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. 2009 Jun 1;3(3):271-281.
doi: 10.2217/phe.09.21.

Nonalcoholic fatty liver disease as a comorbidity of childhood obesity

Nicole J Barshop  1 , Cameron S Francis, Jeffrey B Schwimmer, Joel E Lavine
Affiliations

Nonalcoholic fatty liver disease as a comorbidity of childhood obesity

Nicole J Barshop et al. Ped Health. .

Abstract

Childhood obesity is a worldwide health problem associated with an increase in the prevalence and severity of comorbid conditions including nonalcoholic fatty liver disease (NAFLD). The increasing number of children with NAFLD presents a major public health concern. This review focuses on the recent advancements in the understanding of the epidemiology, diagnosis, histology, pathogenesis and treatment of pediatric NAFLD and highlights ongoing challenges and unmet needs in the area.

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Figures

Figure 1
Figure 1. Photomicrographs of a pediatric liver biopsy
(A) Type 1 nonalcoholic steatohepatitis (NASH). Photomicrograph of a pediatric liver biopsy demonstrating macrovesicular steatosis, ballooning degeneration and perisinusoidal fibrosis, exemplifying a type 1 NASH pattern. (B) Type 2 NASH. Photomicrograph of a pediatric liver biopsy demonstrating macrovesicular steatosis without evidence of cellular injury or lobular inflammation, with mild periportal fibrosis and lack of perisinusoidal fibrosis. This pattern exemplifies a type 2 NASH often seen in children.
Figure 2
Figure 2. Proposed mechanisms for hepatic steatosis in nonalcoholic fatty liver disease
Several mechanisms potentially contribute to the development of fatty liver. (1) Visceral adipose accumulation is associated with adipokine dysregulation and increased delivery of FFAs directly into portal circulation. Oversecretion of leptin and TNF-α and hyposecretion of adiponectin contribute to peripheral insulin resistance. (2) Peripheral insulin resistance results in decreased glucose uptake by muscle and increased FFA liberation from adipose. The result is persistently elevated levels of circulating insulin, FFAs and glucose, which cause a series of changes in hepatic metabolism that ultimately lead to steatosis, (3) increased hepatic DLG from glucose, (4) increased synthesis of TGs from peripherally derived FFAs, (5) decreased hepatic β-oxidation and (6) impaired synthesis of ApoB with decreased export of TG as VLDL. DLG: De novo lipogenesis; FFA: Free fatty acid; Glc: Glucose; TG: Triglyceride.
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References

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