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Brown adipose tissue–specific insulin receptor knockout shows diabetic phenotype without insulin resistance
Carmen Guerra, Paloma Navarro, Angela M. Valverde, Monica Arribas, Jens Brüning, Leslie P. Kozak, C. Ronald Kahn, and Manuel Benito
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Published January 2, 2019 - More info
J Clin Invest. 2019;129(1):437–437. https://doi.org/10.1172/JCI126191.
Copyright © 2019, American Society for Clinical Investigation
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Abstract
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.
Authors
Carmen Guerra, Paloma Navarro, Angela M. Valverde, Monica Arribas, Jens Brüning, Leslie P. Kozak, C. Ronald Kahn, Manuel Benito
Original citation: J Clin Invest. 2001;108(8):1205–1213. https://doi.org/10.1172/JCI13103
Citation for this Expression of Concern: J Clin Invest. 2019;129(1):437. https://doi.org/10.1172/JCI126191
A reader recently contacted the Editors regarding possible duplication of portions of the images presented in Figure 3, A–C, and Figure 4, A and B, that were used to represent distinct samples. The Editors have requested that the corresponding author provide the original data supporting these figures; however, these data are no longer available. As we are unable to evaluate the integrity of these figures, we are publishing this notice to alert readers to the concern.
The corresponding author dissents from the JCI’s decision to issue this Expression of Concern.
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ISSN: 0021-9738 (print), 1558-8238 (online)