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  • Book
    Marina Kurian, Bruce M. Wolfe, Sayeed Ikramuddin, editors.
    Summary: This book provides a concise, state-of-the art review of the surgical treatment of metabolic syndrome and diabetes mellitus. The volume reviews what current practices in surgery and metabolic syndrome and diabetes including the biohormonal effects of the different surgeries. Isolating the effects of the different procedures is critical to the decision tree for type of procedure selected for an individual patient. Specifically for diabetes, this textbook will provide a guide for practitioners to a tailored approach to the treatment. Areas of ongoing research that highlight the minimally invasive approach as well as incorporating what we know of the biochemical results of surgery are presented. Results of established weight loss procedures and ongoing trials are juxtaposed against some of the more novel techniques to ascertain a best practice. Metabolic Syndrome and Diabetes serves as a very useful resource for physicians and researchers dealing with, and interested in, this rising epidemic of metabolic syndrome and diabetes. It provides a concise yet comprehensive summary of the current status of the field that will help guide patient management and stimulate investigative efforts.

    Contents:
    Definition, history and management of the metabolic syndrome and Management Gaps
    Extending current definitions of the Metabolic Syndrome
    Understanding Diabetes Mellitus: Pathophysiology
    Medical Approaches to Weight-Centric Management of Obese Patients with Type 2 Diabetes
    Adipocyte Dysfunction Obesity and Insulin resistance (and inflammation in obesity)
    Type 2 Diabetes Mellitus, Bariatric Surgery, and the Microbiome
    History of Metabolic Surgery
    Obesity and Cancer
    Effect of bariatric surgery on Incretin function
    Effect of Bariatric Surgery on Insulin Secretion
    Gastric banding
    Sleeve Gastrectomy
    Gastric Bypass
    Biliopancreatic Diversion with Duodenal Switch
    Ileal Interposition with Sleeve Gastrectomy for the Treatment of Type 2 Diabetes
    Balancing complications and Metabolic benefit
    Neural Modulation in the Treatment of Obesity
    Endolumenal Sleeve
    Endoscopic primary obesity and balloon therapy.
    Digital Access Springer 2016
  • Article
    Yavin E, Zeigler BP.
    J Biol Chem. 1977 Jan 10;252(1):260-7.
    The patterns of serine metabolism into phospholipids of cultured brain cells was examined. Labeled serine was incorporated predominantly into serine- ad ethanolamine-containing phospholipids and sphingolipids. The highest rates of labeling were observed in the (1)acyl-(2)acyl- and (1)alkyl-(2)acyl-serine phosphoglyceride fractions. Serine incorporation into both compounds appears to proceed via a base exchange mechanism. A decrease in the rate of serine phosphoglycerides labeling and a depletion of the ATP levels were observed when oligomycin or the calcium ionophore A23187 was added to the incubation medium. The inhibition of serine incorporation by A23187 could be partially reversed following addition of 10 mM CaCl2. Based on these findings it is suggested that in addition to demonstrating the energy-independent calcium-stimulated pathway, there may also be an energy related pathway. Formation of ethanolamine phosphoglycerides, as a result of serine phosphoglycerides decarboxylation, has been analyzed by using a simplified compartmental model. Of the 0.67 nmol/mg of protein turned over per h in the diacylserine phosphoglyceride compartment, 0.14 nmol/mg of protein are converted into the ethanolamine phosphoglycerides. In a similar manner, of the 0.09 nmol/mg of protein turned over per h in the (1)alkyl-(2)acyl-serine phosphoglyceride compartment, 0.014 nmol/mg of protein is converted into the (1)alkyl-(2)acyl-ethanolamine phosphoglyceride. These figures provide a first indication that a considerable portion of the ethanolamine phosphoglycerides in cultured brain cells is formed via a direct decarboxylation of the serine phosphoglycerides. In estimating the rates of (1)alkenyl-(2)acyl-ethanolamine phosphoglyceride formation from (1)alkyl-(2)acyl-ethanolamine phosphoglyceride the precursor-product specific activity crossover point could not be established. Mathematical analysis, however, enabled us to estimate the flux from the former into the latter as 0.04 nmol/mg of protein per h. A scheme for the possible metabolic interconversions of the ether bond containing serine and ethanolamine phosphoglycerides is proposed.
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