Guillemin Roger Biography
Guillemin Roger, born in Dijon in 1924, obtained his doctorate in medicine in Lyon and his Ph. D. in experimental medicine and surgery at the University of Montreal. He was then professor of physiology at Baylor University College in Houston from 1953 to 1960, director of the department of experimental endocrinology at the Collège de France from 1960 to 1963, and then again in Houston. In 1970, he and his research group moved to the Salk Institute in La Jolla, California.
Guillemin was awarded the Nobel Prize in Physiology or Medicine in 1977, together with AV Schally, for his research on the hypothalamic regulation of anterior pituitary secretions. His discoveries have provided an important practical contribution to the treatment of some dysendocrinia and the control of fertility. In 1989, Guillemin abandoned the presidency of the neuroendocrinology laboratories of the Salk Institute for Biological Studies in La Jolla, which he had held since 1970. Instead, he decided to follow his artistic passion, creating an original expressive style that takes advantage of the most advanced technologies IT. His works are now exhibited in the main American and European galleries.
The research of Guillemin and his group represented the development, implemented with uncommon technical and financial resources, of the discoveries of GW Harris (1913-71). The latter had demonstrated that the secretions of the adenohypophysis are regulated by substances, then configured as factors releasing the thyrotropic hormones (TRF), luteinizing hormones (LRF) and follicle stimulating hormones (FRF), which reach the gland via the pituitary portal vessels. Guillemin then identified the hypothalamic factors (releasing factors) that promote the pituitary secretion of thyrotropic hormone and luteinizing hormone. He also demonstrated that the latter is also active on follicle-stimulating hormone, of which he identified the peptide structure and carried out the synthesis. His subsequent research focused on endorphins and somatostatin.