Gastric Bypass and Copper Deficiency: A Possible Overlooked Consequence

Medeiros, Denis M.

doi:10.1007/s11695-011-0465-3

Cited by 6 publications

(4 citation statements)

References 11 publications

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“…As described above, surgical obesity treatment has also been strongly implicated in copper deficiency, likely by causing a diminished absorption of copper after a gastric bypass surgery (16)(17)(18). In addition, low copper levels were detected in organs, plasma and tissue of patients with several chronic diseases including cardiovascular disease, central nervous system, and musculoskeletal disorders (25).…”

Section: Low Copper and Human Diseasementioning

confidence: 98%

“…Copper deficiency is rarely diagnosed in humans, with a notable exception of a growing number of reports pointing to copper and other mineral insufficiencies as unintended consequences of bariatric surgeries (16)(17)(18). The under-detection of copper deficiency could be due to limitations of screening using serum or urine samples.…”

Section: Copper In Western Dietmentioning

confidence: 99%

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The Role of Copper as a Modifier of Lipid Metabolism

Burkhead¹,

Lutsenko²

2013

Lipid Metabolism

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Section: Low Copper and Human Diseasementioning

confidence: 98%

Section: Copper In Western Dietmentioning

confidence: 99%

The Role of Copper as a Modifier of Lipid Metabolism

Burkhead¹,

Lutsenko²

2013

Lipid Metabolism

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“…Cu 2þ , on the other hand, may have limited nutritional value and exhibit dichotomous health effects in the body. A fraction of Cu 2þ may bypass the normal uptake process and directly enter the blood stream and increase free Cu levels as described below (Medeiros, 2011).…”

Section: Beneficial and Detrimental Role Of Copper Linking To Admentioning

confidence: 99%

Environmental and Dietary Exposure to Copper and Its Cellular Mechanisms Linking to Alzheimer’s Disease

Hsu

Bondy

Kitazawa

2018

Toxicological Sciences

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Metals are commonly found in the environment, household, and workplaces in various forms, and a significant segment of the population is routinely exposed to the trace amount of metals from variety of sources. Exposure to metals, such as aluminum, lead, iron, and copper, from environment has long been debated as a potential environmental risk factor for Alzheimer's disease (AD) for decades, yet results from in vitro, in vivo, and human population remain controversial. In the case of copper, the neurotoxic mechanism of action was classically viewed as its strong affinity to amyloid-beta (Aβ) to help its aggregation and increase oxidative stress via Fenton reaction. Thus, it has been thought that accumulation of copper mediates neurotoxicity, and removing it from the brain prevents or reverse Aβ plaque burden. Recent evidence, however, suggests dyshomeostasis of copper and its valency in the body, instead of the accumulation and interaction with Aβ, are major determinants of its beneficial effects as an essential metal or its neurotoxic counterpart. This notion is also supported by the fact that genetic loss-of-function mutations on copper transporters lead to severe neurological symptoms. Along with its altered distribution, recent studies have also proposed novel mechanisms of copper neurotoxicity mediated by nonneuronal cell lineages in the brain, such as capillary endothelial cells, leading to development of AD neuropathology. This review covers recent findings of multifactorial toxic mechanisms of copper and discusses the risk of environmental exposure as a potential factor in accounting for the variability of AD incidence.

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“…Even among nondemented elderly population, excess Cu intake from dietary supplements or elevated levels of free Cu in blood is consistently associated with cortical thinning and impaired memory function (Morris et al, 2006;Salustri et al, 2010;Silbert et al, 2018), suggesting a profound adverse effect of Cu dyshomeostasis in the central nervous system and precursor to dementia. Although Cu is an essential transition metal serving as a catalytic cofactor for more than 20 redox enzymes (Itoh et al, 2009), Cu from environment as inorganic cupric (Cu 2þ ) form may enter the blood stream and rapidly increase labile Cu levels to mediate potentially harmful events including the generation of reactive oxygen species in the local microenvironment (Brewer, 2015;Ceko et al, 2014;Hill et al, 1986;Hsu et al, 2018;Medeiros, 2011;Prohaska, 2008). In fact, a very recent study using a mouse model of Down syndrome demonstrates that Cu is abnormally accumulated in cortex and hippocampus and exerts oxidative damage and cognitive decline (Ishihara et al, 2019), although abnormal Cu accumulation in postmortem brains from AD or Down syndrome patients remains controversy (Miller et al, 2006;Rembach et al, 2013), and its neurotoxic mechanism of action is subject to further debates.…”

mentioning

confidence: 99%

Copper-Induced Upregulation of MicroRNAs Directs the Suppression of Endothelial LRP1 in Alzheimer’s Disease Model

Hsu

Rodriguez‐Ortiz

Lim

et al. 2019

Toxicological Sciences

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Chronic exposure to copper and its dyshomeostasis have been linked to accelerated cognitive decline and potentially increasing risk for Alzheimer's disease (AD). We and others have previously demonstrated that exposure to copper through drinking water significantly increased parenchymal amyloid-beta (Ab) plaques and decreased endothelial low-density lipoprotein receptor-related protein 1 (LRP1) in mouse models of AD. In this study, we determined the underlying mechanisms that microRNA critically mediated the copper-induced loss of endothelial LRP1. In human primary microvascular endothelial cells (MVECs), were significantly elevated within the 24-h exposure to copper and returned to baseline after 48-h postexposure, which corresponded with the temporal change of LRP1 expression in these cells. Transient expression of synthetic microRNA-200b-3p, -200c-3p, or -205-5p on MVECs significantly decreased endothelial LRP1, and cotreatment of synthetic antagomirs effectively prevented the loss of LRP1 during copper exposure, collectively supporting the key regulatory role of these microRNAs in copper-induced loss of LRP1. In mice, a significant reduction of LRP1 in cortical vasculature was evident following 9 months exposure to 1.3 ppm copper in drinking water, although the levels of cortical were only marginally elevated. This, however, correlated with increased vascular accumulation of Ab and impairment of spatial memory, indicating that copper exposure has the pivotal role in the vascular damage and development of cognitive decline.

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Gastric Bypass and Copper Deficiency: A Possible Overlooked Consequence

Cited by 6 publications

References 11 publications

The Role of Copper as a Modifier of Lipid Metabolism

The Role of Copper as a Modifier of Lipid Metabolism

Environmental and Dietary Exposure to Copper and Its Cellular Mechanisms Linking to Alzheimer’s Disease

Copper-Induced Upregulation of MicroRNAs Directs the Suppression of Endothelial LRP1 in Alzheimer’s Disease Model

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