Research
Hormonal
Hepatic insulin resistance promotes de novo lipogenesis (DNL) via upregulation of SREBP1c and ChREBP, contributing to liver fat accumulation.
Limiting carbohydrate intake, especially simple sugars, can reduce the substrate and signaling for DNL, thereby lowering liver fat production.
GoodSupportsHIGH confidence
There are two major transcriptional factors for DNL: sterol regulatory element binding protein 1c (SREBP1c), regulated by insulin signaling, and carbohydrate response element binding protein (ChREBP), activated by glucose uptake.
Why this rating
Supported by isotopic tracer studies and molecular biology research.
Source
Role of Insulin Resistance in MAFLD
Yoshitaka Sakurai et al. · International Journal of Molecular Sciences · 2021
DOI 10.3390/ijms22084156
narrative_reviewCited 419×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Systemic and hepatic insulin resistance is the central pathophysiological mechanism driving the development and progression of metabolic dysfunction-associated fatty liver disease (MAFLD).Strong
- Insulin resistance in adipose tissue leads to increased free fatty acid (FFA) release, which drives hepatic fat accumulation and inflammation.Strong
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