion of these patients to RYGB results in further weight loss and resolution of adverse symptoms. This is a challenging procedure, but can usually be performed in a single stage with acceptable morbidity and mortality. These patients should be treated in high-volume, subspecialty bariatric units.

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether.

Exposure of plasmalogen-deficient variants of the murine cell line RAW 264.7 to short-term (0-100 min) treatment with electron transport inhibitors antimycin A or cyanide (chemical hypoxia) resulted in a more rapid loss of viability than in the parent strain. Results suggested that plasmalogen-deficient cells were more sensitive to reactive oxygen species (ROS) generated during chemical hypoxia; the mutants could be rescued from chemical hypoxia by using the antioxidant Trolox, an alpha-tocopherol analogue, and they were more sensitive to ROS generation by plumbagin or by rose bengal treatment coupled with irradiation. In addition, the use of buffers containing 2H2O greatly enhanced the cytotoxic effect of chemical hypoxia, suggesting the involvement of singlet oxygen. We used the unique enzymic deficiencies displayed by the mutants to differentially restore either plasmenylethanolamine (the major plasmalogen species normally found in this cell line) or its biosynthetic precursor, plasmanylethanolamine. Restoration of plasmenylethanolamine, which contains the vinyl ether, resulted in wild-type-like resistance to chemical hypoxia and ROS generators, whereas increasing levels of its precursor, which bears the saturated ether, had no effect on cell survival. These findings identify the vinyl ether double bond as a crucial element in cellular protection under these conditions and support the hypothesis that plasmalogens, through the vinyl ether, act as antioxidants to protect cells against ROS. These phospholipids might protect cells from ROS-mediated damage during events such as chemical hypoxia.

An animal cell mutant with a deficiency in acyl/alkyl-dihydroxyacetone-phosphate reductase activity. Effects on the biosynthesis of ether-linked and diacyl glycerolipids.

In the accompanying paper (James, P. F., and Zoeller, R. A. (1997) J. Biol. Chem. 272, 23532-23539), we reported the isolation of a series of mutants from the fibroblast-like cell line, CHO-K1, that are deficient in the incorporation of the long chain fatty alcohol, hexadecanol, into complex lipids. All but one of these mutants, FAA. K1B, were deficient in long-chain-fatty alcohol oxidase (FAO) activity. We have further characterized this FAO+ isolate. FAA.K1B cells displayed a 40% decrease in [9,10-3H]hexadecanol uptake when compared with the parent strain. Although incorporation of hexadecanol into the phospholipid fraction was decreased by 52%, the cells accumulated label in alkylglycerol (20-fold over wild type). The increase in 1-alkylglycerol labeling corresponded to a 4-fold increase in alkylglycerol mass. Short term labeling with 32Pi showed a 45-50% decrease in overall phospholipid biosynthesis in FAA.K1B. Both diacyl- and ether-linked species were affected, suggesting a general defect in phospholipid biosynthesis. Mutant cells were able to partially compensate for the decreased biosynthesis by decreasing the turnover of the phospholipid pools. The primary lesion in FAA. K1B was identified as a 95% reduction in acyl/alkyl-dihydroxyacetone-phosphate reductase activity. Whole cell homogenates from FAA.K1B were unable to reduce either acyl-dihydroxyacetone phosphate (DHAP) or alkyl-DHAP, supporting the notion that the reduction of these two compounds is catalyzed by a single enzyme. These data suggest that the biosynthesis of diacyl phospholipids, in Chinese hamster ovary cells, begins with the acylation of dihydroxyacetone phosphate as well as glycero-3-phosphate and that the "DHAP pathway" contributes significantly to diacyl glycerolipid biosynthesis. Also, the severe reduction in acyl/alkyl-DHAP reductase activity in FAA.K1B resulted in only a moderate decrease in ether lipid biosynthesis. These latter data together with the observed increase in alkylglycerol levels support the existence of a shunt pathway that is able to partially bypass the enzymatic lesion.