Relationship of body weight with gastrointestinal motor and sensory function: studies in anorexia nervosa and obesity

Abstract

BackgroundWhether gastrointestinal motor and sensory function is primary cause or secondary effect of abnormal body weight is uncertain. Moreover, studies relating continuous postprandial sensations of satiation to measurable pathology are scarce. This work assessed postprandial gastrointestinal function and concurrent sensations of satiation across a wide range of body weight and after weight change.MethodsPatients with anorexia nervosa (AN) and obesity (OB) were investigated in reference to normal weight controls (HC). AN were additionally investigated longitudinally. Gastric emptying, antral contractions and oro-cecal transit after ingestion of a solid meal were investigated by MRI and 13C-lactose-ureide breath test. The dependency of self-reported sensations of satiation on the varying degree of stomach filling during gastric emptying was compared between groups.Results24 AN (BMI 14.4 (11.9–16.0) kg/m2), 16 OB (34.9 (29.6–41.5) kg/m2) and 20 HC (21.9 (18.9–24.9) kg/m2) were studied. Gastric half-emptying time (t50) was slower in AN than HC (p = 0.016) and OB (p = 0.007), and a negative association between t50 and BMI was observed between BMI 12 and 25 kg/m2 (p = 0.007). Antral contractions and oro-cecal transit were not different. For any given gastric content volume, self-reported postprandial fullness was greater in AN than in HC or OB (p < 0.001). After weight rehabilitation, t50 in AN tended to become shorter (p = 0.09) and postprandial fullness was less marked (p < 0.01).ConclusionsA relationship between body weight and gastric emptying as well as self-reported feelings of satiation is present. AN have slower gastric emptying and heightened visceral perception compared to HC and OB. Longitudinal follow-up after weight rehabilitation in AN suggests these abnormalities are not a primary feature, but secondary to other factors that determine abnormal body weight.Trial registrationRegistered July 20, 2009 at ClinicalTrials.gov (NCT00946816).Electronic supplementary materialThe online version of this article (doi:10.1186/s12876-016-0560-y) contains supplementary material, which is available to authorized users.

Delayed gastric emptying and altered antrum protein metabolism during activity‐based anorexia

“…This result suggests that gastric emptying is delayed in ABA mice mainly due to malnutrition. These data are in accordance with previous studies reporting that gastric emptying was normalized after weight restoration in AN patients . However, 2 studies also showed that gastric emptying remained delayed after refeeding .…”

“…34 To our in accordance with previous studies reporting that gastric emptying was normalized after weight restoration in AN patients. [7][8][9] However, 2 studies also showed that gastric emptying remained delayed after refeeding. 10,11 In our study, we did not evaluate gastric emptying after refeeding in LFA and ABA mice.…”

“…However, underlying mechanisms have been poorly documented. Protein malnutrition and secondary gastric amyotrophy seem to be involved as refeeding is associated with an improvement of gastric emptying in several studies . By contrast, maintained delayed gastric emptying after refeeding has also been reported .…”

Gastrointestinal alterations in anorexia nervosa — A systematic review

“…An early study described that from 30 patients diagnosed with primary AN, seven were mistakenly diagnosed and suffered from achalasia instead, indicating that esophageal dysmotility can be misjudged as AN (Stacher et al, 1986). In contrast to gastric dysmotility, esophageal dysmotility (Bozzato et al, 2008;Günther, 1988;Hasler, 1982;Mignogna, Fedele, & Lo Russo, 2004;Price et al, 2008;Walsh et al, 1981;Willershausen, Philipp, Pirke, & Fichter, 1990) Oral health impairment -Vomiting behaviour (Johansson et al, 2012;Touyz et al, 1993) Esophageal dysmotility -Vomiting behaviour ➔ esophageal damage ➔ dysfunction of neural regulation (Benini et al, 2010;Holmes et al, 2012;Stacher et al, 1986) Esophageal cancer -Vomiting behaviour (Brewster et al, 2015;Pacciardi, Cargioli, & Mauri, 2015) Impaired gastric dysmotility -Food restriction, laxative abuse ➔ gastric damage including autonomic nerve dysfunction ➔ dysfunction of neural regulation ➔ bradygastria (Abell et al, 1987;Benini et al, 2004;Bluemel et al, 2017;Domstad et al, 1987;Diamanti et al, 2003;Dubois et al, 1979;Holt et al, 1981;Hutson & Wald, 1990;McCallum et al, 1985;Ogawa et al, 2004;Perez et al, 2013;Ravelli et al, 1993;Rigaud et al, 1988;Robinson, 1989;Robinson et al, 1988;Robinson & Stephenson, 1990;Stacher et al, 1992;Szmukler et al, 1990) Gastric dilatation -Reversible dysfunction of neural regulation ➔ decreased gastric motility and de...…”

“…Associated with disordered gastric motility in AN, further symptoms were reported: increased incidence of gastric dysrhythmia (during fasting, AN: 9.75% vs. controls: 0.48%) and reduced antral contractility (mean motility index, AN: 12.8 vs. controls: 14.2;Abell et al, 1987) with reduced antral contraction amplitudes (Stacher et al, 1992) and increased self-reported postprandial fullness (Bluemel et al, 2017). Typical upper GI symptoms such as nausea, vomiting, and gastric fullness were observed to correlate with delayed emptying (Rigaud et al, 1988), whereas satiety (Robinson, 1989) and body weight (Hutson & Wald, 1990) did not show any correlation with gastric emptying.…”