Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Oliver StöhrDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Ozlem TokDept. Molecular Metabolism, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, USA.
Ana Andres-HernandoDivision of Endocrinology, Metabolism & Diabetes, Univ. of Colorado Anschutz School of Medicine, 12801 East 17th Avenue, Aurora, CO, USA.
Wei QiuDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Baiyu HeDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Caixia WangDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Miguel A LanaspaDivision of Endocrinology, Metabolism & Diabetes, Univ. of Colorado Anschutz School of Medicine, 12801 East 17th Avenue, Aurora, CO, USA.ORCID http://orcid.org/0000-0002-1163-1831
Norbert StefanDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology and Nephrology, University Hospital Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0002-2186-9595
Kyle D CoppsDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Morris F WhiteDivision of Endocrinology Boston Children's Hospital, Harvard Medical School, Boston, MA, USA. morris.white@childrens.harvard.edu.ORCID http://orcid.org/0000-0003-2166-508X
Funding
Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Kanakadurga Singer · 2010 to 2026
$20.3M
Metabolic Crosstalk During Hepatic Insulin ResistanceR01DK098655 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI WHITE, MORRIS F. · 2013 to 2020
$4.0M
Hepatic insulin resistance integrates T2D and NAFLDR01DK137942 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI Morris F. White · 2024 to 2026
$3.2M
Regulation of hippocampal function by central and peripheral IRS signalingR01AG067913 · NIA · BOSTON CHILDREN'S HOSPITAL · PI WHITE, MORRIS F. · 2020 to 2024
$3.1M
Targeting fructokinase, endogenous fructose production and purine degradation for the prevention and treatment of hereditary fructose intoleranceR01DK108859 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Miguel Angel Lanaspa Garcia · 2016 to 2026
$2.4M
Role of TAZ in metabolic regulation in both normal and insulin resistant statesR01DK124328 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI MIAO, JI · 2021 to 2025
$2.2M
Copper and copper-binding proteins in insulin resistance-associated metabolic diseaseR01DK133331 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI MIAO, JI · 2022 to 2025
$1.9M
Anatomical Regulation of Glucose and Lipid Metabolism by Insulin Signaling in HepatocytesR01DK133388 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI Rongya Tao · 2023 to 2026
$1.8M
Hepatic insulin resistance integrates T2D and NAFLDR56DK098655 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI WHITE, MORRIS F. · 2023 to 2023
$150k
NIA NIH HHS R01 AG067913NIDDK NIH HHS P30 DK089503NIDDK NIH HHS R01 DK098655NIDDK NIH HHS R01 DK108859NIDDK NIH HHS R01 DK124328NIDDK NIH HHS R01 DK133331NIDDK NIH HHS R01 DK133388NIDDK NIH HHS R01 DK137942NIDDK NIH HHS R56 DK098655U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) DK098655U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) DK108859U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) DK124328U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) DK133388U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases) DK137942U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging) AG067913
6 · The paper itself
Abstract
MASLD (metabolic-associated steatotic liver disease) and MASH (steatohepatitis) are closely associated with hepatic IR (insulin resistance) and T2D. Regardless, insulin-stimulated hepatic lipogenesis is considered essential for MASLD development, as mouse models of complete hepatic IR become diabetic without MASLD when fed high-fat diets. Challenging this notion, we found that male LDKO mice lacking hepatic insulin receptor substrates acutely developed MASLD if fed a fructose-enriched "MASH diet" (GAN) or high-fructose diet. Fructose potentiated hepatic re-esterification of abundant circulating fatty acids in LDKO mice, evidenced by excess
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Fructose and follistatin potentiate acute MASLD during complete hepatic insulin resistance. · full record | OpenQuestion