1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Background  It is controversial whether serum ghrelin concentration is altered in coeliac disease and whether this alteration is related to nutritional impairment or to inflammatory changes of duodenal mucosa.

Aim  To investigate clinical and histopathological variables affecting circulating ghrelin in coeliac patients by comparison with dyspeptic patients and with healthy controls.

Methods  We measured serum ghrelin and obtained gastric and duodenal biopsies in 44 coeliac patients before and after 1-year gluten-free diet, in 39 dyspeptic patients and 53 healthy controls.

Results  Serum ghrelin concentration was significantly higher in coeliac (531 ± 29 pg/mL, P < 0.05) and in dyspeptic patients (526 ± 14 pg/mL, P < 0.01) than in healthy controls (451 ± 8 pg/mL), and body mass index was significantly lower in coeliac (20 ± 1) and in dyspeptic patients (20 ± 1) than in healthy controls (22 ± 1, P < 0.05). In coeliac patients serum ghrelin concentration was not related to the severity of duodenal lesions. Serum ghrelin reverted to normal (399 ± 30 pg/mL) and body mass index increased significantly (0.6 ± 0.1 kg/m2 increase, P < 0.05) during gluten-free diet despite persistent duodenal lymphocytic infiltration.

Conclusions  Ghrelin concentration is increased and body mass index is decreased in coeliac and in dyspeptic patients irrespective of presence and severity of duodenal inflammation. Nutritional impairment is a key factor in elevating plasma ghrelin levels in coeliac disease.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

The circulating acylated 28-residue peptide ghrelin is at present the only known orexigenic factor1 involved in central regulation of appetite and in the long-term regulation of body weight in rodents2 and humans.3 Serum concentration of this peptide has been reported to decrease in chronic states of positive energy balance,4 and to increase in the fasting state,5 in anorexia nervosa6 and in cancer anorexia.7 This peptide is mainly secreted by enteroendocrine cells of the stomach and of the small intestine and, in addition to a variety of central and peripheral actions,8 it exerts a local protective and anti-inflammatory effect in gastrointestinal mucosa as suggested by animal studies showing increased plasma ghrelin levels in experimental ulcers,9 and by in vitro studies showing increased ghrelin expression and secretion by activated human T cells.10

Coeliac disease (CD) is a gluten-sensitive enteropathy with heterogeneous clinical presentation11, 12 characterized by nutrient malabsorption and increased energy expenditure13 often resulting in impaired nutritional status14 particularly in patients with chronic diarrhoea and weight loss. Villous atrophy and intraepithelial infiltration of activated T lymphocytes in duodenal mucosa are the histopathological hallmark of the disease.15 The combination of these histopathological characteristics with the negative energy balance that characterizes CD may both concur to affect serum ghrelin concentration. Available evidence is, however, conflicting16, 17 and the relative contribution of mucosal and constitutional factors in affecting circulating ghrelin levels is unknown.

By contrast with CD, functional dyspepsia is a syndrome characterized by chronic or recurrent upper abdominal symptoms that may result in mildly impaired nutritional status particularly in women,18 without specific histopathological changes of gastric and duodenal mucosa. We reasoned that comparison of circulating ghrelin levels in CD and in dyspeptic patients could potentially help in distinguishing the role of mucosal from constitutional factors in affecting ghrelin concentration in CD, because patients with these two conditions typically complain of gastrointestinal symptoms that may affect nutritional status, but markedly differ for small intestinal histopathology.

The main aim of our study was to check the relative contribution of constitutional and histopathological factors in affecting circulating ghrelin concentration in CD by comparing untreated patients with patients with functional dyspepsia and with healthy controls, and by assessing the effect of gluten-free diet.

Materials and methods

  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Forty-four consecutive CD patients referred to our CD clinic were admitted to the study. These included 19 patients with malabsorption (defined as a combination of diarrhoea and weight loss), 10 with dermatitis herpetiformis, two with recurrent diarrhoea, two with aphthous stomatitis, two with hypothyroidism, one with epilepsy and eight asymptomatic identified at family screening. In all patients antiendomysial and tissue transglutaminase antibodies tested positive and duodenal histopathology was suggestive of CD. Following diagnosis all CD patients were instructed to adhere to a gluten-free diet under the supervision of a professional dietician. Forty-one of the 44 CD patients entering the study have had a repeat study after 1 year of gluten-free diet.

Thirty-nine consecutive patients referred to our unit for dyspeptic symptoms were also studied. Functional dyspepsia was diagnosed according to Rome II criteria,19 and 32 of the 39 patients reported discomfort centred in the upper abdomen as the predominant symptom associated with abdominal fullness, early satiety, bloating or nausea suggesting dysmotility-like dyspepsia. Seven patients reported ulcer like dyspepsia. Patients with dyspeptic symptoms suggesting gastro-oesophageal reflux disease were not included in the study. All patients tested negative to antiendomysial and tissue transglutaminase antibodies, and had negative endoscopic findings. HLA typing (INNO-LiPA HLA DQ-B1 Update; Innogenetics, Ghent, Belgium) was carried out in 11 seronegative dyspeptic patients with Marsh–Oberhuber type I lesion at duodenal histopathology in order to exclude the relative frequent condition of seronegative CD with mild histopathological lesion.20, 21 All 11 patients tested negative for HLA DQ2 and DQ8 heterodimer, a finding with an extremely high negative predictive value for CD.22 Serum samples of 53 healthy blood donors were obtained from the local blood transfusion centre and information on sex, age and body mass index (BMI) was anonymously obtained from donors file.

Clinical procedure

Biopsies of the gastric antrum (n = 2) and of the distal duodenum (n = 7) were obtained at endoscopy in patients with positive CD serology. A method previously described23 for orientation of endoscopic biopsies using Millipore filters was applied to all cases. The Sydney scoring system24 was applied for histopathological classification of gastric biopsies, and duodenal histopathological lesions were classified according to Marsh's criteria15 as modified by Oberhuber et al.25 According to this classification: type I lesion was normal villous architecture with intraepithelial lymphocytosis; type II, normal villous architecture with intraepithelial lymphocytosis and crypt hyperplasia; and type III mild (IIIA), subtotal (IIIB) and total (IIIC) villous atrophy. CD3+ intraepithelial lymphocytes were counted in duodenal biopsies and counts >40/100 epithelial cells were considered as abnormal.26 For statistical analysis the five Oberhuber histopathological categories were progressively numbered 1–5. Serum samples were collected at time of endoscopy and stored at −80 °C for subsequent one-batch measurement of ghrelin concentration.

Laboratory methods

Serum ghrelin was measured by radioimmunoassay using a commercially available kit (Phoenix Pharmaceuticals, Belmont, CA, USA) that measures total circulating ghrelin concentration. Serum antiendomysial antibodies were measured by indirect immunofluorescence on commercial sections of distal monkey oesophagus (Antiendomysium IgA; Eurospital, Trieste, Italy). Tissue transglutaminase antibodies were measured by ELISA on commercial recombinant human transglutaminase as substrate (Eu-tTG IgA; Eurospital, Trieste, Italy).

Statistical analysis

Results were expressed as means ± standard error of the mean. Statistical analysis27 was performed using Student's t-test for paired and unpaired samples, and Fisher's exact test. Relationship between variables was assessed by linear regression analysis and Spearman coefficient was used as appropriate. P < 0.05 was accepted to reject the null hypothesis.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Clinical and serological characteristics of the study population are shown in Table 1. There was no difference between CD and dyspeptic patients in relation to age, BMI and male/female ratio. BMI was significantly lower in both CD and dyspeptic patients than in healthy controls (Table 1), and was significantly lower in CD patients with malabsorption than in those without malabsorption (18.6 ± 1.2 vs. 21.8 ± 0.6, P < 0.02). Prior to gluten-free diet all CD patients had positive antiendomysial antibodies and transglutaminase antibodies, and these were negative in all dyspeptic patients.

Table 1.  Characteristics of patients and of healthy controls studied
 CoeliacDyspepticHealthy controls
Before dietOn diet
  1. M, male; F, female; BMI, body mass index; t-TG, tissue transglutaminase.

  2. *P < 0.05 and **P < 0.0001; by comparison with coeliac patients before diet; *** = P < 0.01 by comparison with healthy controls. § = P < 0.001, §§ = P < 0.01 by comparison with male.

Age (years)33 ± 234 ± 236 ± 228 ± 1
M/F32 ± 3/35 ± 233 ± 3/36 ± 229 ± 6/38 ± 228 ± 2/27 ± 3
BMI (kg/m2)20.4 ± 0.721 ± 0.7*19.7 ± 0.9***,§23 ± 0.9*
M/F23.2 ± 1.0/19.6 ± 0.8§24.1 ± 0.7/20.2 ± 0.8§§17.8 ± 4.6/14.8 ± 1.6§§24.0 ± 1.0/21.0 ± 2.6§§
Ghrelin (pg/mL)531 ± 29399 ± 30*526 ± 14***451 ± 8*
M/F466 ± 30/552 ± 36327 ± 51/438 ± 35480 ± 24/538 ± 15405 ± 34/484 ± 55
t-TG (U/mL)15.3 ± 2.23.3 ± 0.6**0.5 ± 0.10.4 ± 0.1
M/F14.3 ± 2.2/20.0 ± 3.13.1 ± 0.1/4.7 ± 2.00.2 ± 0.2/0.6 ± 0.10.4 ± 0.1/0.4 ± 0.2

Histopathological characteristics of the study population are shown in Table 2. Gastritis score was similar in CD and in dyspeptic patients. Thirty-one CD patients had atrophic duodenal lesions at histopathology prior to gluten-free diet and 13 had infiltrative lesions. Duodenal histopathology was normal in 30 dyspeptic patients and revealed type I intraepithelial lymphocytic infiltration in 11 patients. All these 11 dyspeptic patients tested HLA DQ 2 and DQ8 negative.

Table 2.  Histopathological characteristics in coeliac patients studied before and during gluten-free diet and in dyspeptic patients
Gastritisn = 44n = 41n = 39
Intestinal metaplasia
Helicobacter pylori +13126
Duodenaln = 44n = 44n = 39

Serum ghrelin concentration

Serum ghrelin concentration was 531 ± 29 pg/mL in CD patients before gluten-free diet, a value similar to that observed in dyspeptic patients (526 ± 14 pg/mL, N.S.) and significantly higher than that observed in healthy subjects (451 ± 8 pg/mL, P < 0.05). Differences between dyspeptic patients and healthy controls were also statistically significant (P < 0.01). There was a tendency for serum ghrelin concentration to be higher in CD patients with malabsorption than in those without malabsorption (545 ± 39 pg/mL vs. 505 ± 31 pg/mL, N.S.). There was no relationship between ghrelin concentration and BMI in CD patients and in dyspeptic patients. In CD patients serum ghrelin concentration increased linearly with age at diagnosis (y = 364.6 + 4.6x, r2 0.1050, P < 0.04, Figure 1), but no relationship with age was detected in dyspeptic patients and in healthy controls.


Figure 1. Correlation between age at diagnosis of coeliac disease and serum ghrelin concentration.

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Ghrelin concentration was significantly lower in CD patients with atrophic gastritis (363 ± 53 pg/mL) than in those without atrophic gastritis (552 ± 33 pg/mL, P < 0.04). There was no significant difference in ghrelin concentration in relation to other histopathological parameters of gastritis and to the presence of Helicobacter pylori infection. Ghrelin concentration was similar in CD patients with infiltrative (510 ± 50 pg/mL) and with atrophic lesions (541 ± 36 pg/mL, N.S.) at duodenal histopathology, and in dyspeptic patients with negative and infiltrative duodenal lesions (520 ± 19 pg/mL vs. 575 ± 24 pg/mL respectively, N.S.).

Effect of gluten-free diet in CD patients

During gluten-free diet duodenal histopathology improved in all CD patients with reversal to normality in seven patients, but lymphocytic infiltration >40 elements/100 epithelial cells persisted in 37 patients including four with persistent mild villous atrophy (Table 2). Gastric histopathology remained unchanged. BMI increased in 28 CD patients during gluten-free diet, decreased in 13 and remained unchanged in three, and mean value significantly increased from 20.4 ± 0.7 to 21.1 ± 0.7 kg/m2 (P < 0.05, Figure 2). Serum transglutaminase antibody concentration decreased in all CD patients during diet from 15 ± 2 to 3 ± 1 Units (P < 0.0001).


Figure 2. Changes of body mass index (BMI) measured before and during gluten free diet in individual coeliac patients (P < 0.05). Mean values are also shown as horizontal bars.

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Serum ghrelin concentration decreased in 38 of the 44 CD patients during gluten-free diet by comparison with pre-diet values (Figure 3), and mean values decreased from 545 ± 39 to 505 ± 31 pg/mL (P < 0.0001). This effect was entirely accounted for by changes in the 36 CD patients identified because of symptoms or associated disease, and ghrelin concentration remained unchanged in the eight asymptomatic CD patients identified by family screening (507 ± 27 pg/mL vs. 395 ± 34 pg/mL, P < 0.001 respectively). Changes in serum ghrelin concentration during gluten-free diet were significantly associated with changes in the severity of duodenal histopathology (y = −1.413 + 0.002x, P < 0.04, Figure 4).


Figure 3. Changes of serum ghrelin concentration measured before and during gluten free diet in individual coeliac patients (P < 0.0001). Mean values are also shown as horizontal bars.

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Figure 4. Correlation between changes (bsl00084) of serum ghrelin concentration and of duodenal histopathology score during gluten free diet in coeliac patients (r2 = 0.1200, P < 0.04).

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  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

Our results show that circulating ghrelin concentration is increased in untreated CD patients by comparison with control subjects and that reverts to normal in individual CD patients studied twice, before and during gluten-free diet. Previous studies have reported contradictory results,16, 17 and we believe that our study may contribute to resolve this uncertainty because, by contrast with previous studies, it was based on a large number of patients, and because the effect of gluten-free diet was assessed within the same large group of patients studied twice, off and on a gluten-free diet. This was not the case for the study of Capristo et al.17 that involved 18 CD patients only, and for the study Peracchi et al.16 that was based on comparison of two different populations of CD patients studied off and on gluten-free diet.

In the present study, we have looked for constitutional and histopathological factors affecting circulating ghrelin concentration in CD patients. We have observed a progressive increase of ghrelin concentration with age at diagnosis in untreated CD patients, but not in dyspeptic patients and in healthy controls. It can be speculated that this age-dependent increase in CD may reflect the duration of exposure to dietary gluten prior to diagnosis as reported, although not consistently, for the age-dependent increase of autoimmune diseases in CD patients.28, 29

We did not find a clear cut inverse relationship between ghrelin and BMI as reported by others16, 17 and as it would theoretically be expected8 given the low BMI of our CD patients and the role of ghrelin as regulator of body weight.3 The finding that BMI increased significantly during gluten-free diet indirectly suggests that our patients as a group were mildly malnourished, a condition that was reverted by gluten-free diet. This mild malnutrition together with the tendency that we found for ghrelin concentration to be particularly elevated in CD patients with clinical diagnosis of malabsorption suggest that circulating ghrelin levels may increase in untreated CD patients as a mechanism for long-term regulation of body weight, a well-documented effect of ghrelin in humans3 and in the experimental animal.2, 30

Although changes of serum ghrelin concentration during gluten-free diet were related with improvement of duodenal histopathology in our CD patients, this phenomenon is unlikely to reflect a cause–effect relationship. This interpretation is based on three main lines of evidence. First, we did not find higher ghrelin levels in patients with duodenal atrophy relative to patients without atrophy as it would be expected from the general concept that growth factors contribute to maintenance of mucosa integrity,31 and from the observation that circulating ghrelin level increases in animals with experimentally induced gastritis and colitis.9, 32 Secondly, marked inflammatory changes with massive intraepithelial lymphocytosis persisted in most of our patients (83%) during diet (Table 2) despite regression of duodenal atrophy, suggesting a minor role for inflammation in influencing circulating ghrelin in CD. Thirdly, circulating ghrelin was similar in dyspeptic patients without and with duodenal infiltration with T lymphocytes, an histopathological characteristic that is often recognized in conditions other than CD.33 Taken together these observations suggest that mucosal inflammation is not a major factor affecting the level of circulating ghrelin and indirectly highlights the role of impaired nutritional status in affecting ghrelin levels in CD.

To our knowledge this is the first report of increased ghrelin concentration in dyspeptic patients. It is noteworthy that BMI was lower in our dyspepsia patients not only than in healthy controls but also than in CD patients, suggesting that impairment of nutritional status may be involved in this effect for dyspeptic as for CD patients. Disordered gastroduodenal motility is among factors implicated in the pathogenesis of functional dyspepsia,34 particularly in patients with dysmotility-like syndrome as the majority of those entering the present study. A motility effect of ghrelin has been well documented,8, 35 and it is theoretically possible that functional abnormalities in dyspepsia may influence the levels of circulating ghrelin as suggested by the finding that ghrelin levels seems to be influenced by the severity of symptoms in a variety of conditions7, 36, 37 including dyspepsia in women.38

Altered gastrointestinal motility is also well described in untreated CD,39, 40 and it is intriguing to speculate that this effect may contribute to affect serum ghrelin concentration in this condition as for dyspepsia. Our preliminary observation41 that the motility defect in response to a physiological meal is not completely reverted to normal during gluten-free diet as reported by others in response to artificial meals,40 suggests that motility may not be an important factor affecting ghrelin concentration in CD.

In conclusion, our study indicates that circulating ghrelin level is increased in CD and reverts to normal during gluten-free diet. Mild malnutrition rather than duodenal mucosal inflammation is the most likely explanation for increased ghrelin concentration in untreated CD patients and in dyspeptic patients, although abnormal gastroduodenal motility may play a role in the latter condition.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References

No external funding was received for this study.


  1. Top of page
  2. Summary
  3. Introduction
  4. Materials and methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. References
  • 1
    Inui A. Ghrelin: an orexigenic and somatotrophic signal from the stomach. Nat Rev Neurosci 2001; 2: 55160.
  • 2
    Tschop M, Smiley DL, Heiman ML. Ghrelin induces adiposity in rodents. Nature 2000; 407: 90813.
  • 3
    Cummings DE, Weigle DS, Frayo RS, et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med 2002; 346: 162330.
  • 4
    Tschop M, Weyer C, Tataranni PA, et al. Circulating ghrelin levels are decreased in human obesity. Diabetes 2001; 50: 7079.
  • 5
    Cummings DE, Purnell JQ, Frayo RS, et al. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 2001; 50: 17149.
  • 6
    Otto B, Cuntz U, Fruehauf E, et al. Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa. Eur J Endocrinol 2001; 145: 66973.
  • 7
    Shimizu Y, Nagaya N, Isobe T, et al. Increased plasma ghrelin level in lung cancer cachexia. Clin Cancer Res 2003; 9: 7748.
  • 8
    Murray CD, Kamm MA, Bloom SR, et al. Ghrelin for the gastroenterologist: history and potential. Gastroenterology 2003; 125: 1492502.
  • 9
    Brzozowski T, Konturek PC, Konturek SJ, et al. Exogenous and endogenous ghrelin in gastroprotection against stress-induced gastric damage. Regul Pept 2004; 120: 3951.
  • 10
    Dixit VD, Schaffer EM, Pyle RS, et al. Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. J Clin Invest 2004; 114: 5766.
  • 11
    Farrell RJ, Kelly CP. Diagnosis of celiac sprue. Am J Gastroenterol 2001; 96: 323746.
    Direct Link:
  • 12
    Fasano A. Celiac disease – how to handle a clinical chameleon. N Engl J Med 2003; 348: 256870.
  • 13
    Capristo E, Addolorato G, Mingrone G, et al. Changes in body composition, substrate oxidation, and resting metabolic rate in adult celiac disease patients after a 1-y gluten-free diet treatment. Am J Clin Nutr 2000; 72: 7681.
  • 14
    Corazza GR, Di Sario A, Sacco G, et al. Subclinical coeliac disease: an anthropometric assessment. J Intern Med 1994; 236: 1837.
  • 15
    Marsh MN. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity (‘celiac sprue’). Gastroenterology 1992; 102: 33054.
  • 16
    Peracchi M, Conte D, Terrani C, et al. Circulating ghrelin levels in celiac patients. Am J Gastroenterol 2003; 98: 24748.
    Direct Link:
  • 17
    Capristo E, Farnetti S, Mingrone G, et al. Reduced plasma ghrelin concentration in celiac disease after gluten-free diet treatment. Scand J Gastroenterol 2005; 40: 4306.
  • 18
    Gee MI, Grace MG, Wensel RH, et al. Nutritional status of gastroenterology outpatients: comparison of inflammatory bowel disease with functional disorders. J Am Diet Assoc 1985; 85: 15919.
  • 19
    Talley NJ, Stanghellini V, Heading RC, et al. Functional gastroduodenal disorders. Gut 1999; 45(Suppl. 2):II3742.
  • 20
    Rostami K, Kerckhaert J, Tiemessen R, et al. Sensitivity of antiendomysium and antigliadin antibodies in untreated celiac disease: disappointing in clinical practice. Am J Gastroenterol 1999; 94: 88894.
    Direct Link:
  • 21
    Lanzini A, Villanacci V, Apillan N, et al. Epidemiological, clinical and histopathologic characteristics of celiac disease: results of a case-finding population-based program in an Italian community. Scand J Gastroenterol 2005; 40: 9507.
  • 22
    Sollid LM, Lie BA. Celiac disease genetics: current concepts and practical applications. Clin Gastroenterol Hepatol 2005; 3: 84351.
  • 23
    Villanacci V, Cornolti G, Lanzarotto F, et al. [Histopathological diagnosis of celiac disease in children and adults: 3 years’ experience]. Pathologica 2002; 94: 1621.
  • 24
    Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996; 20: 116181.
  • 25
    Oberhuber G, Granditsch G, Vogelsang H. The histopathology of coeliac disease: time for a standardized report scheme for pathologists. Eur J Gastroenterol Hepatol 1999; 11: 118594.
  • 26
    Ferguson A, Murray D. Quantitation of intraepithelial lymphocytes in human jejunum. Gut 1971; 12: 98894.
  • 27
    Armitage P, Berry G. Statistical Methods in Clinical Research, 3rd edn. Oxford: Blackwell Scientific Publications, 1994.
  • 28
    Ventura A, Magazzu G, Greco L. Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease. SIGEP Study Group for Autoimmune Disorders in Celiac Disease. Gastroenterology 1999; 117: 297303.
  • 29
    Sategna GC, Solerio E, Scaglione N, et al. Duration of gluten exposure in adult coeliac disease does not correlate with the risk for autoimmune disorders. Gut 2001; 49: 5025.
  • 30
    Nakazato M, Murakami N, Date Y, et al. A role for ghrelin in the central regulation of feeding. Nature 2001; 409: 1948.
  • 31
    Kitazawa T, De Smet B, Verbeke K, et al. Gastric motor effects of peptide and non-peptide ghrelin agonists in mice in vivo and in vitro. Gut 2005; 54: 107884.
  • 32
    Pawlik M, Brzozowski T, Kwiecien S. Role of exogenous and endogenous leptin and ghrelin in healing of colonic damage in experimental ulcerative colitis. Gastroenterology 2004; 126: A575.
  • 33
    Kakar S, Nehra V, Murray JA, et al. Significance of intraepithelial lymphocytosis in small bowel biopsy samples with normal mucosal architecture. Am J Gastroenterol 2003; 98: 202733.
    Direct Link:
  • 34
    Tack J, Bisschops R, Sarnelli G. Pathophysiology and treatment of functional dyspepsia. Gastroenterology 2004; 127: 123955.
  • 35
    Peeters TL. Ghrelin: a new player in the control of gastrointestinal functions. Gut 2005; 54: 163849.
  • 36
    Ariyasu H, Nakao K, Kangawa K. [Role of ghrelin in anorexia nervosa]. Nippon Rinsho 2004; 62(Suppl. 9):4103.
  • 37
    Nagaya N, Uematsu M, Kojima M, et al. Elevated circulating level of ghrelin in cachexia associated with chronic heart failure: relationships between ghrelin and anabolic/catabolic factors. Circulation 2001; 104: 20348.
  • 38
    Shinomiya T, Fukunaga M, Akamizu T, et al. Plasma acylated ghrelin levels correlate with subjective symptoms of functional dyspepsia in female patients. Scand J Gastroenterol 2005; 40: 64853.
  • 39
    Spiller RC, Lee YC, Edge C, et al. Delayed mouth-caecum transit of a lactulose labelled liquid test meal in patients with steatorrhoea caused by partially treated coeliac disease. Gut 1987; 28: 127582.
  • 40
    Lanzini A, Lanzarotto F. Review article: the ‘mechanical pumps’ and the enterohepatic circulation of bile acids–defects in coeliac disease. Aliment Pharmacol Ther 2000; 14(Suppl. 2): 5861.
  • 41
    Lanzini A, Benini F, Mora A, et al. Postprandial Gallbladder Emptying and Small Intestinal Transit in Celiac Patients: A Distinct Effect of Gluten Free Diet? BSG Annual Meeting, 20–23 March 2006, Birmingham Abstract, Gut 2006.