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Review
. 2021 Apr 13;17(3):191-195.
doi: 10.1002/cld.1008. eCollection 2021 Mar.

Hepatic Steatosis in the Pediatric Population: An Overview of Pathophysiology, Genetics, and Diagnostic Workup

Claudia Phen  1 , Charina M Ramirez  1
Affiliations
Review

Hepatic Steatosis in the Pediatric Population: An Overview of Pathophysiology, Genetics, and Diagnostic Workup

Claudia Phen et al. Clin Liver Dis (Hoboken). .
No abstract available

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Figures

FIG 1
FIG 1
(A) Development of steatosis. Glucose (from the carbohydrate) is converted into pyruvate, which enters the Krebs cycle and is subsequently converted into acetyl‐CoA, then into malonyl‐CoA, and eventually to FFAs and TGs. White adipose tissue (WAT) takes up fatty acids (FA) from chylomicron (CM) particles via lipoprotein lipase. Additional source of FFAs comes from lipolysis in WAT. These processes lead to accumulation of hepatic FFAs and TGs. 2 , 4 (B) Progression of NAFLD. Accumulation of FFAs and TGs within the cytosol leads to impaired mitochondrial‐β‐oxidation and inadequate disposal of FFAs. Increased production of lipotoxic lipids, unesterified cholesterol, and ceramides causes damage to hepatocytes and increases inflammation. Further hepatocellular injury occurs with recruitment of inflammatory cytokines. Adipokines, oxidative stress, lipid peroxidation, and formation of aldehyde products contribute to further damage. ATP depletion also occurs. Lipopolysaccharides, by‐products from gut microbiome, induce TLR‐4 expression, which promotes hepatic inflammation. 7 With Kupffer cell and HSC activation, collagen production increases with a net matrix deposition and fibrosis ensues. 8 This process leads to cirrhosis, which can become decompensated cirrhosis or predispose to hepatocellular carcinoma.
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