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Tag: obesity (page 2 of 8)

II reunión científica Immunothercan-CM (13 December 2018)

El próximo jueves 13 de diciembre de 2018 tendrá lugar la segunda reunión científica del consorcio Immunothercan-CM, en el Centro Nacional de Biotecnología (Campus Universidad Autónoma).

En esta reunión, los investigadores pre y postdoctorales de los distintos grupos presentarán los últimos avances en los proyectos que se desarrollan en el marco del consorcio. Además, se discutirán aspectos que fomenten la colaboración entre los grupos.

Immunothercan

Programa de la II reunión científica Immunothercan-CM

El impacto de la genética en las enfermedades y sus tratamientos (10 December 2018)

Guadalupe Sabio y Adrián Llerena participarán en la conferencia de divulgación científica sobre el impacto de la genética en las enfermedades sus tratamientos, que celebra el 10 de diciembre de 2018, en horario de 11:30 a 14:00 horas, en las instalaciones del Parque Científico y Tecnológico de Extremadura, en Badajoz.

Protein kinase D1 deletion in adipocytes enhances energy dissipation and protects against adiposity

Mona C. Löffler, Alexander E. Mayer, Jonathan Trujillo Viera, Angel Loza Valdes, Rabih El‐Merahbi, Carsten P. Ade, Till Karwen, Werner Schmitz, Anja Slotta, Manuela Erk, Sudha Janaki‐Raman, Nuria Matesanz, Jorge L. Torres, Miguel Marcos, Guadalupe Sabio, Martin Eilers, Almut Schulze, Grzegorz Sumara.

Nutrient overload in combination with decreased energy dissipation promotes obesity and diabetes. Obesity results in a hormonal imbalance, which among others activates G protein‐coupled receptors utilizing diacylglycerol (DAG) as secondary messenger. Protein kinase D1 (PKD1) is a DAG effector, which integrates multiple nutritional and hormonal inputs, but its physiological role in adipocytes is unknown.

Correlation between PKD1 and HOMA‐IR

Correlation between PKD1 expression and HOMA‐IR levels in human sWAT (Image: Nuria Matesanz).

Here, we show that PKD1 promotes lipogenesis and suppresses mitochondrial fragmentation, biogenesis, respiration, and energy dissipation in an AMP‐activated protein kinase (AMPK)‐dependent manner. Moreover, mice lacking PKD1 in adipocytes are resistant to diet‐induced obesity due to elevated energy expenditure. Beiging of adipocytes promotes energy expenditure and counteracts obesity. Consistently, deletion of PKD1 promotes expression of the β3‐adrenergic receptor (ADRB3) in a CCAAT/enhancer binding protein (C/EBP)‐α‐ and δ‐dependent manner, which leads to the elevated expression of beige markers in adipocytes and subcutaneous adipose tissue. Finally, deletion of PKD1 in adipocytes improves insulin sensitivity and ameliorates liver steatosis.

Our results showed that p38δ is activated in BAT by cold exposure, and lack of this kinase specifically in adipose tissue (p38δFab-KO) resulted in overweight together with reduced energy expenditure and lower body and skin surface temperature in the BAT region. These observations indicate that p38α probably blocks BAT thermogenesis through p38δ inhibition. Consistent with the results obtained in animals, p38α was reduced in visceral and subcutaneous adipose tissue of subjects with obesity and was inversely correlated with body mass index (BMI).

Thus, depletion of PKD1 in adipocytes increases energy dissipation by several complementary mechanisms and might represent an attractive strategy to treat obesity and its related complications.

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