Asami Hagiwara
First author of a 2012 mouse study from Michael Hall's lab showing that liver mTORC2 tells the liver that the animal has eaten, by switching on sugar breakdown and fat production
Biozentrum, University of Basel, Michael N. Hall group (at the time of the study, 2012)
After a meal, insulin tells the liver to stop making glucose and to start burning it and storing the extra as fat. Asami Hagiwara was first author of the 2012 Cell Metabolism study in this Atlas (HAG2012), from Michael Hall's lab in Basel, which asked what role mTORC2, the second mTOR complex, plays in that switch. The team deleted rictor, a core part of mTORC2, only in the liver of mice.
In fed mice without liver mTORC2, the kinase Akt lost its activating phosphate at serine 473, and the enzyme glucokinase and the fat-making regulator SREBP1c became less active. The liver kept making glucose while glycolysis (sugar breakdown) and fat synthesis fell, as if it could not sense that the animal had eaten. The mice developed high blood sugar and high insulin with low blood lipids. In liver cells lacking mTORC2, an always-active form of Akt2 restored both sugar breakdown and fat production, while extra glucokinase restored only the sugar side, so Akt is the main route from mTORC2 to these outputs. The study, in mice and mouse liver cells, placed mTORC2 at the centre of the liver's response to insulin.
PubMed lists Hagiwara at the Biozentrum of the University of Basel on this paper. No other paper could be tied to this person with confidence, so the later career is not known.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2012 | A | Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c HAG2012 First author: showed in mice that liver mTORC2 activates glycolysis and fat synthesis through Akt, glucokinase and SREBP1c. |
Co-authors in the Atlas 5
People with a profile here who share at least one study with Asami Hagiwara.
ShowHide
- Charles Betz Traced mTORC2 to a specific address inside the cell — the mitochondria-ER contact site
- Marion Cornu Physiologist from Michael Hall's Basel lab who showed in mice that mTORC1 in the liver controls body temperature, movement and fat metabolism through the hormone FGF21
- Markus A. Rüegg Neurobiologist at the Biozentrum of the University of Basel who studies how muscles and the nerve connections that drive them develop, age and fail, including the role of mTOR signalling in muscle.
- Michael N. Hall Discovered TOR in yeast in 1991 and established it as a central controller of cell growth that responds to nutrients. His lab later showed that TOR works in two distinct complexes, TORC1 and TORC2, only one of which is blocked by rapamycin
- Nadine Cybulski Cell biologist from Michael Hall's Basel lab who showed that mTORC2 in fat tissue helps control how big the whole body grows
Every researcher with a profile →
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.
Thank you. Your answer was counted anonymously.