| First Author | Moura-Assis A | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 18015 |
| PubMed ID | 34504172 | Mgi Jnum | J:313887 |
| Mgi Id | MGI:6766284 | Doi | 10.1038/s41598-021-97291-7 |
| Citation | Moura-Assis A, et al. (2021) TLR4-interactor with leucine-rich repeats (TRIL) is involved in diet-induced hypothalamic inflammation. Sci Rep 11(1):18015 |
| abstractText | Obesity and high-fat diet (HFD) consumption result in hypothalamic inflammation and metabolic dysfunction. While the TLR4 activation by dietary fats is a well-characterized pathway involved in the neuronal and glial inflammation, the role of its accessory proteins in diet-induced hypothalamic inflammation remains unknown. Here, we demonstrate that the knockdown of TLR4-interactor with leucine-rich repeats (Tril), a functional component of TLR4, resulted in reduced hypothalamic inflammation, increased whole-body energy expenditure, improved the systemic glucose tolerance and protection from diet-induced obesity. The POMC-specific knockdown of Tril resulted in decreased body fat, decreased white adipose tissue inflammation and a trend toward increased leptin signaling in POMC neurons. Thus, Tril was identified as a new component of the complex mechanisms that promote hypothalamic dysfunction in experimental obesity and its inhibition in the hypothalamus may represent a novel target for obesity treatment. |
