The lab is mainly focusing on healthy expansion of white adipose tissue (WAT).
WAT is a critical metabolic organ that contributes to energy storage, endocrine homeostasis, and metabolic flexibility by efficiently storing the surplus of fuel and quickly mobilising lipids/energy to supply peripheral organs. In the context of the current obesity epidemic, the demands imposed on the expandability and functionality of WAT are paramount, overwhelming WAT capacity to store and mobilise fat promoting the development of metabolic comorbidities.
Whereas most research aims to understand why obese people develop comorbidities, we will study the opposite paradigm, why some obese people are resilient and do not develop comorbidities. Knowing all the molecular layers explaining how to uncouple having excess adiposity from developing metabolic complications is essential to keep obese people healthy. There is plenty of information about the unhealthy inflamed human adipose tissue. Paradoxically, there is a paucity of knowledge about the critical molecular components driving human WAT development and healthy expansion against comorbidities.
Our question is not why obese patients develop comorbidities but how to make them resilient, and we hypothesise that this depends on the mechanisms that keep their adipose tissue healthy irrespectively of its size.
To answer this question we will
- Identify genetic variants associated with increased risk of obesity but have protective cardiometabolic effects, and vice versa.
- Prioritise and genetically mutate the candidate genes using a human stem cell approach and CRIPRs/Cas9 technology
- Validate tin vitro and in vivo the functionality of the candidate genes.
Using the same approaches, we are also interested to prioritise and study candidate genes involved in human brown/beige adipocytes differentiation and activation as a strategy to counteract obesity and metabolic complications.
Get to know us better
The people who make it all possible
Mª Carmen Navarro González
Our scientific contributions
Unraveling the Developmental Roadmap toward Human Brown Adipose Tissue
S. CAROBBIO, A. GUENANTIN, M. BAHRI, S. RODRIGUEZ-FDEZ, F. HONIG, I. KAMZOLAS, I. SAMUELSON, K. LONG, S. AWAD, D. LUKOVIC, S. ERCEG, A. BASSETT, S. MENDJAN, L. VALLIER, B. ROSEN, D. CHIARUGI and A. VIDAL-PUIG
Stem Cell Reports, 2021 Mar,  DOI:  10.1016/j.stemcr.2021.01.013,  Vol. 16,  pag. 641-655
Genome-wide discovery of genetic loci that uncouple excess adiposity from its comorbidities.
Huang LO, Rauch A, Mazzaferro E, Preuss M, Carobbio S, Bayrak CS, Chami N, Wang Z, Schick UM, Yang N, Itan Y, Vidal-Puig A, den Hoed M, Mandrup S, Kilpeläinen TO and Loos RJF
Nature Metabolism, 2021 Feb,  DOI:  10.1038/s42255-021-00346-2,  Vol. 3,  pag. 228-243
Brown and beige fat: From molecules to physiology and pathophysiology.
Carobbio S, Guénantin AC, Samuelson I, Bahri M and Vidal-Puig A
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 2019 Jan,  DOI:  10.1016/j.bbalip.2018.05.013,  Vol. 1864,  pag. 37-50
Adaptive changes of the Insig1/SREBP1/SCD1 set point help adipose tissue to cope with increased storage demands of obesity.
Carobbio S, Hagen RM, Lelliott CJ, Slawik M, Medina-Gomez G, Tan CY, Sicard A, Atherton HJ, Barbarroja N, Bjursell M, Bohlooly-Y M, Virtue S, Tuthill A, Lefai E, Laville M, Wu T, Considine RV, Vidal H, Langin D, Oresic M, Tinahones FJ, Fernandez-Real JM, Griffin JL, Sethi JK, López M and Vidal-Puig A
DIABETES, 2013 Nov,  DOI:  10.2337/db12-1748,  Vol. 62,  pag. 3697-3708
BMP8B increases brown adipose tissue thermogenesis through both central and peripheral actions.
Whittle AJ, Carobbio S, Martins L, Slawik M, Hondares E, Vázquez MJ, Morgan D, Csikasz RI, Gallego R, Rodriguez-Cuenca S, Dale M, Virtue S, Villarroya F, Cannon B, Rahmouni K, López M and Vidal-Puig A
CELL, 2012 May,  DOI:  10.1016/j.cell.2012.02.066,  Vol. 149,  pag. 871-885