Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 20 P591

Department of Endocrinology, Metabolism and Internal Diseases, University of Medical Sciences, Poznan, Poland.


The role of ghrelin in the pathogenesis of acromegaly is doubtful. Ghrelin also regulates glucose and adipose tissue metabolism. It has not been demonstrated whether it contributes to the development of metabolic complications of acromegaly.

Aim: The aim of the study was to assess: (1) whether serum concentrations of total and acyl ghrelin in patients with acromegaly differ in relation to coexisting metabolic complications (hypercholesterolemia, hyperinsulinemia, hyperglicemia). (2) correlations between concentrations of ghrelin and concentrations of GH, IGF-1, cholesterol, insulin and glucose in patients with acromegaly.

Materials: Twenty-four patients with previously diagnosed acromegaly (16 women and 8 men, 27–71 years old) (11 subjects with active and 13 subjects with inactive disease) and 12 healthy subjects. Twenty-three subjects were treated in the past with neurosurgery, 3 subjects with radiotherapy. Seven patients were receiving octreotide LAR at the time of the study. Methods: In all studied subjects the concentrations of total ghrelin, acyl ghrelin, GH, IGF-1, insulin, glucose, total cholesterol, LDL cholesterol, HDL cholesterol, triglicerydes, were measured.

Results: (1) Mean concentrations of total and acyl ghrelin were significantly higher in patients with acromegaly and hypercholesterolemia compared with patients with normocholesterolemia (P=0.01 total ghrelin; P=0.05 acyl ghrelin). (2) In patients with hypercholesterolemia the ratio of acyl/total ghrelin was 16%. (3) In patients with active acromegaly there was a statistically significant positive correlation between the concentration of total ghrelin and the concentration of total cholesterol (P=0.03, r=0.63) and LDL cholesterol (P=0.03, r=0.64). There was also a positive correlation between the concentration of acyl ghrelin and LDL cholesterol (without statistical significance, P=0.07). (4) In patients with inactive acromegaly there was a statistically significant positive correlation between the concentration of acyl ghrelin and the concentration of triglycerides (P=0.03, r=0.6) and a positive correlation between total ghrelin and triglycerides, but statistically insignificant (P=0.08).

Conclusions: Ghrelin might be the factor contributing to development of hypercholesterolemia in patients with acromegaly. Presumably, some metabolic complications of the disease result not only from GH hypersecretion but also from altered ghrelin secretion.

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