Andoni Lancha1, Santiago López-Garrido2, Amaia Rodríguez3, Victoria Catalán3, Beatriz Ramírez3, Víctor Valentí4, Rafael Moncada5, Camilo Silva6, María J Gil7, Javier Salvador8, Gema Frühbeck9, Javier Gómez-Ambrosi10. 1. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain. 2. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain. 3. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain. 4. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain; Department of Surgery, Clínica Universidad de Navarra, Pamplona, Spain. 5. Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain; Department of Anesthesia, Clínica Universidad de Navarra, Pamplona, Spain. 6. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain; Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain. 7. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain; Department of Biochemistry, Clínica Universidad de Navarra, Pamplona, Spain. 8. CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain. 9. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain; Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain. 10. Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain; Obesity and Adipobiology Group, Instituto de Investigación Sanitaria de Navarra, Pamplona, Spain. Electronic address: jagomez@unav.es.
Abstract
BACKGROUND AND AIMS: Obesity is associated with increased adipose tissue inflammation as well as with the development of type 2 diabetes (T2D). Syntaxin 8 (STX8) is a protein required for the transport of endosomes. In this study we analyzed the relationship of STX8 with the presence of T2D in the context of obesity. METHODS: With this purpose, 21 subjects (seven lean [LN], eight obese normoglycemic [OB-NG] and six obese with type 2 diabetes [OB-T2D]) were included in the study. Gene and protein expression levels of STX8 and GLUT4 were analyzed in visceral adipose tissue (VAT). RESULTS: mRNA (p = 0.008) and protein (p <0.001) expression levels of STX8 were significantly increased in VAT of OB-T2D patients. Moreover, gene expression levels of SLC2A4 (GLUT4) were downregulated (p = 0.002) in VAT of obese patients. We found that STX8 was positively correlated (p <0.05) with fasting glucose concentrations, plasma glucose 2 h after an OGTT and C-reactive protein. Interestingly, the expression of STX8 was negatively correlated (p <0.05) with the expression of SLC2A4 in VAT. CONCLUSIONS: Increased STX8 expression in VAT appears to be associated with the presence of T2D in obese patients through a mechanism that may involve GLUT4.
BACKGROUND AND AIMS: Obesity is associated with increased adipose tissue inflammation as well as with the development of type 2 diabetes (T2D). Syntaxin 8 (STX8) is a protein required for the transport of endosomes. In this study we analyzed the relationship of STX8 with the presence of T2D in the context of obesity. METHODS: With this purpose, 21 subjects (seven lean [LN], eight obese normoglycemic [OB-NG] and six obese with type 2 diabetes [OB-T2D]) were included in the study. Gene and protein expression levels of STX8 and GLUT4 were analyzed in visceral adipose tissue (VAT). RESULTS: mRNA (p = 0.008) and protein (p <0.001) expression levels of STX8 were significantly increased in VAT of OB-T2Dpatients. Moreover, gene expression levels of SLC2A4 (GLUT4) were downregulated (p = 0.002) in VAT of obesepatients. We found that STX8 was positively correlated (p <0.05) with fasting glucose concentrations, plasma glucose 2 h after an OGTT and C-reactive protein. Interestingly, the expression of STX8 was negatively correlated (p <0.05) with the expression of SLC2A4 in VAT. CONCLUSIONS: Increased STX8 expression in VAT appears to be associated with the presence of T2D in obesepatients through a mechanism that may involve GLUT4.
Authors: Tamara Camino; Nerea Lago-Baameiro; Susana B Bravo; Aurelio Sueiro; Iván Couto; Fernando Santos; Javier Baltar; Felipe F Casanueva; María Pardo Journal: Int J Mol Sci Date: 2020-03-24 Impact factor: 5.923