Ricquier specializes in the
physiology and biochemistry of mitochondria,
adipose tissue and
thermogenic mechanisms. He is an expert on
brown adipose tissue. His work has contributed towards identifying a family of proteins involved in mitochondrial respiration,
ATP yield, heat production and mitochondrial control of the level of cellular oxygenated
free radicals. Ricquier described in 1976 a mitochondrial membrane protein specific for brown adipocytes, later named UCP (
uncoupling protein) and identified by David Nicholls as the protein responsible for
heat energy dissipation. Having isolated antibodies specific to this protein, he demonstrated brown adipocytes in
neonates and adult patients and demonstrated that the
sympathetic nervous system controls the development of brown adipose tissue and the synthesis of DCS in animals and humans. With Fréderic Bouillaud, in 1984 and in collaboration with
Jean Weissenbach at the
Pasteur Institute, he isolated and sequenced the complementary
DNA of the UCP and the UCP gene from rodents and humans. He then analyzed the mechanisms of control of the tissue-specific transcription of the UCP gene. In addition, he studied the functional organization of this membrane protein. Ricquier identified and characterized in 1997 a second UCP protein called UCP2, the brown adipocyte UCP being renamed UCP1. He also identified a new cerebral mitochondrial transporter, BMCP, an avian UCP and a renal mitochondrial transporter KMCP and contributed to the identification of the first plant UCP protein. He was able to obtain mice without the UCP2 gene, demonstrating the essential role of this gene in innate immunity and the limitation of free radical levels, particularly in macrophages in collaboration with Denis Richard at
Laval University. This function of UCP2 has been confirmed by the demonstration of a protective role of UCP2 against atherosclerosis. Ricquier has demonstrated that mutations in the UCP2 protein induce
congenital hyperinsulinism in children at birth. He also described a protective role for UCP2 against autoimmune diabetes. Applications of the work include metabolic diseases (obesity, diabetes), nutrition,
degenerative diseases and
autoimmune diseases involving oxygenated free radicals in
atherosclerosis and
neurodegeneration. == Honours ==