| Autor: |
Monibas, Rafael Mayoral, Johnson, Andrew M. F., Osborn, Olivia, Traves, Paqui G., Mahata, Sushil K., Zhihong Yang, Castro-Alves, Victor Costa |
| Předmět: |
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| Zdroj: |
Frontiers in Endocrinology; 12/6/2016, Vol. 7, p1-8, 8p |
| Abstrakt: |
Obesity is a complex metabolic disorder associated with the development of noncommunicable diseases such as cirrhosis, non-alcoholic fatty liver disease, and type 2 diabetes. In humans and rodents, obesity promotes hepatic steatosis and inflammation, which leads to increased production of pro-inflammatory cytokines and acute-phase proteins. Liver macrophages (resident as well as recruited) play a significant role in hepatic inflammation and insulin resistance (IR). Interestingly, depletion of hepatic macrophages protects against the development of high-fat-induced steatosis, inflammation, and IR. Kupffer cells (KCs), liver-resident macrophages, are the first-line defense against invading pathogens, clear toxic or immunogenic molecules, and help to maintain the liver in a tolerogenic immune environment. During high fat diet feeding and steatosis, there is an increased number of recruited hepatic macrophages (RHMs) in the liver and activation of KCs to a more inflammatory or M1 state. In this review, we will focus on the role of liver macrophages (KCs and RHMs) during obesity. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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