The neurohormonal regulation of energy intake in relation to bariatric surgery for obesity

St. Luke's-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY 10025, USA.
Physiology & Behavior (Impact Factor: 2.98). 07/2010; 100(5):549-59. DOI: 10.1016/j.physbeh.2010.04.032
Source: PubMed


Obesity has reached pandemic proportions, with bariatric surgery representing the only currently available treatment demonstrating long-term effectiveness. Over 200,000 bariatric procedures are performed each year in the US alone. Given the reliable and singular success of bariatric procedures, increased attention is being paid to identifying the accompanying neurohormonal changes that may contribute to the resulting decrease in energy intake. Numerous investigations of postsurgical changes in gut peptides have been conducted, suggesting greater alterations in endocrine function in combination restrictive and malabsorptive procedures (e.g., Roux-en-Y gastric bypass) as compared to purely restrictive procedures (e.g., gastric banding), which may contribute to the increased effectiveness of combination procedures. However, very few studies have been performed and relatively little is known about changes in neural activation that may result from bariatric procedures, which likely interact with changes in gut peptides to influence postsurgical caloric intake. This review provides a background in the neurohormonal regulation of energy intake and discusses how differing forms of bariatric surgery may affect the neurohormonal network, with emphasis on Roux-en-Y gastric bypass, the most commonly performed procedure worldwide. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009.

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Available from: Christopher Ochner
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    • "neurohormones, as playing important roles (Ochner et al. 2010; Berthoud et al. 2011). Several excellent reviews have highlighted the paracrine action of the GI neurohormones in normal conditions to activate vagal afferent signalling to the brainstem and regulate visceral and GI reflex homeostasis (Raybould & Tache, 1988; Holzer et al. 1994; Owyang, 1996; Raybould, 1998, 2007; Takahashi & Owyang, 1999; Li et al. 2001), although direct actions at the level of the brainstem neurocircuits should not be ignored or underplayed (Branchereau et al. 1993; Blevins et al. 2000; Appleyard et al. 2005; van de Wall et al. 2005; Zheng et al. 2005; Baptista et al. 2007; Sullivan et al. 2007; Wan et al. 2007a; Holmes et al. 2009). "
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    ABSTRACT: Diet-induced obesity (DIO) has been shown to alter the biophysical properties and pharmacological responsiveness of vagal afferent neurones and fibers, although the effects of DIO on central vagal neurones have never been investigated. The aims of this study were to investigate whether high-fat diet (HFD)-induced DIO also affects the properties of vagal efferent motoneurones, and to investigate whether these effects were reversed following weight-loss induced by Roux-en-Y gastric bypass surgery (RYGB). Whole cell patch clamp recordings were made from rat dorsal motor nucleus of the vagus (DMV) neurones in thin brainstem slices. DMV neurones from rats exposed to HFD for 12-14 weeks, were less excitable, with a decreased membrane input resistance and decreased ability to fire action potentials in response to direct current pulse injection. DMV neurones were also less responsive to superfusion with the satiety neuropeptides cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1). RYGB reversed all of these DIO-induced effects. DIO also affected the morphological properties of DMV neurons, increasing their dendritic arborization; RYGB did not reverse these morphological alterations. Remarkably, independent of diet, RYGB also reversed age-related changes of membrane properties and occurrence of charybdotoxin-sensitive (BK) calcium dependent potassium current. These findings represent the first direct evidence for the plausible effect of RYGB to improve vagal neuronal health in the brain by reversing some effects of chronic high fat diet. Vago-vagal neurocircuits appear to remain open to modulation and adaptation throughout life and understanding these mechanisms may help to develop novel interventions to alleviate environmental (e.g. dietary) ailments.
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    • "presurgery , based on the supposition that larger post-vs. pre-surgery difference in satiety hormone levels were driving postoperative changes in neural responsivity (Ochner et al., 2010). Data from this study again failed to support the relevant a priori hypothesis, with results showing a trend opposite in direction to that hypothesized. "
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    ABSTRACT: Reductions in mesolimbic responsivity have been noted following Roux-en-Y gastric bypass (RYGB; Ochner et al., 2011a). Given potential for postoperative increases in postprandial gut (satiety) peptides to affect mesolimbic neural responsivity, we hypothesized that: (1) post RYGB changes in mesolimbic responsivity would be greater in the fed relative to the fasted state and; (2) fasted vs. fed state differences in mesolimbic responsivity would be greater post-relative to pre-surgery. fMRI was used to asses neural responsivity to high- and low-calorie food cues in five women 1 mo pre- and 1 mo post-RYGB. Scans were repeated in fasted and fed states. Significant post RYGB decreases in the insula, ventromedial prefrontal cortex (vmPFC) and dorsolateral prefrontal cortex (dlPFC) responsivity were found in the fasted state. These changes were larger than neural changes in the fed state, which were non-significant. Preoperatively, fasted vs. fed differences in neural responsivity were greater in the precuneus, with large but nonsignificant clusters in the vmPFC and dlPFC. Postoperatively, however, no fasted vs. fed differences in neural responsivity were noted. Results were opposite to that predicted and appear inconsistent with the initial hypothesis that postoperative increases in postprandial gut peptides are the primary driver of postoperative changes in neural responsivity.
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