Higher fructose intake is inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults

Kanerva, Noora; Sandboge, Samuel; Kaartinen, Niina E.; Männistö, Satu; Eriksson, Johan G.

doi:10.3945/ajcn.114.086074

Cited by 57 publications

(51 citation statements)

References 39 publications

(44 reference statements)

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“…However, his condition was suddenly, drastically worsened, likely due to the elevated insulin and subsequent hyperphagia. The NAFLD in the current case was certainly worsened by over-consumption of fruits rich in fructose, which is linked to NAFLD by increased hepatic de novo synthesis of fatty acids [8,9]. In addition, despite BMI of less than 25.0 before the hypoglycemic attack, increased bodyweight, particularly increased body fat, may have played a role in the progression of the disease.…”

Section: Case Presentationmentioning

confidence: 68%

A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease

et al. 2015

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Abstract. Nonalcoholic fatty liver disease (NAFLD) is a serious health-related condition all over the world; the number of patients is increasing in Asian countries including Japan. Better understanding of its pathophysiology is required to develop effective therapeutics, as patients may go on to develop non-alcoholic steatohepatitis and hepatocellular carcinomas. While NAFLD is believed to be associated with metabolic risk factors such as obesity, diabetes, and dyslipidemia, its etiology remains largely unknown and the development or co-existence of NAFLD in patients with insulinoma has not been investigated. A 33-year-old male with an insulinoma, who had been hypoglycemic during the previous four years, developed abnormally elevated levels of liver enzymes and histological fatty liver characteristic of NAFLD by the time of admission to our hospital for resection of an insulinoma. His medical records for the previous eight years revealed that his bodyweight had increased gradually from 60 kg to 71 kg for seven years and then acutely increased to 79 kg in the latest one-year period. This sudden increase was thought to be due to the patient's self-described overeating of fruits to forestall hypoglycemia. Fresh fruits are rich in fructose, and the patient's triglycerides, alanine and aspartate transaminases showed an acute increase in the previous one-year period. After resection of the insulinoma, the levels of these parameters all were mostly restored, which suggests that hyperinsulinemia and subsequent hyperphagia played a role in the development of NAFLD in this case. This is the first report of patient with NAFLD and an insulinoma.Key words: Insulinoma, Non-alcoholic fatty liver disease, Fibroscan, Fructose steatohepatitis and hepatocellular carcinomas [1][2]. While NAFLD is associated with metabolic risk factors such as obesity, diabetes, and dyslipidemia, its etiology remains largely unknown and the development or co-existence of NAFLD in patients with insulinoma has not been investigated [1][2][3][4]. Here we report a case of insulinoma with NAFLD, in which surgical resection of the tumor drastically improved NAFLD-related parameters and hypoglycemia. Case PresentationA 33-year-old male suspected of insulinoma was referred to Kansai Electric Power Hospital for surgical resection of the tumor. His fasting plasma glucose lev-

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Section: Case Presentationmentioning

confidence: 68%

A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease

et al. 2015

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“…In a 4-wk randomized, controlled, double-blinded beverage intervention study, Jin et al [80] demonstrated that reduction of dietary fructose in Hispanic-American adolescents with NAFLD improved several important factors related to cardiovascular disease risk, including adipose insulin sensitivity, high sensitivity C-reactive protein and low-density lipoprotein oxidation. On the other side a recent study by Kanerva et al [81] found that high fructose intake was inversely associated with risk of NAFLD in older Finnish adult. A latest meta-analysis of 21 intervention studies concluded that there was insufficient evidence to draw a conclusion for effects of HFCS or sucrose on NAFLD [82] .…”

Section: Fructosementioning

confidence: 94%

Role of diet on non-alcoholic fatty liver disease: An updated narrative review

Papandreou

Andreou

2015

WJH

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The purpose of this article review is to update what is known about the role of diet on non-alcoholic fatty liver disease (NAFLD). NAFLD is the most common cause of chronic liver disease in the developed world and is considered to be a spectrum, ranging from fatty infiltration of the liver alone (steatosis), which may lead to fatty infiltration with inflammation known as non alcoholic steatohepatitis While the majority of individuals with risk factors like obesity and insulin resistance have steatosis, only few people may develop steatohepatitis. Current treatment relies on weight loss and exercise, although various insulin-sensitizing medications appear promising. Weight loss alone by dietary changes has been shown to lead to histological improvement in fatty liver making nutrition therapy to become a cornerstone of treatment for NAFLD. Supplementation of vitamin E, C and omega 3 fatty acids are under consideration with some conflicting data. Moreover, research has been showed that saturated fat, trans-fatty acid, carbohydrate, and simple sugars (fructose and sucrose) may play significant role in the intrahepatic fat accumulation. However, true associations with specific nutrients yet to be clarified.

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“…While the experimental and clinical studies suggest an association of fructose intake with NAFLD, there is one epidemiological study from Finland that found an inverse relationship between fructose intake and NAFLD, but in this population less than 10 percent consumed soft drinks, and fruit intake was much more prevalent (57). While fruits contain fructose, they are less likely to induce metabolic syndrome due to the lower fructose content per fruit (compared to a soft drink) and also because they contain constituents (flavonols, epicatechin, ascorbate, and other antioxidants) that may combat the effects of fructose (58).…”

Section: Soft Drinks and Added Sugar Are Associated With Fatty Livermentioning

confidence: 99%

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease

Jensen

Abdelmalek

Sullivan

et al. 2018

Journal of Hepatology

652

490

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Nonalcoholic Fatty Liver Disease (NAFLD) is the hepatic manifestation of metabolic syndrome, and its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high fructose corn syrup (HFCS)) not only increases the risk for NAFLD, but also, nonalcoholic steatohepatitis (NASH). Here we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked with metabolism of fructose by fructokinase C, resulting in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations in gut permeability, microbiome, and associated endotoxemia contributes to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.

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Higher fructose intake is inversely associated with risk of nonalcoholic fatty liver disease in older Finnish adults

Cited by 57 publications

References 39 publications

A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease

A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease

Role of diet on non-alcoholic fatty liver disease: An updated narrative review

Fructose and sugar: A major mediator of non-alcoholic fatty liver disease

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