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Chronic arsenic exposure impairs adaptive thermogenesis in male C57BL/6J mice.
Authors Castriota F, Zushin PH, Sanchez SS, Phillips RV, Hubbard A, Stahl A, Smith MT,
Wang JC, La Merrill MA
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal American journal of physiology. Endocrinology and metabolism
Year 2020
Date Published 5/1/2020
Volume : Pages 318 : E667 - E677
PubMed Reference 32045263
Abstract The global prevalence of type 2 diabetes (T2D) has doubled since 1980. Human
epidemiological studies support arsenic exposure as a risk factor for T2D,
although the precise mechanism is unclear. We hypothesized that chronic arsenic
ingestion alters glucose homeostasis by impairing adaptive thermogenesis, i.e.,
body heat production in cold environments. Arsenic is a pervasive environmental
contaminant, with more than 200 million people worldwide currently exposed to
arsenic-contaminated drinking water. Male C57BL/6J mice exposed to sodium
arsenite in drinking water at 300 µg/L for 9 wk experienced significantly
decreased metabolic heat production when acclimated to chronic cold tolerance
testing, as evidenced by indirect calorimetry, despite no change in physical
activity. Arsenic exposure increased total fat mass and subcutaneous inguinal
white adipose tissue (iWAT) mass. RNA sequencing analysis of iWAT indicated that
arsenic dysregulated mitochondrial processes, including fatty acid metabolism.
Western blotting in WAT confirmed that arsenic significantly decreased TOMM20, a
correlate of mitochondrial abundance; PGC1A, a master regulator of mitochondrial
biogenesis; and, CPT1B, the rate-limiting step of fatty acid oxidation (FAO).
Our findings show that chronic arsenic exposure impacts the mitochondrial
proteins of thermogenic tissues involved in energy expenditure and substrate
regulation, providing novel mechanistic evidence for arsenic's role in T2D


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