Fructose and carbonyl metabolites as endogenous toxins

Lee, O.; Bruce, W. R.; Dong, Qiang; Bruce, Jeff; Mehta, Rhea; O’Brien, Peter J.

doi:10.1016/j.cbi.2008.10.011

Cited by 90 publications

(69 citation statements)

References 54 publications

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“…42,59 There is some evidence about the potential interaction of industrial toxins namely high-fructose corn syrup have a role in NASH, and there is increasing interest in the potential interaction of industrial toxins and nutrients. 42,[59][60][61] On the other hand, decreased physical activity in obese patients could promote IR 62 and fatty infiltration of the liver. 26,37 Owing to the close relation to IR and obesity-related inflammation, dietary and lifestyle factors are thought to have a key role in pathogenesis of NAFLD.…”

Section: Nutrition-sedentary Lifestylementioning

confidence: 99%

Nonalcoholic fatty liver disease: a challenge for pediatricians

Widhalm

Ghods

2010

Int J Obes

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Background: Nonalcoholic fatty liver disease (NAFLD) is the most common cause of pediatric liver disease. Its prevalence is related to the growing epidemic in childhood obesity during the past decades. At present, NAFLD and nonalcoholic steatohepatitis (NASH) are increasingly recognized worldwide. In spite of alarming trend in the epidemiology in pediatric field and growing risk of end stage liver disease, there is no significant advance in its diagnosis and treatment. Aim: To provide a detailed review for diagnosis and management of NAFLD and NASH. Methods: By using Pubmed to find review articles and relevant research. Results: The prevalence ranges from at least 3% in children overall to about 50% in obese children. The noninvasive biomarkers can be used to identify NAFLD/NASH patients. Diagnostic criteria based on biochemical and immunological indicators in the high-risk group of children could prevent about half of cases from receiving an invasive test. The pharmacological and surgical interventions have shown a growing role in pediatric NAFLD. Novel treatment modalities, such as probiotics, have hardly been studied. Conclusion: Early diagnosis by using noninvasive screening methods in high-risk groups is the most effective strategy against the NAFLD. The biology of early growth and development, including hepatic metabolism, may hold the key to pediatric NAFLD. Prevention of overweight children and childhood obesity is undoubtedly the best strategy for treating NAFLD.

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Section: Nutrition-sedentary Lifestylementioning

confidence: 99%

Nonalcoholic fatty liver disease: a challenge for pediatricians

Widhalm

Ghods

2010

Int J Obes

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“…Using sham-operated rats as controls, we allowed 5/6Nx rats to develop clear symptoms of CKD for 6 wk, then subsequently fed either a high-fructose or -glucose diet for an additional 4 wk and determined the classical blood and bone markers of renal disease. No study has related fructose consumption to vitamin D metabolism, yet the liver and the kidney, the main sites of vitamin D synthesis, are organs adversely affected by both chronic fructose consumption 20,21 and renal failure 10,11 ; therefore, we next tested the hypothesis that fructose consumption aggravates the already adverse effects of ESRD on the synthesis of the major active form of vitamin D, 1,25-(OH) 2 D 3 . Because 1,25-(OH) 2 D 3 regulates intestinal Ca and Pi absorption, 22,23 we also examined rates of transepithelial transport of these minerals as well as determined expression levels of transporters and proteins involved in their uptake.…”

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confidence: 99%

Dietary Fructose Inhibits Intestinal Calcium Absorption and Induces Vitamin D Insufficiency in CKD

Douard

Asgerally²,

Sabbagh³

et al. 2010

Journal of the American Society of Nephrology

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Renal disease leads to perturbations in calcium and phosphate homeostasis and vitamin D metabolism. Dietary fructose aggravates chronic kidney disease (CKD), but whether it also worsens CKD-induced derangements in calcium and phosphate homeostasis is unknown. Here, we fed rats diets containing 60% glucose or fructose for 1 mo beginning 6 wk after 5/6 nephrectomy or sham operation. Nephrectomized rats had markedly greater kidney weight, blood urea nitrogen, and serum levels of creatinine, phosphate, and calcium-phosphate product; dietary fructose significantly exacerbated all of these outcomes. Expression and activity of intestinal phosphate transporter, which did not change after nephrectomy or dietary fructose, did not correlate with hyperphosphatemia in 5/6-nephrectomized rats. Intestinal transport of calcium, however, decreased with dietary fructose, probably because of fructosemediated downregulation of calbindin 9k. Serum calcium levels, however, were unaffected by nephrectomy and diet. Finally, only 5/6-nephrectomized rats that received dietary fructose demonstrated marked reductions in 25-hydroxyvitamin D 3 and 1,25-dihydroxyvitamin D 3 levels, despite upregulation of 1␣-hydroxylase. In summary, excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease. Future studies should evaluate the relevance of monitoring fructose consumption in patients with CKD.

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“…Interestingly, Lee et al (2009) showed that a low, noncytotoxic dose of H 2 O 2 dramatically increases the cytotoxicity of fructose and glyoxal, a fructose metabolite. Indeed, under normal circumstances, hepatocytes are highly resistant to H 2 O 2 , and fructose also exerts its cytotoxicity at fairly high concentrations (Nomura & Yamanouchi 2012).…”

Section: Genes To Cells (2016) 21 1320-1332mentioning

confidence: 99%

Dietary fructose‐induced hepatocellular carcinoma development manifested in mice lacking apoptosis inhibitor of macrophage (AIM)

et al. 2016

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The consumption of fructose, including the use of high-fructose corn syrup as a sweetener, has increased continuously in recent decades. Although the involvement of fructose in the development of metabolic diseases has been emphasized recently, whether fructose intake increases susceptibility to steatosis-associated hepatocellular carcinoma (HCC) is unclear. Here, we investigated this issue using mice lacking a circulating protein, apoptosis inhibitor of macrophage (AIM, encoded by cd5l). AIM does not induce carcinogenesis of hepatocytes, but provokes necrotic death specifically in AIM-bound cancer cells through complement cascade activation, thereby preventing HCC tumor development in wild-type mice. When subjected to a high-fructose diet (HFrD), AIM-deficient (AIM -/-) mice showed liver steatosis and subsequent liver inflammation as well as fibrosis, but at much milder levels compared with mice fed a high-fat diet. However, AIM -/-mice were markedly susceptible to HCC tumor development, whereas no wild-type mice developed the disease. Systemic metabolic states, including obesity and insulin resistance, were similar in both types of mice after HFrD challenge, indicating no influence of AIM on HFrD-induced metabolic changes. Our results suggest that dietary fructose increases the risk for liver carcinogenesis and that individuals with low blood AIM levels may be susceptible to HCC under chronic fructose intake.

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Fructose and carbonyl metabolites as endogenous toxins

Cited by 90 publications

References 54 publications

Nonalcoholic fatty liver disease: a challenge for pediatricians

Nonalcoholic fatty liver disease: a challenge for pediatricians

Dietary Fructose Inhibits Intestinal Calcium Absorption and Induces Vitamin D Insufficiency in CKD

Dietary fructose‐induced hepatocellular carcinoma development manifested in mice lacking apoptosis inhibitor of macrophage (AIM)

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