Fig. 6 Schematic representation of Mr activation as a possible peripheral mechanism leading to adiposity in Pomc mutants. The left panel shows the hypothalamus-pituitary-interrenal (HPI) axis function in the wildtype larvae leading to normal growth post-feeding. The right panel shows that the loss of Pomc leads to a lack of Acth and this leads to a reduced Gr responsiveness and an enhanced Mr responsiveness, which regulates adipogenic genes, including pparg, lpl and fasn, leading to adiposity. Acth, Adrenocorticotropic hormone; Crh, Corticotropin-releasing hormone; fasn, Fatty acid synthase; Gr, Glucocorticoid receptor; lpl, Lipoprotein lipase; Mr, Mineralocorticoid receptor; Pomc, Proopiomelanocortin; ppary, Peroxisome proliferator-activated receptor gamma.
Image
Figure Caption
Acknowledgments
This image is the copyrighted work of the attributed author or publisher, and
ZFIN has permission only to display this image to its users.
Additional permissions should be obtained from the applicable author or publisher of the image.
Full text @ J. Cell. Physiol.