Hormonal
Obese humans with Non-Alcoholic Steatohepatitis (NASH) exhibit decreased expression of cytochromes P450 involved in bioactive lipid synthesis, mirroring findings in MyD88-deficient mice.
In advanced liver disease (NASH), the liver's ability to produce protective fats (via CYP450 enzymes) is reduced. This suggests that liver health is a critical component of overall metabolic health, and protecting the liver from fat accumulation may preserve these protective pathways.
Similar to what is seen in hepatocyte Myd88 deleted mice, human obese subjects developing non-alcoholic steatohepatitis (NASH) are characterised by a decreased expression of different cytochromes P450 involved in bioactive lipids synthesis.
Why this rating
Observational human data, smaller sample size implied by 'stratified based on severity', but consistent with animal model.
Source
Hepatocyte MyD88 affects bile acids, gut microbiota and metabolome contributing to regulate glucose and lipid metabolism
Thibaut Duparc et al. · Gut · 2016
DOI 10.1136/gutjnl-2015-310904
More from this paper
- Hepatocyte-specific deletion of MyD88 causes glucose intolerance, hepatic insulin resistance, and inflammation independently of body weight or fat mass gain.Good
- Hepatocyte MyD88 regulates bile acid synthesis and profile, which in turn influences gut microbiota composition and host glucose/lipid metabolism.Good
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