The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease

Yu, Siyu; Li, Chunlin; Ji, Guang; Zhang, Li

doi:10.3389/fphar.2021.783393

Cited by 31 publications

(42 citation statements)

References 129 publications

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“…Children's sugar intake, such as fructose, is of concern. Dietary fructose promotes hepatic de novo lipogenesis (DNL) via acetate from the gut microbiota (21)(22)(23). The World Health Organization recommends that the average daily sugar intake should not exceed 25 g (24,25).…”

Section: The Relationship Between Diets and Obesitymentioning

confidence: 99%

Roles of gut microbiota and metabolites in overweight and obesity of children

Zhang

Dang

2022

Front. Endocrinol.

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The prevalence of overweight and obesity in children and adolescents is an increasing public health problem. Pediatric overweight and obesity result from multiple factors, including genetic background, diet, and lifestyle. In addition, the gut microbiota and their metabolites play crucial roles in the progression of overweight and obesity of children. Therefore, we reviewed the roles of gut microbiota in overweight/obese children. The relationship between pediatric overweight/obesity and gut metabolites, such as short-chain fatty acids, medium-chain fatty acids, amino acids, amines, and bile acids, are also summarized. Targeting gut microbiota and metabolites might be a promising strategy for interventions aimed at reducing pediatric overweight/obesity.

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Section: The Relationship Between Diets and Obesitymentioning

confidence: 99%

Roles of gut microbiota and metabolites in overweight and obesity of children

Zhang

Dang

2022

Front. Endocrinol.

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“…When the diet was once again revised, the patient assumed high levels of consumption of added sugars, particularly fructose-sweetened beverages. The liver is the primary organ to metabolize fructose, and overwhelming fructose consumption is a driving force in the development of NAFLD/NASH via de novo lipogenesis, hepatic insulin resistance, lipotoxicity, and oxidative stress ( 13 , 32 ). Fructose overconsumption also induces gut dysbiosis, visceral adiposity, and intracellular cortisol concentration ( 12 , 33 ).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, to develop a fatty liver, it usually takes at least 8–24 weeks on a high-fructose diet ( 9 ), which correlates well with the rapid development of graft steatosis in our patient. The pattern of fructose consumption is important in the pathogenesis of NAFLD because if it is accompanied by dietary fiber, fructose absorption will be slower, in contrast to diets with sugar additives and sugar-sweetened beverages, most commonly sucrose and the sweetener high-fructose corn syrup, which have the most detrimental effect ( 13 ).…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, the worldwide increase in pediatric overweight and obesity parallels the global diet modifications including the rise of sucrose (table sugar) and fructose consumption, mainly present in sugar-sweetened beverages ( 8 – 10 ). The hepatic oversupply of these substrates is a major mediator of non-alcoholic fatty liver disease (or “ fructoholic liver disease”) ( 8 , 9 , 11 – 13 ), correlating with the severity of hepatic fibrosis in a dose-dependent manner ( 14 , 15 ).…”

Section: Introductionmentioning

confidence: 99%

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Case report: NAFLD and maple syrup urine disease: Is there an interplay between branched-chain amino acids and fructose consumption?

et al. 2022

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BackgroundThe worldwide increase in pediatric overweight and obesity, in parallel with the global increase in the consumption of sucrose and fructose, is associated with non-alcoholic fatty liver disease (NAFLD). Elevated branched-chain amino acids (BCAAs) are a metabolic feature related to obesity and an early risk factor for insulin resistance and NAFLD. However, few studies have assessed metabolic risk factors and nutritional status in maple syrup urine disease (MSUD) patients under restricted BCAA and high carbohydrate diets.Methods and resultsHerein, we present a pilot report of a 17-year-old boy with classic MSUD with poor diet compliance and high fructose consumption, mainly during early adolescence. At that time, he was overweight and developed features of metabolic syndrome, including persistently elevated liver enzymes and hepatic steatosis. He underwent liver transplantation at the age of 13 years to prevent the risk of progressive cognitive impairment. Two months later, NAFLD relapsed in the graft, despite a better BCAA balance and weight loss. Nevertheless, 6 months after dietary restriction of fructose consumption, NAFLD had sustainably improved.ConclusionChildhood overweight and fructose overconsumption are wellestablished driving forces in the development of pediatric NAFLD. However, their role in the early onset and progression of NAFLD in the allograft remains to be established. Furthermore, it is not known whether the dysmetabolic state associated with elevated BCAAs may be contributory. Further studies are required with a cohort of MSUD subjects to validate our findings and to ascertain the possible interaction between a BCAA imbalance and dietary intake in the development of NAFLD.

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“…Despite intense research efforts throughout the last decade, mechanisms underlying the effects of elevated fructose intake on insulin, and even more so, the development of hyperinsulinemia and insulin resistance are not yet fully understood. Results of some animal studies suggest that hepatic insulin resistance may be related to fructose-induced hepatic steatosis (for an overview see [80,81] and below). Indeed, results of studies suggest that the intake of fructose adds through an increase in hepatic diacylglycerol accumulation, activation of protein kinase C and alterations of insulin-mediated Akt to the development of steatosis [82][83][84].…”

Section: Effect Of Fructose On Insulin Signaling and The Development ...mentioning

confidence: 99%

Fructose, a trigger of metabolic diseases?—a narrative review

2022

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Worldwide the number of individuals being overweight or obese has dramatically increased during the last decades, which is also associated with a similar dramatic increase of individuals afflicted with metabolic disorders like dyslipidemia, hypertension, and non-alcoholic fatty liver disease (NAFLD). Genetic predisposition may account for some of the increases in body weight and the development of metabolic disorders; however, much is probably also related to the changes in physical activity and dietary pattern. Indeed, results of epidemiological studies suggest that a ‘western-type dietary pattern’ composed of highly processed foods, sweetened foods, and beverages, all adding to a low fiber but high sugar and saturated fat intake, may increase the odd of developing overweight and metabolic disorders. Consumption of sugar, and especially, fructose has repeatedly been discussed to be a key contributor to the development of health disturbances including hypertension, dyslipidemia, insulin resistance as well as NAFLD. However, despite intense research effort, the question if and how (high) dietary fructose intake interferes with human health has not yet been fully answered also as findings are sometimes contradictory. In the present narrative review, results of recent studies assessing the effect of fructose consumption on the development of metabolic disorders including hypertension, dyslipidemia, cardiovascular diseases (CVDs), hyperinsulinemia, and NAFLD as well as underlying molecular mechanisms are reviewed, thereby, aiming to further address the question if (high) fructose intake is a trigger of metabolic diseases.

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The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease

Cited by 31 publications

References 129 publications

Roles of gut microbiota and metabolites in overweight and obesity of children

Roles of gut microbiota and metabolites in overweight and obesity of children

Case report: NAFLD and maple syrup urine disease: Is there an interplay between branched-chain amino acids and fructose consumption?

Fructose, a trigger of metabolic diseases?—a narrative review

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