2026-06-30T03:25:33Zhttps://riubu.ubu.es/oai/request

oai:riubu.ubu.es:10259/99242025-01-16T01:05:34Zcom_10259_4862com_10259_5086com_10259_2604col_10259_4863

Herrerías-González, Fernando Yeramian, Andrée Baena-Fustegueras, Juan Antonio Bueno, Marta Fleitas, Catherine de la Fuente, Maricruz Serrano, José C. E. Granado-Serrano, Ana Santamaría, Maite Yeramian Hakim, Nadine Zorzano-Martínez, Marta Mora, Conchi Lecube, Albert PKN1 Visceral adipose tissue Insulin resistance Type 2 diabetes Adipocyte Glucose metabolism Adipocyte dysfunction is the driver of obesity and correlates with insulin resistance and the onset of type 2 diabetes. Protein kinase N1 (PKN1) is a serine/threonine kinase that has been shown to contribute to Glut4 translocation to the membrane and glucose transport. Here, we evaluated the role of PKN1 in glucose metabolism under insulin-resistant conditions in primary visceral adipose tissue (VAT) from 31 patients with obesity and in murine 3T3-L1 adipocytes. In addition, in vitro studies in human VAT samples and mouse adipocytes were conducted to investigate the role of PKN1 in the adipogenic maturation process and glucose homeostasis control. We show that insulinresistant adipocytes present a decrease in PKN1 activation levels compared to nondiabetic control counterparts. We further show that PKN1 controls the adipogenesis process and glucose metabolism. PKN1-silenced adipocytes present a decrease in both differentiation process and glucose uptake, with a concomitant decrease in the expression levels of adipogenic markers, such as PPARγ, FABP4, adiponectin and CEBPα. Altogether, these results point to PKN1 as a regulator of key signaling pathways involved in adipocyte differentiation and as an emerging player of adipocyte insulin responsiveness. These findings may provide new therapeutic approaches for the management of insulin resistance in type 2 diabetes. 2025-01-15 2025-01-15 2023-05 info:eu-repo/semantics/article http://hdl.handle.net/10259/9924 10.3390/nu15102414 2072-6643 spa Nutrients. V. 15, n. 10, p. 2414 https://doi.org/10.3390/nu15102414 http://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess Atribución 4.0 Internacional MDPI