title: Neural and humoral changes associated with the adjustable gastric band: insights from a rodent model.
abstract: BACKGROUND
  Bariatric surgical procedures, including the laparoscopic adjustable gastric band (LAGB), are currently the only effective treatments for morbid obesity, however, there is no clear understanding of the mechanisms underpinning the efficacy of LAGB. The aim of this study is to examine changes in activation of the sensory neuronal pathways and levels of circulating gut hormones associated with inflation of an AGB.
  
  
  RESULTS
  The trajectory within the central nervous system of polysynaptic projections of sensory neurons innervating the stomach was determined using the transsynaptically transported herpes simplex virus (HSV). Populations of HSV-infected neurons were present in the brainstem, hypothalamus and cortical regions associated with energy balance. An elevation of Fos protein was present within the nucleus of the solitary tract, a region of the brainstem involved in the control of food intake, following acute and chronic band inflation. Two approaches were used to test (1) the impact of inflation of the band alone (on a standard caloric background) or (2) the impact of a standard caloric meal (on the background of the inflated band) on circulating gut hormones. Importantly, there was a significant elevation of glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) following oral gavage of a liquid meal in animals with pre-inflated bands. There was no impact of inflation of the band alone on circulating GLP-1, PYY or ghrelin in animals on a standard caloric background.
  
  
  CONCLUSIONS
  These data are consistent with the notion that the LAGB exerts its effects on satiety, reduced food intake and reduced body weight by the modulation of both neural and hormonal responses with the latter involving an elevation of meal-related levels of GLP-1 and PYY. These data are contrary to the view that the surgery is purely 'restrictive'.
authors.affiliation: Department of Physiology, Monash University, Clayton, Victoria, Australia.
authors.forename: J
authors.initials: J
authors.lastname: Kampe
authors.forename: A
authors.initials: A
authors.lastname: Stefanidis
authors.forename: S H
authors.initials: SH
authors.lastname: Lockie
authors.forename: W A
authors.initials: WA
authors.lastname: Brown
authors.forename: J B
authors.initials: JB
authors.lastname: Dixon
authors.forename: A
authors.initials: A
authors.lastname: Odoi
authors.forename: S J
authors.initials: SJ
authors.lastname: Spencer
authors.forename: J
authors.initials: J
authors.lastname: Raven
authors.forename: B J
authors.initials: BJ
authors.lastname: Oldfield
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000821:virology; D031204:Caloric Restriction; D004195:Disease Models, Animal; D004435:Eating; D005753:Gastric Mucosa / Q000378:metabolism*; D015391:Gastroplasty / Q000379:methods; D054439:Ghrelin / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D010535:Laparoscopy; D008297:Male; D009767:Obesity, Morbid / Q000378:metabolism* / Q000601:surgery*; D019894:Peptide YY / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012527:Satiation; D011984:Sensory Receptor Cells / Q000378:metabolism* / Q000821:virology; D015398:Signal Transduction; D018139:Simplexvirus / Q000378:metabolism*; D013270:Stomach / Q000294:innervation / Q000601:surgery; D015431:Weight Loss
chemical_list: D054439:Ghrelin; D019894:Peptide YY; D052216:Glucagon-Like Peptide 1