Serum concentration of adiponectin, leptin and resistin in obese children with non-alcoholic fatty liver disease

Dm, Lebensztejn; Wojtkowska, Małgorzata; Skiba, Elżbieta; Werpachowska, Irena; Tobolczyk, Jolanta; Kaczmarski, Maciej

doi:10.2478/v10039-009-0047-y

Cited by 45 publications

(31 citation statements)

References 33 publications

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“…The data suggest an importance of the leptin axis in regulating downstream effects of CR on expression of transcription factors and drug processing genes. Serum levels of leptin are known to correlate with the severity of steatosis (54,55). Hepatic and central leptin resistance is known to cause insulin resistance and obesity (56).…”

Section: Discussionmentioning

confidence: 99%

Effect of Caloric Restriction and AMPK Activation on Hepatic Nuclear Receptor, Biotransformation Enzyme, and Transporter Expression in Lean and Obese Mice

Kulkarni

Donepudi

et al. 2013

Pharm Res

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Purpose Fatty liver alters liver transporter expression. Caloric restriction (CR), the recommended therapy to reverse fatty liver, increases Sirtuin1 deacetylase activity in liver. This study evaluated whether CR and CR mimetics reversed obesity-induced transporter expression in liver and hepatocytes. Methods mRNA and protein expression was determined in adult lean (lean) and leptin-deficient obese (OB) mice fed ad libitum or placed on 40% (kCal) reduced diet. Hepatocytes were isolated from lean and OB mice, treated with AMP Kinase activators, and gene expression was determined. Results CR decreased Oatp1a1, Oatp1b2, and Abcb11 mRNA expression in lean, but not OB mice. CR increased Abcc2 mRNA OB livers, whereas protein expression increased in both genotypes. CR increased Abcc3 protein expression increased in OB livers. CR did not alter Abcc1, 4 and 5 mRNA expression in lean mice but decreased expression in livers of OB mice. CR increased Abcc4 protein in lean, but not OB mice. Conclusions CR restriction reversed the expression of some, but not all transporters in livers of OB mice. Overall, these data indicate a potential for CR to restore some hepatic transporter changes in OB mice, but suggest a functional leptin axis is needed for reversal of expression for some transporters.

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Section: Discussionmentioning

confidence: 99%

Effect of Caloric Restriction and AMPK Activation on Hepatic Nuclear Receptor, Biotransformation Enzyme, and Transporter Expression in Lean and Obese Mice

Kulkarni

Donepudi

et al. 2013

Pharm Res

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“…Adiponectin levels have been shown to correlate negatively with early markers of atherosclerosis and the MS in obese children [65]. More importantly, adiponectin levels are lower in children with NAFLD compared with lean controls, which may increase their risk for developing atherosclerosis [66]. Bugianesi et al showed that decreased levels of circulating adiponectin in NAFLD is related to hepatic insulin sensitivity and to the amount of hepatic fat content but not to fibrosis or necroinflammation [67].…”

Section: Nafld and Systemic Inflammationmentioning

confidence: 99%

Atherogenic dyslipidemia and cardiovascular risk in children with nonalcoholic fatty liver disease

Alkhouri

Carter–Kent

Elias

et al. 2011

Clinical Lipidology

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Nonalcoholic fatty liver disease is now regarded as the most common form of chronic liver disease in adults and children. The close association between nonalcoholic fatty liver disease (NAFLD) and the metabolic syndrome has been extensively described. Moreover, a growing body of evidence suggest that NAFLD by itself confers a substantial cardiovascular risk independent of the other components of the metabolic syndrome. Given the significant potential for morbidity and mortality in these patients, and the large proportion of both pediatric and adult population affected, it is important that we clearly define the overall risk, identify early predictors for cardiovascular disease progression, and establish management strategies. In this article, we will focus on current data linking NAFLD and the severity of liver damage present in children with cardiovascular risk.

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“…Low levels of adiponectin have been reported in pediatric patients with NASH. 54 Zou et al 55 evaluated adiponectin levels in 113 obese children and 37 nonobese controls. They found that adiponectin levels were significantly lower (3.63 vs 5.79 μg/mL; P < .001) in the obese children than in controls.…”

Section: Biochemical Findingsmentioning

confidence: 99%

Pediatric Nonalcoholic Fatty Liver Disease

Cohen¹,

Gonzales-Pacheco²

2013

Topics in Clinical Nutrition

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Serum concentration of adiponectin, leptin and resistin in obese children with non-alcoholic fatty liver disease

Cited by 45 publications

References 33 publications

Effect of Caloric Restriction and AMPK Activation on Hepatic Nuclear Receptor, Biotransformation Enzyme, and Transporter Expression in Lean and Obese Mice

Effect of Caloric Restriction and AMPK Activation on Hepatic Nuclear Receptor, Biotransformation Enzyme, and Transporter Expression in Lean and Obese Mice

Atherogenic dyslipidemia and cardiovascular risk in children with nonalcoholic fatty liver disease

Pediatric Nonalcoholic Fatty Liver Disease

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