Gama Perez 2023 MiP2023
 |
Link: MiP2023 Obergurgl AT
Gama Perez Pau (2023)
Event: MiP2023 Obergurgl AT
Authors: Gama Perez Pau, Dahdah Norma, Kulis Marta, Chapaprieta Vicente, Espino-Guarch Meritxell, Martin-Subero Jose Ignacio, Garcia-Roves Pablo M
Aging is perhaps the most paradigmatic example of metabolic plasticity loss, and mitochondrial derangements play a critical role in this process. Several studies have evidenced a particular exhaustion of this organelle as we age, which favors the onset of many associated pathologies. Of note, adipose tissue has been proved to be one of the most vulnerable tissues during aging progression with a remarkable metabolic impairment that ultimately compromise its plasticity. Obesity, on the other hand, has also a strong detrimental impact on mitochondrial performance and metabolic health. In our laboratory we have evidenced that this fingerprint persists particularly in the visceral adipose tissue of young animals even after the successful implementation of weight-loss strategies, which suggests the tissue exceeded a similar “point of no return” to that described in aged models. With all this, we aim to explore the adipose tissue phenotype of young obese and formerly obese mice from an aging perspective in order to test the idea of obesity being an early instigator of age-associated metabolic deterioration. We will present data of transcriptional changes occurring in our obesity model compared with data from aging models available in public repositories, and we will explore the commonality of biological processes mostly affected by both stressors, mainly mitochondria, immune system, and inflammation. In addition, we will complement this comparative analysis with transcriptional and functional data obtained from adipose precursor cells, since they host most of the indelible marks associated with aging and play a fundamental role in tissue remodeling processes.
Labels: Pathology: Aging;senescence, Obesity
Event: E2
