Dr. Rahbani aims at elucidating new basic molecular mechanisms that could provide opportunities for developing novel treatments to limit tumor progression, improve cachexia in cancer patients and combat obesity. The first focus of his laboratory is to understand the multiplex interplay of energy wasting pathways in cancer-associated cachexia. In particular, he is interested in identifying how futile cycles and thermogenesis in adipose tissues contribute to muscle atrophy and how fat and skeletal muscle adapt their metabolism during early stages of cachexia. The second focus of his laboratory is to constrain tumor growth by targeting adipose tissue metabolism and promoting the greatest amount of energy expenditure. Understanding the significant capacity for mitochondria in adipocytes to coordinate various biological outcomes by exerting control over cellular bioenergetics, biosynthesis and signaling will extend insight towards recognizing how to offset metabolic diseases, such as cancer, obesity and diabetes.
Goodman Cancer Institute
Canada
PDF - Biochemistry
2024
McGill University
Canada
Ph.D - Chemical Biology
2018
American University of Beirut
Lebanon
MSc - Chemistry
2012
Coenzyme A is a redox sensing cofactor for malic enzyme 2 regulating oxidative stress and mitochondrial metabolism.
Coenzyme A is a redox sensing cofactor for malic enzyme 2 regulating oxidative stress and mitochondrial metabolism. bioRxiv. 2026 Apr 28.
PMID: 42094367
Glycerol-driven TNAP activation in thermogenesis and mineralization.
Glycerol-driven TNAP activation in thermogenesis and mineralization. Nature. 2026 Jun; 654(8117):198-208.
PMID: 42020733
Creatine kinase B regulates glycolysis and de novo lipogenesis pathways to control lipid accumulation during adipogenesis.
Creatine kinase B regulates glycolysis and de novo lipogenesis pathways to control lipid accumulation during adipogenesis. Cell Rep. 2025 11 25; 44(11):116489.
PMID: 41196679
Cold exposure induces the constitutively active thermogenic receptor, GPR3, via ERRa and ERR?.
Cold exposure induces the constitutively active thermogenic receptor, GPR3, via ERRa and ERR?. Mol Metab. 2026 Jan; 103:102277.
PMID: 41173363
The Futile Creatine Cycle powers UCP1-independent thermogenesis in classical BAT.
The Futile Creatine Cycle powers UCP1-independent thermogenesis in classical BAT. Nat Commun. 2025 Apr 04; 16(1):3221.
PMID: 40185737
Parallel control of cold-triggered adipocyte thermogenesis by UCP1 and CKB.
Parallel control of cold-triggered adipocyte thermogenesis by UCP1 and CKB. Cell Metab. 2024 03 05; 36(3):526-540.e7.
PMID: 38272036
ADRA1A-Gaq signalling potentiates adipocyte thermogenesis through CKB and TNAP.
ADRA1A-Gaq signalling potentiates adipocyte thermogenesis through CKB and TNAP. Nat Metab. 2022 11; 4(11):1459-1473.
PMID: 36344764
A brown fat-selective mechanism of mitochondrial calcium import?
A brown fat-selective mechanism of mitochondrial calcium import? Cell Metab. 2022 09 06; 34(9):1231-1233.
PMID: 36070679
Creatine transport and creatine kinase activity is required for CD8+ T cell immunity.
Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. Cell Rep. 2022 03 01; 38(9):110446.
PMID: 35235777
Measurement of Futile Creatine Cycling Using Respirometry.
Measurement of Futile Creatine Cycling Using Respirometry. Methods Mol Biol. 2022; 2448:141-153.
PMID: 35167096