title: Hormonal and metabolic responses to acute ghrelin administration in patients with bulimia nervosa.
abstract: Ghrelin is generally influenced by energy balance status and is inversely associated with body mass index (BMI), being reduced in simple obesity, notable exception being Prader Willi syndrome, and elevated in several conditions of undernutrition, including anorexia nervosa (AN). Interestingly, ghrelin levels have also been found elevated in patients with bulimia nervosa (BN) in spite of normal BMI. In humans, intravenous (iv) ghrelin administration induces endocrine (increase in GH, PRL, ACTH and cortisol) and metabolic (increase in glucose and decrease in insulin) effects as well as an increase in appetite and food intake. In AN, ghrelin administration surprisingly leads to a decreased GH response and absence of glycemic variations but normal PRL, ACTH and insulin response. This pattern would reflect a decrease in sensitivity to ghrelin or, alternatively, the metabolic status of AN. To further clarify the function of ghrelin in eating disorders, the endocrine and metabolic response to acute iv ghrelin (1.0 microg/kg) was studied in seven young women with purging BN (BW, BMI, mean+/-SEM: 20.3+/-0.5 kg/m2). Circulating total ghrelin levels were also measured. The results in BW were compared to those recorded in a group of nine healthy women (HW; BMI 22.3+/-2.5 kg/m2). The GH response to ghrelin in BW overlapped with that in HW. Ghrelin administration also led to a similar increase in PRL, ACTH, cortisol and glucose levels in the two groups. Insulin levels were not significantly modified by ghrelin administration in either group. The overlapping endocrine and metabolic response to ghrelin in the two groups occurred with regard to circulating total ghrelin levels which were higher in BW than in HW. In conclusion, BN, a condition of ghrelin hypersecretion, is connoted by a normal endocrine and metabolic response to exogenous ghrelin administration.
authors.affiliation: Division of Psychiatry, Department of Neuroscience, University of Turin, Via Cherasco 11, 10126 Turin, Italy. secondo.fassino@unito.it
authors.forename: S
authors.initials: S
authors.lastname: Fassino
authors.forename: G Abbate
authors.initials: GA
authors.lastname: Daga
authors.forename: V
authors.initials: V
authors.lastname: Mondelli
authors.forename: A
authors.initials: A
authors.lastname: Pierò
authors.forename: F
authors.initials: F
authors.lastname: Broglio
authors.forename: A
authors.initials: A
authors.lastname: Picu
authors.forename: R
authors.initials: R
authors.lastname: Giordano
authors.forename: M
authors.initials: M
authors.lastname: Baldi
authors.forename: E
authors.initials: E
authors.lastname: Arvat
authors.forename: E
authors.initials: E
authors.lastname: Ghigo
authors.forename: L
authors.initials: L
authors.lastname: Gianotti
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000502:physiology; D002032:Bulimia / Q000503:physiopathology*; D004435:Eating / Q000502:physiology*; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D054439:Ghrelin; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D016555:Matched-Pair Analysis; D036361:Peptide Hormones / Q000008:administration & dosage / Q000502:physiology*; D011388:Prolactin / Q000097:blood; D012016:Reference Values; D018709:Statistics, Nonparametric
chemical_list: D001786:Blood Glucose; D054439:Ghrelin; D007328:Insulin; D036361:Peptide Hormones; D019382:Human Growth Hormone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D006854:Hydrocortisone