In the present study, we therefore analyzed both, AcG and UnG, in a large cohort of metabolically well-characterized individuals covering a large BMI range at baseline as well as after oral glucose ingestion to address the questions if, first, AcG is also diminished in obesity and whether the proportion of AcG and UnG is altered, second circulating ghrelin (AcG and UnG) is associated with insulin resistance independent of obesity and third, post-glucose (oGTT) ghrelin alterations are associated with obesity or insulin resistance. This evidence concerns the gene GHRL and obesity due to melanocortin 4 receptor deficiency.