Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

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diabetes mellitus 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hypertriglyceridemia 3 endocrinologydiseases
metabolic syndrome 21 endocrinologydiseases
obesity 9 endocrinologydiseases
testosterone 2 endocrinologydiseasesdrugs
allopurinol 3 endocrinologydiseasesdrugs

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allopurinol 30172 absorption and metabolism provide clues for mechanisms of copper-fructose interactions. Rats treated with allopurinol , a competitive inhibitor of xanthine oxidase, displayed improved symptoms induced by copper deficient
allopurinol 30439 decreased mortality, and this was associated with a dramatic reduction of uric acid. The beneficial role of allopurinol is likely attributable to protection against the catabolism of purines and increased nucleotides pool
allopurinol 42031 deficient diet compared to adequate copper diet [[201]]. However, inhibition of uric acid generation with allopurinol showed beneficial effects on copper-fructose interactions [[160]]. Recent studies pointed out that sexual
testosterone 40710 copper deficiency and sex is not well established. Experimental study from rats implies the level of testosterone in the males may play a role in the severity of copper deficiency [[195]]. In line with this, evidence
testosterone 40864 severity of copper deficiency [[195]]. In line with this, evidence from a murine study demonstrated that testosterone robustly suppressed hepcidin transcription through epidermal growth factor receptor (Egfr) signaling,
Select Disease Character Offset Disease Term Instance
diabetes mellitus 10225 184,000 global deaths in 2010 were attributable to consumption of sugary beverages, with 72.3% from diabetes mellitus , 24.2% from cardiovascular diseases (CVDs) and 3.5% from cancer. United States is ranked second in SSB-related
hyperglycemia 17035 reduction is less than 3% of total glucose utilization, whereas more than 30% glucose is used by AR under hyperglycemia [[109],[110]].The causal role of fructose in the pathogenesis of NAFLD has been demonstrated in numerous
hypertriglyceridemia 33200 Copper-Fructose Interaction and HyperlipidemiaCopper-fructose interactions-induced hypercholesterolemia and hypertriglyceridemia have been well demonstrated [[48],[50],[72],[142],[147],[148],[170],[171],[172],[173]]. In a population-based
hypertriglyceridemia 34147 diet high in saturated fat, but not polyunsaturated fat. However, copper-fructose interaction induced hypertriglyceridemia can be exacerbated by both high saturated fat diet and high polyunsaturated fat diet [[72],[171],[173]].
hypertriglyceridemia 34287 by both high saturated fat diet and high polyunsaturated fat diet [[72],[171],[173]]. Of note, both hypertriglyceridemia and hypercholesterolemia are associated with hepatic iron overload and are ameliorated by dietary iron
metabolic syndrome 1058 11/2018AbstractCompelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of
metabolic syndrome 1179 and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose
metabolic syndrome 1420 been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients.
metabolic syndrome 2006 of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis
metabolic syndrome 2381 evidence has shown that increased fructose consumption parallels the rises in the obesity epidemic, metabolic syndrome and NAFLD in the United States and worldwide [[1],[2],[3],[4],[5],[6],[7],[8]]. Moreover, fructose consumption
metabolic syndrome 3098 metabolism [[14]] and limited absorption [[15],[16]]. The role of fructose in the induction of components of metabolic syndrome , as well as NAFLD, has been well documented in numerous animal studies [[17],[18],[19],[20]]. A recent
metabolic syndrome 3932 highlighting the importance of the gut-liver axis in the pathogenesis of dietary fructose associated NAFLD and metabolic syndrome . Despite the major progress that has been made over the past two decades, the mechanisms underlying
metabolic syndrome 4078 that has been made over the past two decades, the mechanisms underlying fructose-induced NAFLD and metabolic syndrome are still incompletely understood. Even with increased de novo lipogenesis, only a small amount of fructose
metabolic syndrome 4702 compelling epidemiologic data support the critical role of dietary fructose in the epidemic of the metabolic syndrome [[2],[8],[28],[29],[30],[31]], a causal link between fructose consumption and the metabolic syndrome
metabolic syndrome 4803 metabolic syndrome [[2],[8],[28],[29],[30],[31]], a causal link between fructose consumption and the metabolic syndrome has not been firmly established in human studies [[32],[33],[34],[35],[36]]. Most of studies on fructose
metabolic syndrome 6143 pathways. We and others have demonstrated copper-fructose interactions in inducing the components of metabolic syndrome and NAFLD in rat model [[47],[48],[49],[50],[51]].A growing body of evidence indicates that hepatic
metabolic syndrome 7502 In this review, we will discuss the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and NAFLD and discuss potential underlying mechanisms.2. Epidemiology of NAFLD, Fructose Consumption,
metabolic syndrome 8256 obesity, type 2 diabetes (T2D), insulin resistance and hypertension [[8],[73]]—all hallmarks of the metabolic syndrome . In particular, the prevalence of suspected NAFLD in adolescents increased at an alarming rate, from
metabolic syndrome 15130 [[23],[101]]. Depletion of KHK-C or KHK-A and -C, but not KHK-A alone, protects against fructose-induced metabolic syndrome [[23],[103],[104]]. A reduction of intracellular phosphate leads to the activation of adenosine monophosphate
metabolic syndrome 16624 that endogenous fructose, generated from polyol pathway, plays a critical role in the development of metabolic syndrome and NASH (in addition to dietary fructose) [[22],[104]]. The polyol pathway is an alternate route of
metabolic syndrome 20511 copper levels than those with simple steatosis. Hepatic copper level is lower in NAFLD patients with the metabolic syndrome and T2D compared to those without metabolic syndrome and T2D [[52]]. Moreover, NAFLD patients with lower
metabolic syndrome 20564 copper level is lower in NAFLD patients with the metabolic syndrome and T2D compared to those without metabolic syndrome and T2D [[52]]. Moreover, NAFLD patients with lower serum copper and lower liver copper exhibited higher
metabolic syndrome 23200 1980’s demonstrated that dietary copper-fructose interactions worsened copper deficiency-induced metabolic syndrome . The severity of experimental copper deficiency was exacerbated by a diet containing high fructose compared
metabolic syndrome 26870 overload is considered as a partial potential mechanism underlying copper deficiency and fructose induced metabolic syndrome [[147],[148],[149],[150]]. We showed that marginal copper deficient and high fructose diet markedly
metabolic syndrome 42619 interactions likely contributes to sex variances in fructose metabolism and susceptibility to NAFLD/ metabolic syndrome .7. ConclusionsHigh fructose consumption and low copper availability are two risk factors identified
metabolic syndrome 43600 copper/ceruloplasmin. A beneficial role for restricting dietary fructose intake to improve obesity and the metabolic syndrome has been clearly demonstrated and further studies may confirm the additional role of low copper availability.Figure
obesity 1049 11/2018AbstractCompelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity , metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose
obesity 2363 IntroductionAccumulating evidence has shown that increased fructose consumption parallels the rises in the obesity epidemic, metabolic syndrome and NAFLD in the United States and worldwide [[1],[2],[3],[4],[5],[6],[7],[8]].
obesity 3627 ketohexokinase (KHK), a key enzyme of fructose metabolism, markedly attenuated high fructose diet-induced NAFLD, obesity and other metabolic effects [[22],[23],[24]]. Similarly, toll like receptor 4 (TLR4) mutation or oral
obesity 5175 [[37]]. Of note, isocaloric dietary fructose restriction has been reported to be beneficial in improving obesity and metabolic parameters [[38],[39],[40]]. Animal studies also showed the essential role of fructose
obesity 8154 and is 24.13% in North America [[8]]. The increased prevalence of NAFLD parallels the increases in obesity , type 2 diabetes (T2D), insulin resistance and hypertension [[8],[73]]—all hallmarks of the metabolic
obesity 9423 time-trend data over the past 3 decades have shown that the increased consumption of SSBs parallels the obesity epidemic and is associated with increased T2D risk in the United States [[2]]. The prevalence of obesity
obesity 9528 obesity epidemic and is associated with increased T2D risk in the United States [[2]]. The prevalence of obesity increased from approximately 5% (early 1970’s) to 17% (2011–2014) in children and adolescents, and
obesity 38841 fructose (w/v) in the drinking water and AIN-76 based rodent diet (ad libitum) for four weeks exhibited an obesity phenotype characterized by a markedly increased ratio of Firmicutes/Bacteroides, and this effect was
obesity 43584 depressed serum copper/ceruloplasmin. A beneficial role for restricting dietary fructose intake to improve obesity and the metabolic syndrome has been clearly demonstrated and further studies may confirm the additional

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