Effects of arsenic on adipocyte metabolism: Is arsenic an obesogen?

Ceja-Galicia, Zeltzin Alejandra; Daniel, Alberto; Salazar, Ana Marı́a; Pánico, Pablo; Ostrosky‐Wegman, Patricia; Dı́az-Villaseñor, Andrea

doi:10.1016/j.mce.2017.05.008

Cited by 41 publications

(23 citation statements)

References 95 publications

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“…Thus, arsenite contaminated drinking water has been considered as a contributing factor for numerous health concerns in humans such as diabetes, lung and skin diseases, and cancer 23–25 . Recent evidence suggests that exposure to arsenite may lead to adipose tissue dysfunction and lipodystrophy as well as inhibition of adipogenesis 26,27 . Arsenite inhibits adipogenesis and adipocyte function in human mesenchymal stem cells 28 , 3T3-L1 preadipocytes 29 , and C3H 10T1/2 preadipocytes 30 .…”

Section: Introductionmentioning

confidence: 99%

Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

Bae

Jang

Kim

et al. 2019

Sci Rep

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Arsenite, a trivalent form of arsenic, is an element that occurs naturally in the environment. Humans are exposed to high dose of arsenite through consuming arsenite-contaminated drinking water and food, and the arsenite can accumulate in the human tissues. Arsenite induces oxidative stress, which is linked to metabolic disorders such as obesity and diabetes. Brown adipocytes dissipating energy as heat have emerging roles for obesity treatment and prevention. Therefore, understanding the pathophysiological role of brown adipocytes can provide effective strategies delineating the link between arsenite exposure and metabolic disorders. Our study revealed that arsenite significantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respiration, leading to attenuated thermogenesis via decreasing UCP1 expression. Oral administration of arsenite in mice resulted in heavy accumulation in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis. Mechanistically, arsenite exposure significantly inhibited autophagy necessary for homeostasis of brown adipose tissue through suppression of Sestrin2 and ULK1. These results clearly confirm the emerging mechanisms underlying the implications of arsenite exposure in metabolic disorders.

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Section: Introductionmentioning

confidence: 99%

Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

Bae

Jang

Kim

et al. 2019

Sci Rep

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“…Arsenite at physiologically relevant concentrations also shows an inhibitory effect on the expression of peroxisome proliferator‐activated receptor γ, a nuclear hormone receptor important for activating insulin action (Tseng, ). In fact, CAsE has been associated with diabetes mellitus type 2 (Navas‐Acien et al, ) as well as with obesity (Ceja‐Galicia et al, ).…”

Section: Discussionmentioning

confidence: 99%

Chronic arsenic intoxication diagnostic score (CAsIDS)

Dani

Walter

2017

J of Applied Toxicology

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Arsenic and its compounds are well-established, potent, environmentally widespread and persistent toxicants with metabolic, genotoxic, mutagenic, teratogenic, epigenetic and carcinogenic effects. Arsenic occurs naturally in the Earth's crust, but anthropogenic arsenic emissions have surmounted the emissions from important natural sources such as volcanism. Inorganic arsenicals exhibit acute and chronic toxicities in virtually all cell types and tissues, and hence arsenic intoxication affects multiple systems. Whereas acute arsenic intoxication is rare and relatively easy to diagnose, chronic arsenic intoxication (CAsI) is common but goes often misdiagnosed.Based on a review of the literature as well as our own clinical experience, we propose a chronic arsenic intoxication diagnostic score (CAsIDS). A distinctive feature of CAsIDS is the use of bone arsenic load as an essential criterion for the individual risk assessment of chronic arsenic intoxication, combined with a systemic clinical assessment. We present clinical examples where CAsIDS is applied for the diagnosis of CAsI, review the main topics of the toxicity of arsenic in different cell and organ systems and discuss the therapy and prevention of disease caused or aggravated by chronic arsenic intoxication. CAsIDS can help physicians establish the diagnosis of CAsI and associated conditions.

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“…In the current study, postmenopausal women had a significant correlation with increasing arsenic concentrations and obesity. Fat distribution in women changes with menopausal status, where central/abdominal obesity is more prevalent among postmenopausal women, as are various hormone stores within this white adipose tissue (Garaulet et al 2002;Ferrara et al 2002;Hodson et al 2015;Lovejoy, 2003;Ceja-Galicia et al 2017). The decreased urinary arsenic concentration associated with an increase in BMI could possibly be explained by the urinary quantification.…”

Section: Figmentioning

confidence: 99%

Low-Level Environmental Heavy Metals are Associated with Obesity Among Postmenopausal Women in a Southern State

Stahr

Chiang²,

Bauer³

et al. 2021

Expo Health

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Both arsenic and cadmium are reported to be toxic to humans. The use of saliva as a biomarker of low-level exposures to these elements has not been adequately explored, and the putative relationship between exposure and obesity is unclear. This cross-sectional study aims to investigate the relationship between salivary arsenic and cadmium concentrations and their association with obesity. Arsenic and cadmium concentrations were analyzed in human saliva samples by Inductively Coupled Plasma-Mass Spectrometry on 270 randomly selected women who participated in the Arkansas Rural Community Health Study. Multivariable logistic regression was performed to evaluate the association between heavy metal concentrations and obesity. Stratified logistic regression was performed based on menopausal status. Generalized linear models were used to evaluate weight gain velocity. Significant positive associations were observed in postmenopausal women for both arsenic (OR = 4.43, 95% CI 1.91–10.28) and cadmium (OR = 2.72, 95% CI 1.23–5.99) concentrations, as well as significant trends among tertiles (p < 0.01 and p = 0.01, respectively). No relationship with obesity was evident among premenopausal women for either metal. A dose–response relationship was observed between increasing weight gain velocity and increasing metal concentrations. At concentrations well below governmental and industrial standards for acute toxicity, significant associations between obesity and concentration of these heavy metals are evident. The rate at which individuals gain weight is affected by metal concentrations and may play a role in the rapid increase in weight in postmenopausal women. These results might explain, in part, the missing variability in the increasing obesity pandemic in certain population exposed to these environmental toxicants.

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Effects of arsenic on adipocyte metabolism: Is arsenic an obesogen?

Cited by 41 publications

References 95 publications

Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

Chronic arsenic intoxication diagnostic score (CAsIDS)

Low-Level Environmental Heavy Metals are Associated with Obesity Among Postmenopausal Women in a Southern State

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