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Related Experiment Video

Updated: Oct 9, 2025

Assessment of Murine Exercise Endurance Without the Use of a Shock Grid: An Alternative to Forced Exercise

Assessment of Murine Exercise Endurance Without the Use of a Shock Grid: An Alternative to Forced Exercise

Published on: August 14, 2014

CHOP is dispensable for exercise-induced increases in GDF15.

Logan K Townsend^1,2, Kyle Medak¹, Alyssa J Weber¹

¹Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.

Journal of Applied Physiology (Bethesda, Md. : 1985)

|December 16, 2021

Summary

Exercise increases Growth Differentiation Factor 15 (GDF15), a cellular stress marker. This study found that exercise-induced GDF15 increases occur independently of endoplasmic reticulum stress and the CHOP protein.

Keywords:

CHOP ER stress GDF15 exercise obesity

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Last Updated: Oct 9, 2025

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Area of Science:

Cellular Biology
Endocrinology
Exercise Physiology

Background:

Growth Differentiation Factor 15 (GDF15) is a secreted hormone and a marker of cellular stress.
CHOP (C/EBP homologous protein) is a key transcriptional regulator of GDF15 and an endoplasmic reticulum stress protein.
Exercise is known to increase GDF15 levels, but the regulatory mechanisms are unclear.

Purpose of the Study:

To investigate whether CHOP regulates GDF15 expression and secretion during exercise.
To explore the relationship between ER stress, obesity, and exercise-induced GDF15.

Main Methods:

Examined circulating GDF15 and tissue GDF15 mRNA expression in response to acute exercise.
Utilized lean, obese, trained, sedentary, and CHOP-deficient mouse models.
Assessed markers of endoplasmic reticulum stress.

Main Results:

Obesity augmented exercise-induced GDF15, despite similar ER stress markers in lean and obese mice.
Exercise-induced GDF15 increased similarly in trained and sedentary mice at the same relative intensity.
Exercise-induced GDF15 increases were preserved in CHOP-deficient mice.

Conclusions:

Exercise-induced GDF15 expression and secretion are independent of ER stress and CHOP.
The findings suggest alternative pathways mediate GDF15 regulation during physical activity.