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עמוד בית
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February 2012
D. Boltin and Y. Niv
Eradication of Helicobacter pylori is accompanied by an array of metabolic and hormonal changes in the host. Weight gain following H. pylori eradication is a poorly understood phenomenon and probably results from an interaction between multiple factors. Ghrelin, a peptide hormone secreted by the stomach, is involved in the regulation of food intake and appetite and may account for some of these changes. Although several observational studies have demonstrated that H. pylori infection suppresses circulating ghrelin levels, it has yet to be proven that ghrelin levels increase following eradication. On the other hand, gastric expression of ghrelin, also suppressed by H. pylori, clearly increases following eradication. The determinants of plasma ghrelin levels remain elusive, as do the effects of eradication on these levels. Weight gain following H. pylori eradication may be attributable to changes in plasma and gastric ghrelin however, this hypothesis needs to be further investigated.
August 2002
Fabio Broglio, MD, Emanuela Arvat, MD, Andrea Benso, MD, Cristina Gottero, MD, Flavia Prodam, MD, Riccarda Granata, PhD, Mauro Papotti, MD, Giampiero Muccioli, PhD, Romano Deghenghi, PhD and Ezio Ghigo, MD

Ghrelin, a 28 amino acid acylated peptide predominantly produced by the stomach, displays strong growth hormone-releasing activity mediated by the hypothalamus-pituitary GH[1] secretagogue receptors that were found to be specific for a family of synthetic, orally active GH secretagogues. The discovery of ghrelin brings us to a new understanding of the regulation of GH secretion. However, ghrelin is much more than simply a natural GH secretagogue. It also acts on other central and peripheral receptors and exhibits other actions, including stimulation of lactotroph and corticotroph secretion, orexigenia, influences gastroenteropancreatic functions, and has metabolic, cardiovascular and anti-proliferative effects. Knowledge of the whole spectrum of biologic activities of this new hormone will provide new understanding of some critical aspects of neuroscience, metabolism and internal medicine. In fact, GHS[2] were born more than 20 years ago as synthetic molecules, eliciting the hope that orally active GHS could be used to treat GH deficiency as an alternative to recombinant human GH. However, the dream did not become reality and the usefulness of GHS as an anabolic anti-aging intervention restoring the GH/IGF-I[3] axis in somatopause is still unclear. Instead, we now face the theoretic possibility that GHS analogues acting as agonists or antagonists could become candidate drugs for the treatment of pathophysiologic conditions in internal medicine totally unrelated to disorders of GH secretion. 




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[1]
GH = growth hormone

[2] GHS = GH secretagogues

[3] GH/IGF-1 = growth hormone/insulin-like growth factor-I

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