2026-04-29T12:23:45Zhttps://repisalud.isciii.es/rest/oai/request
oai:repisalud.isciii.es:20.500.12105/230902024-11-29T15:20:12Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud author Guerra, C author Navarro, P author Valverde, A M author Arribas, M author Brüning, J author Kozak, L P author Kahn, C R author Benito, M funder NIH - National Cancer Institute (NCI) (Estados Unidos) 2024-09-16T08:16:59Z 2024-09-16T08:16:59Z 2001-10 J Clin Invest . 2001;108(8):1205-13. 10.1172/JCI13103 0021-9738 The Journal of clinical investigation 11602628 https://hdl.handle.net/20.500.12105/23090 Although insulin regulates metabolism in both brown and white adipocytes, the role of these tissues in energy storage and utilization is quite different. Recombination technology using the Cre-loxP approach allows inactivation of the insulin receptor in a tissue-specific manner. Mice lacking insulin receptors in brown adipocytes show an age-dependent loss of interscapular brown fat but increased expression of uncoupling protein-1 and -2. In parallel, these mice develop an insulin-secretion defect resulting in a progressive glucose intolerance, without insulin resistance. This model provides direct evidence for not only a role for the insulin receptors in brown fat adipogenesis, the data also suggest a novel role of brown adipose tissue in the regulation of insulin secretion and glucose homeostasis. eng Brown adipose tissue-specific insulin receptor knockout shows diabetic phenotype without insulin resistance. research article