Endocrine Abstracts

Background: Although acyl–ghrelin has been considered essential for ghrelin’s GH-releasing activity, several recent in vitro studies have shown that desacyl–ghrelin exhibits biological activities on metabolism and proliferation of adipocytes, myocytes, cardiomyocytes, and myelocytes. The full desacyl–ghrelin biological activity still remains a matter of debate.

Aims: To assess desacyl–ghrelin circulating levels and its R51Q polymorphism as a risk factor for obesity in women.

Materials and methods: Seventy three healthy women (35.9±8.1 years) and ninety one obese women (34.7±8.0 years) were included in the study. Obese women were characterized by a BMI=43.1±8.1 kg/m², waist=117±1.50 cm, hip=133±1.35 cm and absence of kidney, hepatic, inflammatory or neoplasic disease. The ghrelin polymorphism was assessed by real time PCR with Taqman probes. Desacyl–ghrelin plasma levels were obtained by ELISA (Cayman). All statistical analyses were performed using the software SPSS, version 15.0.

Results: Desacyl–ghrelin levels were significantly lower in the obese group (P<0.001) and significantly inverse associations were found between this form of ghrelin and BMI, waist and hip circumferences and percentage of total body fat (P<0.001 for all). Despite the absence of significance in allele or genotype frequency between groups, R allele was significantly associated with higher desacyl–ghrelin in non-obese women (P<0.001).

Conclusion: These results support recent in vitro findings that desacyl–ghrelin may induce a negative energy balance in contrast to the acylated form and that could be genetically determined. Better understanding of the role of desacyl–ghrelin may provide a new therapeutic approach for the treatment of obesity.