August Krogh / CWS Seminar

Nuclear Receptors and the Hunger Game

v/ Ronald M. Evans, Professor and Director, Salk Institute for Biological Studies, La Jolla, California


Survival requires the ability to adapt to cycles of feast and famine yet the underlying mechanisms to maintain metabolic balance during extremes of nutrient challenge remain poorly understood. As part of a screen to identify genes that respond to feast and famine cues, we discovered that FGF1 is induced in white adipose tissue (WAT) in response to high-fat-diet (HFD) and repressed during a fast, pointing to an unexpected metabolic function. Thus, FGF1 participates in both fed-state and fasted-state responses.  In WAT, FGF1 is induced by HFD through a PPAR-gamma dependent mechanism.  On HFD, FGF1 deficient mice develop an aggressive diabetic phenotype, with adipose tissue becoming inflamed and unable to adapt to nutrient excess. As loss ofFGF1 results in a diabetic phenotype, synthetic FGF1 could be as a new class of insulin sensitizer.  

Mammalian metabolism is highly circadian and major hormonal circuits involving nuclear hormone receptors display interlinked diurnal cycling. However, mechanisms that logically explain the coordination of nuclear hormone receptors and the clock are poorly understood. Recently we have shown that two circadian co-regulators, Cryptochrome 1/2 (Cry 1 and 2), and Rev-erb a&b act in the liver to control both lipogenic and gluconeogenic programs.  These observations expand our understanding of how metabolism is coordinated with geophysical time.


This seminar is presented in collaboration with the research programme "Physical activity and nutrition for improvement of health" funded by the UCPH Excellence Programme for Interdisciplinary Research (2016).


1 November 2013

15:00-16:00: Seminar and discussion
16:00-16:30: Post seminar servings and socializing


Auditorium 1, August Krogh Building, Universitetsparken 13, DK-2100 Copenhagen


Participation is free, but please register here.

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Christian Frøsig,, mobile +45 2875 1617

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