ArticleCell reports2026
Glycogen and lactate metabolism in mouse fetal Sertoli cells sustain the germ line.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Protocol for ex vivo mouse paired single-gonad screening platform for phenotypical characterization.STAR protocols · 2026Article
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8 authors.
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Abstract
Metabolites are key regulators of cell fate decisions, chromatin remodeling, and lineage commitment. While genetic pathways governing testis differentiation are well studied, the role of metabolism remains poorly understood. In this study, we investigate the transient, male-specific accumulation of glycogen in supporting cells of the fetal testis in mice, between embryonic days 11.5 and 13.5. Blocking glycogen metabolism/accumulation in vivo and in vitro is dispensable for Sertoli cell differentiation. However, its disruption leads to reduced lactate production and reduced germ cell number in the testis. Inhibiting lactate transport reveals a critical metabolic coupling between Sertoli and germ cells during early testis development. Surprisingly, external lactate or glucose supplementation fails to rescue the germ cell phenotype. These findings suggest that glycogen accumulation supports a critical developmental window in which both Sertoli and germ cells are metabolically constrained and unable to rely on external carbon sources.
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