ReviewCureus2026
Nonalcoholic Fatty Liver Disease as a Risk Marker for Incident Type 2 Diabetes Mellitus: A Systematic Review.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD), now largely encompassed by the newer metabolic dysfunction-associated steatotic liver disease (MASLD) nomenclature, is increasingly recognized as a marker of systemic metabolic dysfunction. This systematic review synthesized longitudinal evidence from adults examining NAFLD and related steatotic liver disease definitions in relation to incident type 2 diabetes mellitus. PubMed/MEDLINE and Scopus were searched from inception, the supplementary search was repeated to capture recently published studies. Eligible longitudinal reports excluded participants with diabetes at baseline or clearly identified new-onset diabetes during follow-up. Because the included cohorts differed in liver disease definitions, diabetes ascertainment, populations, follow-up structures, and reported effect measures, the findings were synthesized narratively. The protocol was prepared before screening but was not prospectively registered. A total of 61 reports were included. Risk of bias was generally low to moderate where adequately assessed, while reports with incomplete domain-level information were interpreted cautiously. NAFLD or MASLD was generally associated with higher estimates of incident diabetes risk, although the magnitude varied and was attenuated after adjustment for metabolic factors in some studies. Persistent or newly developed steatosis and a greater liver fat or fibrosis burden were associated with higher estimates of future diabetes occurrence, whereas the resolution or reduction of liver fat was associated with lower estimates. Reported subgroup differences arose largely from individual or overlapping cohorts and were not sufficiently consistent to establish uniform effect modification. Overall, the evidence supports NAFLD or MASLD as a clinical risk marker rather than a stand-alone individualized prediction tool and supports standardized longitudinal assessments in future studies.
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