Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Do RPE cells have a preferred ketogenic substrate?
Author Affiliations & Notes
  • Kriti Pandey
    Biochemistry, University of Washington, Seattle, Washington, United States
  • Daniel Hass
    Biochemistry, University of Washington, Seattle, Washington, United States
  • Gillian Autterson
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan, United States
  • Jason Matthew Lewis Miller
    Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan, United States
  • James Hurley
    Biochemistry, University of Washington, Seattle, Washington, United States
    Ophthalmology, University of Washington, Seattle, Washington, United States
  • Footnotes
    Commercial Relationships   Kriti Pandey None; Daniel Hass None; Gillian Autterson None; Jason Miller None; James Hurley None
  • Footnotes
    Support  J.B.H. is supported by NEI R01EY06641, R01EY017863, R21032597 and Foundation Fighting Blindness TA-NMT-0522-0826-UWA-TRAP. D.T.H is supported by a Brightfocus Foundation Postdoctoral Fellowship (M2022003F) and NEI K99EY034881.
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 187. doi:
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      Kriti Pandey, Daniel Hass, Gillian Autterson, Jason Matthew Lewis Miller, James Hurley; Do RPE cells have a preferred ketogenic substrate?. Invest. Ophthalmol. Vis. Sci. 2024;65(7):187.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : RPE cells can oxidize both glucose and fatty acids to produce acetyl-CoA. They can use acetyl-CoA from fatty acid oxidation to produce citrate in the Krebs cycle or ketone bodies such as β-hydroxybutyrate (β-HB) in ketogenesis. In biochemistry textbooks, it’s taught that ketogenesis in liver cells occurs when glucose is scarce due to insufficient levels of oxaloacetate, which would limit utilization of acetyl-CoA by the Krebs cycle. We have observed formation of β-HB in RPE cells supplied with palmitate in the presence of abundant glucose. We therefore hypothesize that glucose supplied to RPE cells is poorly oxidized by RPE mitochondria relative to the fatty acid palmitate.

Methods : We cultured primary human fetal RPE cells in serum free Miller media either with 5.5 mM 13C-glucose and 300 μM unlabeled palmitate, or with 5.5 mM unlabeled glucose and 300 μM 13C-palmitate. Medium was collected at 0, 2, 4, 7, 10, and 13 hours after the medium change. Glucose and palmitate remaining in the medium were quantified. 13C labeling of glycolytic and Krebs cycle intermediates was determined by GC-MS.

Results : Labeling of intermediates from 13C glucose increased steadily over time. Labeling of intermediates from 13C palmitate increased and then decreased as the RPE cells depleted palmitate rapidly from the medium. We found that citrate can be labeled with 13C from glucose or from palmitate demonstrating that the RPE cells use carbons from both glucose and from palmitate to make acetyl-CoA, which is a substrate for synthesis of citrate and for β-HB. Remarkably, we found that β-HB incorporates 13C only from palmitate, but not from glucose.

Conclusions : The design of this experiment and our findings from it show that RPE cells can sort acetyl-CoA derived from fatty acids away from acetyl-CoA derived from glucose, using acetyl-CoA produced only from fatty acids for ketogenesis. This sorting mechanism may contribute to the ability of RPE cells to synthesize β-HB even when glucose is abundant.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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