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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

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Reduced voluntary wheel running behaviour in Kiss1r knockout mice.

Raj Patel¹, Aaron Gomes¹, Shane K Maloney¹

¹School of Human Sciences, The University of Western Australia, 35 Stirling Highway, Crawley, Western Australia 6009, Perth, Australia.

Physiology & Behavior

|September 24, 2024

Summary

Kisspeptin signaling regulates circadian activity in male mice. Kisspeptin receptor knockout mice show reduced running, but obesity is prevented with voluntary exercise.

Keywords:

Circadian rhythm Inflammation Kisspeptin Microglia Obesity

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Area of Science:

Neuroendocrinology
Circadian Biology
Metabolic Regulation

Background:

Kisspeptin and its receptor (Kiss1r) are implicated in energy balance, thermoregulation, and circadian rhythms.
Kiss1r knockout (KO) mice exhibit hypogonadism and obesity, providing a model to study kisspeptin's broader functions.

Purpose of the Study:

To investigate the role of kisspeptin signaling in circadian locomotor behavior using Kiss1r KO mice.
To assess the impact of gonadectomy (GDX) on activity levels and body mass in relation to kisspeptin signaling.

Main Methods:

Voluntary wheel running activity was measured in intact and gonadectomized Kiss1r KO and wild-type (WT) mice.
Body mass, tissue histology (WAT, BAT, muscle), and neuronal marker expression (orexin, dopamine, Iba1) were analyzed.

Main Results:

Kiss1r KO mice exhibited significantly reduced running distance compared to WT controls, particularly in males.
Gonadectomy affected running activity in WT mice, with a less pronounced decrease in GDX Kiss1r KO males.
Obesity was not observed in GDX Kiss1r KO mice engaging in voluntary activity, despite the genetic background.
Increased microglial activation (Iba1) was noted in the arcuate nucleus of male Kiss1r KO mice.

Conclusions:

Kisspeptin signaling is crucial for normal circadian locomotor activity in male mice.
Voluntary physical activity can mitigate the development of obesity in Kiss1r KO mice, suggesting a complex interplay between energy expenditure and kisspeptin pathways.