Evaluations of Lifestyle, Dietary, and Pharmacologic Treatments for Pediatric Nonalcoholic Fatty Liver Disease: A Systematic Review

Mann, Jake; Tang, George; Nobili, Valério; Armstrong, Matthew J.

doi:10.1016/j.cgh.2018.05.023

Cited by 36 publications

(47 citation statements)

References 50 publications

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“…In children and young people, biomarkers of NAFLD have been shown to improve following weight loss secondary to lifestyle modifications [54]. However, lifestyle interventions, such as low-calorie diets or exercise programmes, that do not culminate in weight loss, also appear to be beneficial [54]. There is no compelling high-quality evidence to recommend one nutritional intervention over another.…”

Section: Lifestyle Interventionsmentioning

confidence: 99%

“…Whilst low fructose, low fat and low glycaemic index diets have shown limited results, preliminary data on the efficacy of a low free sugar diet is promising [55]. General healthy eating advice and physical activity is currently recommended to promote weight loss in paediatric NAFLD, although the amount of weight loss necessary remains unclear [54,56,57].…”

Section: Lifestyle Interventionsmentioning

confidence: 99%

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Non-alcoholic fatty liver disease and childhood obesity

Shaunak

Byrne

Davis³

et al. 2020

Arch Dis Child

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Non-alcoholic fatty liver disease (NAFLD) in children and adolescents has an estimated prevalence of 36.1% in the context of obesity. This figure is anticipated to increase in conjunction with the global obesity epidemic. Worryingly, NAFLD in childhood persisting into adulthood is likely to be harmful, contributing to significant hepatic and extrahepatic morbidities. Early disease detection is required, although the optimum timing, frequency and mode of screening remains undetermined. While the efficacy of several medications, antioxidants, fatty acid supplements and probiotics has been investigated in children, healthy eating and physical activity remain the only prevention and treatment strategies for paediatric NAFLD. This short review discusses the epidemiology, diagnosis, pathogenesis and management of NAFLD in childhood obesity.

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Section: Lifestyle Interventionsmentioning

confidence: 99%

Section: Lifestyle Interventionsmentioning

confidence: 99%

Non-alcoholic fatty liver disease and childhood obesity

Shaunak

Byrne

Davis³

et al. 2020

Arch Dis Child

View full text Add to dashboard Cite

show abstract

“…As not all overweight/obese children have NAFLD [17], the current review focused exclusively on the NAFLD population and not just overweight or obese individuals without an NAFLD diagnosis per se. This further highlights the novelty of current review, as most of the existing reviews were not conducted exclusively on NAFLD patients [3,6,21,22].…”

Section: Discussionmentioning

confidence: 91%

“…Therefore, considering all overweight/obese children to have NAFLD is inappropriate, suggesting that a precise diagnosis of NAFLD per se is needed. Although this has been highlighted by previous published systematic reviews assessing the efficacy of lifestyle modifications on pediatric NAFLD [3,6,[20][21][22], the majority of the included studies were focused on overweight or obese individuals, without a NAFLD diagnosis per se [3,6,21,22].…”

Section: Introductionmentioning

confidence: 99%

Effects of Dietary and Lifestyle Interventions on Liver, Clinical and Metabolic Parameters in Children and Adolescents with Non-Alcoholic Fatty Liver Disease: A Systematic Review

et al. 2020

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Non-alcoholic fatty liver disease (NAFLD) affects 5.5–10.3% of children worldwide, while in obese individuals, it increases to almost 34%. Pediatric NAFLD is consistently associated with metabolic syndrome and insulin resistance. As no pharmacological agents exist for the treatment of NAFLD, lifestyle modifications remain the only therapy. However, as not all overweight/obese children have NAFLD, high-quality data, focused exclusively on NAFLD population are needed. Therefore, the present systematic review assessed the efficacy of lifestyle (diet or exercise) based on randomized controlled clinical trials (RCTs) on liver, anthropometric, glucose, and lipid parameters in children, with imaging or biopsy-proven NAFLD. In general, the results were inconclusive and therefore no specific recommendations could be drawn. In most studies, differences were derived from within group comparisons, which are known to be highly misleading. However, both low-carbohydrate and low-fat diets could benefit liver outcomes, as long as weight loss is achieved, but not necessary glucose and lipid parameters. No RCTs were found on exercise alone, as compared to no intervention on pediatric NAFLD. Concerning diet plus exercise interventions, all studies led to improvements in liver outcomes accompanied with weight loss. Resolution of NAFLD was found in considerably high percentages, while improvements were also seen in glucose but were modest in lipid parameters.

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“…A combination of drugs and lifestyle intervention is ideal for obesity [62][63][64][65][66]. An anti-obesity drug should also prevent or delay other metabolic diseases, as even a 5-10% weight loss significantly reduces risks of cardiovascular and kidney diseases, osteoarthritis and NAFLD/NASH [67,68]. According to the Food and Drug Administration (FDA) guidelines, a compound that decreases body weight by 5% over a long period without causing significant side-effects, should be encouraged as a potential anti-obesity drug [67].…”

Section: Obesity Insulin Resistance and Naflmentioning

confidence: 99%

Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases

2020

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In mammals, a family of three inositol hexakisphosphate kinases (IP6Ks) synthesizes the inositol pyrophosphate 5-IP7 from IP6. Genetic deletion of Ip6k1 protects mice from high fat diet induced obesity, insulin resistance and fatty liver. IP6K1 generated 5-IP7 promotes insulin secretion from pancreatic β-cells, whereas it reduces insulin signaling in metabolic tissues by inhibiting the protein kinase Akt. Thus, IP6K1 promotes high fat diet induced hyperinsulinemia and insulin resistance in mice while its deletion has the opposite effects. IP6K1 also promotes fat accumulation in the adipose tissue by inhibiting the protein kinase AMPK mediated energy expenditure. Genetic deletion of Ip6k3 protects mice from age induced fat accumulation and insulin resistance. Accordingly, the pan IP6K inhibitor TNP [N2-(m-trifluorobenzyl), N6-(p-nitrobenzyl)purine] ameliorates obesity, insulin resistance and fatty liver in diet induced obese mice by improving Akt and AMPK mediated insulin sensitivity and energy expenditure. TNP also protects mice from bone loss, myocardial infarction and ischemia reperfusion injury. Thus, the IP6K pathway is a potential target in obesity and other metabolic diseases. Here, we summarize the studies that established IP6Ks as a potential target in metabolic diseases. Further studies will reveal whether inhibition of this pathway has similar pleiotropic benefits on metabolic health of humans.

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Evaluations of Lifestyle, Dietary, and Pharmacologic Treatments for Pediatric Nonalcoholic Fatty Liver Disease: A Systematic Review

Cited by 36 publications

References 50 publications

Non-alcoholic fatty liver disease and childhood obesity

Non-alcoholic fatty liver disease and childhood obesity

Effects of Dietary and Lifestyle Interventions on Liver, Clinical and Metabolic Parameters in Children and Adolescents with Non-Alcoholic Fatty Liver Disease: A Systematic Review

Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases

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