Nicholas Michael Morton
Corresponding author: Nicholas M. Morton
Name/email consistency: high
- Optimal Elevation of β-Cell 11β-Hydroxysteroid Dehydrogenase Type 1 Is a Compensatory Mechanism That Prevents High-Fat Diet-Induced β-Cell Failure. Turban, S., Liu, X., Ramage, L., Webster, S.P., Walker, B.R., Dunbar, D.R., Mullins, J.J., Seckl, J.R., Morton, N.M. Diabetes (2012)
- Dietary manipulation reveals an unexpected inverse relationship between fat mass and adipose 11{beta}-hydroxysteroid dehydrogenase type 1. Man, T.Y., Michailidou, Z., Gokcel, A., Ramage, L., Chapman, K.E., Kenyon, C.J., Seckl, J.R., Morton, N.M. Am. J. Physiol. Endocrinol. Metab. (2011)
- Obesity and corticosteroids: 11beta-hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease. Morton, N.M. Mol. Cell. Endocrinol. (2010)
- A polygenic model of the metabolic syndrome with reduced circulating and intra-adipose glucocorticoid action. Morton, N.M., Densmore, V., Wamil, M., Ramage, L., Nichol, K., Bünger, L., Seckl, J.R., Kenyon, C.J. Diabetes (2005)
- Down-regulation of adipose 11beta-hydroxysteroid dehydrogenase type 1 by high-fat feeding in mice: a potential adaptive mechanism counteracting metabolic disease. Morton, N.M., Ramage, L., Seckl, J.R. Endocrinology (2004)
- Novel adipose tissue-mediated resistance to diet-induced visceral obesity in 11 beta-hydroxysteroid dehydrogenase type 1-deficient mice. Morton, N.M., Paterson, J.M., Masuzaki, H., Holmes, M.C., Staels, B., Fievet, C., Walker, B.R., Flier, J.S., Mullins, J.J., Seckl, J.R. Diabetes (2004)
- Improved lipid and lipoprotein profile, hepatic insulin sensitivity, and glucose tolerance in 11beta-hydroxysteroid dehydrogenase type 1 null mice. Morton, N.M., Holmes, M.C., Fiévet, C., Staels, B., Tailleux, A., Mullins, J.J., Seckl, J.R. J. Biol. Chem. (2001)









