Given the remarkable effects of CNTF on rodent white adipose tissue and its potential to treat human obesity, we performed a series of experiments to characterize the signaling systems, transcriptional changes, glucose uptake and inflammatory responses modulated by acute and/or long-term CNTF treatment using cultured adipose cells differentiated from human multipotent adipose tissue-derived stem (hMADS) cells (26, 27). This evidence concerns the gene CNTF and obesity due to melanocortin 4 receptor deficiency.