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Short-term exposure to air pollution (PM_2.5) induces hypothalamic inflammation, and long-term leads to leptin resistance and obesity via Tlr4/Ikbke in mice.

ABSTRACT: A previous study demonstrated that a high-fat diet (HFD), administered for one-three-days, induces hypothalamic inflammation before obesity's established, and the long term affects leptin signaling/action due to inflammation. We investigate whether exposure to particulate matter of a diameter of ≤2.5 μm (PM_2.5) in mice fed with a chow diet leads to similar metabolic effects caused by high-fat feeding. Compared to the filtered air group (FA), one-day-exposure-PM_2.5 did not affect adiposity. However, five-days-exposure-PM_2.5 increased hypothalamic microglia density, toll-like-receptor-4 (Tlr4), and the inhibitor-NF-kappa-B-kinase-epsilon (Ikbke) expression. Concurrently, fat mass, food intake (FI), and ucp1 expression in brown adipose tissue were also increas

SUBMITTER: Campolim CM

PROVIDER: S-EPMC7311527 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Dataset Information

Short-term exposure to air pollution (PM_2.5) induces hypothalamic inflammation, and long-term leads to leptin resistance and obesity via Tlr4/Ikbke in mice.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Short-term exposure to air pollution (PM2.5) induces hypothalamic inflammation, and long-term leads to leptin resistance and obesity via Tlr4/Ikbke in mice.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Short-term exposure to air pollution (PM_2.5) induces hypothalamic inflammation, and long-term leads to leptin resistance and obesity via Tlr4/Ikbke in mice.