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Abstract
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.
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Details
1 University of Campinas, Laboratory of Cell Signalling-Obesity and Comorbidities Research Center, Campinas, Brazil (GRID:grid.411087.b) (ISNI:0000 0001 0723 2494)
2 University of Campinas (UNICAMP), Multidisciplinary Laboratory of Food and Health (LABMAS), School of Applied Sciences (FCA), Limeira, Brazil (GRID:grid.411087.b) (ISNI:0000 0001 0723 2494)
3 University of Sao Paulo, Department of Physiology and Biophysics, Institute of Biomedical Sciences, Sao Paulo, Brazil (GRID:grid.11899.38) (ISNI:0000 0004 1937 0722)
4 University of Campinas, Laboratory of Cell Signalling-Obesity and Comorbidities Research Center, Campinas, Brazil (GRID:grid.411087.b) (ISNI:0000 0001 0723 2494); National Institute of Science and Technology on Neuroimmunomodulation, Rio de Janeiro, Brazil (GRID:grid.411087.b)