Reduced plasma ghrelin concentration in celiac disease after gluten-free diet treatment.

Capristo E, Farnetti S, Mingrone G, Certo M, Greco AV, Addolorato G, Gasbarrini G.  Scand J Gastroenterol. 2005;40(4):430-6.

Abstract.

OBJECTIVE:

Celiac disease (CD) is characterized by malabsorption, weight loss and increased energy expenditure. The aim of this study was to investigate the relationship between circulating ghrelin and leptin, which are produced at gastrointestinal level and are involved in energy balance regulation, and changes in body composition and energy metabolism in CD patients before and after gluten-free diet (GFD)-induced restoration of the intestinal mucosa.

MATERIAL AND METHODS:

Body composition (by dual-energy X-ray absorptiometry), resting metabolic rate and substrate oxidation rates (by indirect calorimetry) were assessed in 18 adult women with the classic form of CD (age 31.4 +/- 7.8 years, body mass index (BMI) 20.6 +/- 2.1 kg/m2) before and at least 2 years after GFD treatment and in 22 age-matched healthy women (age 33.1 +/- 7.2 years, BMI 22.9 +/- 2.1 kg/m2). Plasma leptin and ghrelin concentrations were assessed by the ELISA and RIA procedures, respectively.

RESULTS:

Fat-free mass was reduced before and after GFD compared to control subjects (p < 0.01), while fat mass increased after treatment (p < 0.01). Plasma leptin concentration was similar between groups and correlated only with BMI (r = 0.84; p < 0.0001) and percentage body fat (r = 0.86; p < 0.0001). Circulating ghrelin levels (pg/ml) were similar between untreated patients and control subjects, but decreased after GFD treatment (untreated CD: 282.6 +/- 55.5 versus treated 109.2 +/- 49.9; p < 0.0001 and versus control subjects 262.2 +/- 30.0; p < 0.0001) and were negatively correlated with BMI in CD patients (r = -0.32; p < 0.01).

CONCLUSIONS:

The low plasma ghrelin concentration found in CD patients after GFD treatment could only be partially explained by the slight increase in body-weight and fat mass. Further studies are needed to better ascertain the role played by an incomplete functional or quantitative recovery of ghrelin-producing cells in CD.