Plasma Leptin Concentrations and Esophageal Hypomotility in Obese Patients

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Abstract

BACKGROUND: Although esophageal hypomotility is prevalent in obese patients, its cause remains unknown. Leptin, a hormone derived from adipose tissue, may be involved in this phenomenon because it has been shown to decrease gastric and intestinal motility in animals. It has been hypothesized that elevated plasma leptin concentration is a risk factor for esophageal dysmotility in obese patients.

OBJECTIVE: To determine whether plasma leptin concentrations are higher in obese patients with esophageal hypomotility than in obese patients with a normal motility profile.

METHOD: Fasting plasma leptin concentration (assessed by radioimmuoassay) was measured in all patients who were included in a study protocol investigating esophageal manometry before bariatric surgery. The patients completed standardized surveys regarding epidemiological data, upper gastrointestinal symptoms, medical history and medication(s). Basal levels of leptin, as well as corrected leptin scores adjusted for sex and body mass index, were compared in patients with and without esophageal dysmotility.

RESULTS: Nine patients without dysmotility and eight with dysmotility were included. Both groups were comparable with regard to age (42±9 versus 38±9 years), sex (78% versus 75% women) and body mass index (49±10 kg/m ²versus 42±7 kg/m ²). There were no significant differences regarding medication(s) and comorbidities between the two groups. When compared with normal predicted values, the corrected leptin scores were 30% higher in patients with dysmotility than in the control group with normal motility (P≤0.05).

CONCLUSION: Obese patients with esophageal dysmotility exhibited elevated plasma leptin concentrations, suggesting a role for leptin in promoting esophageal hypomotility.

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Most cited references 7

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Diverse roles of leptin in the gastrointestinal tract: modulation of motility, absorption, growth, and inflammation.

Shadi S. Yarandi, Gautam Hebbar, Cary G Sauer … (2011)

Leptin was discovered in 1994 as a hormone produced by adipose tissue with a modulatory effect on feeding behavior and weight control. Recently, the stomach has been identified as an important source of leptin and growing evidence has shown diverse functions for leptin in the gastrointestinal tract. Using leptin as a keyword in PubMed, more than 17 000 articles were identified, of which more than 500 articles were related to the role of leptin in the gastrointestinal tract. Available abstracts were reviewed and more than 200 original articles were reviewed in detail. The available literature demonstrated that leptin can modulate several important functions of the gastrointestinal tract. Leptin interacts with the vagus nerve and cholecystokinin to delay gastric emptying and has a complex effect on motility of the small bowel. Leptin modulates absorption of macronutrients in the gastrointestinal tract differentially in physiologic and pathologic states. In physiologic states, exogenous leptin has been shown to decrease carbohydrate absorption and to increase the absorption of small peptides by the PepT1 di-/tripeptide transporter. In certain pathologic states, leptin has been shown to increase absorption of carbohydrates, proteins, and fat. Leptin has been shown to be upregulated in the colonic mucosa in patients with inflammatory bowel disease. Leptin stimulates gut mucosal cell proliferation and inhibits apoptosis. These functions have led to speculation about the role of leptin in tumorigenesis in the gastrointestinal tract, which is complicated by the multiple immunoregulatory effects of leptin. Leptin is an important modulator of major aspects of gastrointestinal tract functions, independent of its more well-described roles in appetite regulation and obesity. Copyright © 2011 Elsevier Inc. All rights reserved.

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Esophageal motility disorders in the morbidly obese population.

V A Botoman, L Poggi, Tara Rosenthal … (2007)

Most studies investigating esophageal motility among the morbidly obese have focused on the relationship between lower esophageal sphincter (LES) pressure and gastroesophageal reflux disease (GERD). Very few studies in the literature have examined motility disorders among the morbidly obese population in general outside the context of GERD. This study aimed to determine the prevalence of esophageal motility disorders in obese patients selected for bariatric surgery. A total of 116 obese patients (81 women and 35 men) selected for laparoscopic gastric banding underwent manometric evaluation of their esophagus from January to March 2003. Tracings were retrospectively reviewed for the end points of LES resting pressure, LES relaxation, and esophageal peristalsis. The study patients had a body mass index (BMI) of 42.9 kg/m2, and a mean age of 48.6 years. The following abnormal manometric findings were demonstrated in 41% of the patients: nonspecific esophageal motility disorders (23%), nutcracker esophagus (peristaltic amplitude >180 mmHg) (11%), isolated hypertensive LES pressure (>35 mmHg) (3%), isolated hypotensive LES pressure (<12 mmHg) (3%), diffuse esophageal spasm (1%), and achalasia (1%). Only one patient with abnormal esophageal motility reported noncardiac chest pain. Despite a high prevalence of esophageal dysmotility in our morbidly obese study population, there was a conspicuous absence of symptoms. Although the patients in this study were not directly questioned with regard to esophageal symptoms, several studies in the literature support our conclusion.