Wafa B'chir
Metabolism researcher in Vincent Giguère's laboratory at McGill who studies how the nuclear receptor ERR-alpha controls fat handling in the liver, including the fatty liver caused by rapamycin
Goodman Cancer Institute, McGill University, Montreal (papers 2018–2026) · INRA Human Nutrition Unit and Université Clermont 1, Clermont-Ferrand, France (papers to 2013)
Wafa B'chir was first author of a 2026 Journal of Endocrinology study (BCH2026) on a side effect of rapamycin. Rapamycin blocks mTORC1, the growth-control complex, and is used to prevent organ rejection. In mice it can also cause fatty liver, where fat builds up inside liver cells. The team added chloroquine, an old antimalarial drug, and found that it made the rapamycin-induced fatty liver milder. Measuring all the genes switched on in the liver showed that chloroquine undid much of rapamycin's push on fat-handling genes, and the nuclear receptor ERR-alpha, a master switch for energy metabolism, came out as a top controller. In mice lacking ERR-alpha, chloroquine no longer helped. This is a mouse study, and it does not show that the combination is safe or useful in patients.
B'chir came to this from nutrition and stress biology. In 2013, at the INRA Human Nutrition Unit in Clermont-Ferrand, France, B'chir was first author of a Nucleic Acids Research paper showing that when amino acids run out, the GCN2 and PERK stress kinases act through ATF4 and CHOP to switch on a whole set of autophagy genes. At McGill's Goodman Cancer Research Centre B'chir moved to the liver: a 2018 first-author paper in Endocrinology found that mice without ERR-alpha are protected from fatty liver on a high-fat diet but cannot clear fat from the liver normally when fed again after fasting.
B'chir has continued with the Giguère group at the Goodman Cancer Institute on work about ERR-alpha in the heart (2022) and in the progression of fatty liver to liver inflammation in mice (2023).
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | Rapamycin-induced fatty liver in mice is attenuated by chloroquine co-treatment in an ERRα-dependent manner BCH2026 First author: showed in mice that chloroquine softens rapamycin-induced fatty liver and that this rescue needs ERR-alpha. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Wafa B'chir.
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- Julie St-Pierre Biochemist and Vice-President, Research and Innovation at the University of Ottawa who studies how cancer cells adapt their metabolism, and a co-author on McGill work linking mTORC1 to mitochondria and to rapamycin-induced fatty liver
- Vincent Giguère Studies how nuclear receptors, especially the estrogen-related receptors (ERRs), control energy metabolism, and showed that mTOR and ERRα share target genes involved in lipid and TCA-cycle metabolism
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