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Comment
. 2023 Jan 19;186(2):238-240.
doi: 10.1016/j.cell.2022.12.045.

SON-light activation of glucose regulation

Gisela Geoghegan  1 , Judith Simcox  2
Affiliations
Comment

SON-light activation of glucose regulation

Gisela Geoghegan et al. Cell. .

Abstract

Body temperature maintenance is an important regulator of glucose homeostasis. In this issue of Cell, Meng et al. discover a regulatory axis in which light activation of photoreceptive retinal ganglia stimulates the supraoptic nucleus (SON) to inhibit brown adipose tissue (BAT) thermogenesis and impair glucose homeostasis. This could explain the impact of constant light exposure on metabolism.

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Conflict of interest statement

Declaration of interests The authors declare no competing interests.

Figures

Figure 1.
Figure 1.. Light modulation of brown fat activity.
Top panel: When light is detected by intrinsically photosensitive retinal ganglion cells (ipRGC) located in the retina, a conformational change occurs in the photopigment melanopsin (OPN4) leading to its activation, GTP attachment to the Gα subunit leading to translocation and binding to Phospholipase C (PLC). PLC then cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) to inositol triphosphate (IP3) and diacylglycerol (DAG) to activate ion channels for depolarization to generate an action potential down the neuron where it innervates and activates the supraoptic nucleus (SON) (not shown). This signal goes through several more areas of the brain before it is finally transduced to the brown adipose tissue (BAT) where it inhibits β3AR dependent glucose uptake and thermogenesis. Bottom panel: In the absence of light, the signal from the ipRGCs is not activated and leads to a loss of inhibition on β3AR dependent glucose uptake and thermogenesis in BAT.
See this image and copyright information in PMC

Comment on

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