ArticlebioRxiv : the preprint server for biology2025
BDH1-Dependent Ketone Body Metabolism Maintains Müller Cell Homeostasis and Retinal Function.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ketone body metabolism serves as an auxiliary regulator of cellular energetics and redox balance, particularly during prolonged fasting and carbohydrate restriction, yet its role in retinal homeostasis under physiological conditions remains poorly defined. β-hydroxybutyrate dehydrogenase 1 (BDH1) is a mitochondrial enzyme that interconverts acetoacetate and β-hydroxybutyrate, and is required for efficient ketone utilization. Here, we investigated the impact of impaired endogenous ketone metabolism on retinal function using global and retinal pigment epithelium (RPE)-specific BDH1 knockout (KO) mice. Global BDH1 KO mice showed reduced circulating β-hydroxybutyrate and blunted fasting-induced ketone elevations, accompanied by ganglion cell loss, structural abnormalities on fundus and OCT imaging, and diminished scotopic and photopic electroretinogram (ERG) a- and b-wave amplitudes, consistent with impaired photoreceptor responses and downstream bipolar and Müller cell signaling. In contrast, RPE-specific BDH1 KO mice exhibited no changes in ERG responses or retinal morphology. Transcriptomic and molecular analyses in global KO retinas revealed disrupted Müller cell homeostasis, including reduced CAMKII-CREB activation, which is required for EAAT1 glutamate transporter expression. Administration of exogenous β-hydroxybutyrate,
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