Abstract
Desacyl ghrelin is produced in the gastric mucosa and plasma by deacylation of ghrelin. It occurs in considerably larger amounts than ghrelin in various regions in the organisms of rats and mice. It exerts biological activities in vitro as different as stimulating adipogenesis or inhibiting glucose output in hepatocytes. In fasted rats, desacyl ghrelin levels decreased under catabolic metabolic conditions and in mice, high desacyl ghrelin concentrations went along with decreased food intake. These observations suggest an influence of the peptide on food intake and energy homeostasis. Behavioral studies led to controversial results, but several suggest an anorexigenic effect. Studies on desacyl ghrelin-induced modulation of food intake indicate the involvement of central nervous pathways, since it is said to cross the blood–brain barrier and to induce increased neuronal activity hypothalamic nuclei. It is likely to be involved in the regulation of the synthesis of anorexigenic hypothalamic mediators. Quite possibly, there might be means of interaction between desacyl ghrelin and its supposable precursor ghrelin.
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