En masse organoid phenotyping informs metabolic-associated genetic susceptibility to NASH
Open accessAbstract
Genotype-phenotype associations for common diseases are often compounded by pleiotropy and metabolic state. Here, we devised a pooled human organoid-panel of steatohepatitis to investigate the impact of metabolic status on genotype-phenotype association. En masse population-based phenotypic analysis under insulin insensitive conditions predicted key non-alcoholic steatohepatitis (NASH)-genetic factors including the glucokinase regulatory protein (GCKR)-rs1260326:C>T. Analysis of NASH clinical cohorts revealed that GCKR-rs1260326-T allele elevates disease severity only under diabetic state but protects from fibrosis under non-diabetic states. Transcriptomic, metabolomic, and pharmacological analyses indicate significant mitochondrial dysfunction incurred by GCKR-rs1260326, which was not reversed with metformin. Uncoupling oxidative mechanisms mitigated mitochondrial dysfunction and permitted adaptation to increased fatty acid supply while protecting against oxidant stress, forming a basis for future therapeutic approaches for diabetic NASH. Thus, "in-a-dish" genotype-phenotype association strategies disentangle the opposing roles of metabolic-associated gene variant functions and offer a rich mechanistic, diagnostic, and therapeutic inference toolbox toward precision hepatology. VIDEO ABSTRACT.
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iPSC-derived MASH organoids from different donors have been used to screen for MASH susceptibility loci, identifying the GCKR allele rs1260326[T] which increases lipid loading in hepatocytes.
“Furthermore, iPSC-derived MASH organoids from different donors have been used to screen for MASH susceptibility loci, leading to the identification of the glucokinase regulator (GCKR) allele rs1260326[T] which increases lipid loading in hepatocytes (242).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [242]
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Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH)
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- Authors
- Kimura, M., Iguchi, T., Iwasawa, K., Dunn, A., Thompson, W. L., Yoneyama, Y., Chaturvedi, P., Zorn, A. M., Wintzinger, M., Quattrocelli, M., Watanabe-Chailland, M., Zhu, G., Fujimoto, M., Kumbaji, M., Kodaka, A., Gindin, Y., Chung, C., Myers, R. P., Subramanian, G. M., Hwa, V., & Takebe, T.
- Affiliations
- Cincinnati Children's Hospital Medical Center (US)
- Tokyo Medical and Dental University (JP)
- Advanced Medical Research Center, Yokohama City University (JP)
- Gilead Sciences (United States) (US)
- Corresponding author
- Takebe, Takanori
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2022-10
- Volume
- 185
- Issue
- 22
- Pages
- 4216-4232.e16
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC9617783
- OpenAlex
- W4305013887
- Cited by
- 115
- References
- 70
- Citations by year
- 2026: 23 · 2025: 33 · 2024: 38 · 2023: 21
- FWCI
- 16.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 391 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (DP2 DK128799-01)
- Core Research for Evolutional Science and Technology (JP22gm1210012)
- Japan Society for the Promotion of Science (JP18H02800, HL158531, DK121875, AG078174, DK130908)
- Japan Science and Technology Agency (JPJSBP220203101)
- Takeda Science Foundation
- New York Stem Cell Foundation
- Japan Agency for Medical Research and Development (UG3/UH3 DK119982)
- Cincinnati Children’s Research Foundation
- Mitsubishi Foundation (JP21bm0404045, AMED JP20fk0210037, JP20bm0704025, JP22fk0210106, JP22fk0210091, JP21fk0210060)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- nonalcoholic steatohepatitis, human organoids, genotype-phenotype correlation, GCKR, insulin resistance, diabetes mellitus, liver fibrosis, mitochondrial dysfunction, oxidative stress, metformin, uncoupling, fatty acid metabolism, metabolic status
- MeSH terms
- Alleles, Humans, Liver, Organoids, Genetic Predisposition to Disease, Genetic Association Studies, Non-alcoholic Fatty Liver Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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