Endometrium and endometriosis tissue mitochondrial energy metabolism in a nonhuman primate model

Hannah M Atkins, Hannah Atkins, Manish S Bharadwaj, Anderson O'Brien Cox, Anderson O. Cox, Cristina M Furdui, Susan E Appt, David L Caudell
Reproductive biology and endocrinology : RB&E · 2019 · vol. 17(1) , pp. 70 · doi:10.1186/s12958-019-0513-8 · PMID:31445519 · PMC6708555 · W2969948750
article OA: gold CC0 ⤵ 38 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometriosis and affected endometrium in nonhuman primates exhibit reduced mitochondrial energy metabolism, with specific decreases in key metabolites involved in energy production and amino acid biosynthesis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study analyzed mitochondrial energy metabolism in endometrium (from clinically healthy nonhuman primates) and endometriosis tissue from a nonhuman primate model of spontaneous endometriosis, using mitochondrial respirometry to measure oxidative phosphorylation across different respiratory states and targeted metabolomics to quantify metabolites in energy and amino acid biosynthesis pathways. The authors found reduced mitochondrial function in endometriosis-associated tissues, including lower complex II- (endometrium) and complex I-mediated oxygen consumption and respiratory control rates, alongside decreased levels of key energy- and redox-related metabolites such as carnitine, creatine phosphate, NADH, and FAD in endometriosis tissue, with similar decreases in endometrium from animals with endometriosis. A major caveat is that mitochondrial and metabolomics analyses were performed on relatively small tissue subsets (mitochondrial assays n=9 animals total), with tissue handling limitations noted for unusable complex-II respiration data from one animal. This paper is centrally about endometriosis — it directly measures mitochondrial energy metabolism and tissue metabolite changes in endometriosis tissue and adjacent endometrium in a nonhuman primate model.

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Abstract

BACKGROUND: Endometriosis is the growth of uterine lining (endometrium) outside of the uterus. In other chronic inflammatory diseases, mitochondrial dysfunction is suspected of playing a role in disease pathogenesis. However, little is known about endometriosis mitochondrial function or its effects on tissue metabolism. The objectives of this study were to analyze mitochondrial function in nonhuman primate (NHP) endometrium and endometriosis tissue and to identify the metabolic features of these tissues that may contribute to disease. METHODS: Mitochondrial function in endometriosis tissue and endometrium was measured using mitochondrial respirometry analysis to determine if changes in oxidative phosphorylation exist in endometrium and endometriosis tissue compared to control endometrium from clinically healthy NHPs. Targeted metabolomics and multidimensional statistical analysis were applied to quantify key metabolites in energy and amino acid biosynthesis pathways. RESULTS: Mitochondrial respirometry assays showed endometrium from NHPs with endometriosis had reduced complex II-mediated oxygen consumption rates (OCR) across all energy states (basal, p = 0.01; state 3, p = 0.02; state 3u, p = 0.04; state 4o, p = 0.008) and endometriosis tissue had reduced state 3, complex I-mediated OCR (p = 0.02) and respiratory control rates (p = 0.01) compared to normal endometrium. Targeted metabolomics performed on tissue revealed carnitine (p = 0.001), creatine phosphate (p = 0.01), NADH (p = 0.0001), FAD (p = 0.001), tryptophan (p = 0.0009), and malic acid (p = 0.005) were decreased in endometriosis tissue compared to normal endometrium samples. FAD (p = 0.004), tryptophan (p = 0.0004) and malic acid (p = 0.03) were significantly decreased in endometrium from NHPs with endometriosis compared to normal endometrium. Significant metabolites identified in endometriosis and endometrium samples from animals with endometriosis were part of amino acid biosynthesis or energy metabolism pathways. CONCLUSIONS: Here, endometrial mitochondrial energy production and metabolism were decreased in endometrium and endometriosis tissue. Decreased mitochondrial energy production may be due to oxidative stress-induced damage to mitochondrial DNA or membranes, a shift in cell metabolism, or decreased energy substrate; however, the exact cause remains unknown. Additional research is needed to determine the implications of reduced mitochondrial energy production and metabolism on endometriosis and endometrium.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Energy Metabolism Macaca fascicularis Macaca mulatta Mitochondria Animals Electron Transport Chain Complex Proteins Electron Transport Chain Complex Proteins Endometriosis Endometriosis Endometrium Female Humans Macaca fascicularis Macaca mulatta Mitochondria Primates Primates Primates

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