Mechanistic insight into high-fat diet-induced metabolic inflammation in the arcuate nucleus of the hypothalamus - 18/09/21
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Abstract |
A high-fat diet (HFD) is linked with cytokines production by non-neuronal cells within the hypothalamus, which mediates metabolic inflammation. These cytokines then activate different inflammatory mediators in the arcuate nucleus of the hypothalamus (ARC), a primary hypothalamic area accommodating proopiomelanocortin (POMC) and agouti-related peptide (AGRP) neurons, first-order neurons that sense and integrate peripheral metabolic signals and then respond accordingly. These mediators, such as inhibitor of κB kinase-β (IKKβ), suppression of cytokine signaling 3 (SOCS3), c-Jun N-terminal kinases (JNKs), protein kinase C (PKC), etc., cause insulin and leptin resistance in POMC and AGRP neurons and support obesity and related metabolic complications. On the other hand, inhibition of these mediators has been shown to counteract the impaired metabolism. Therefore, it is important to discuss the contribution of neuronal and non-neuronal cells in HFD-induced hypothalamic inflammation. Furthermore, understanding few other questions, such as the diets causing hypothalamic inflammation, the gender disparity in response to HFD feeding, and how hypothalamic inflammation affects ARC neurons to cause impaired metabolism, will be helpful for the development of therapeutic approaches to prevent or treat HFD-induced obesity.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | A high-fat diet activates glial cells to produce and release cytokines. |
• | Cytokines then activate inflammatory mediators in POMC and AGRP neurons. |
• | Inflammatory mediators cause insulin and leptin resistance. |
• | Insulin and leptin resistance leads to decreased POMC and increased AGRP expression. |
• | Compromised POMC and AGRP expression result in increased food intake, reduced energy expenditure, and obesity. |
Keywords : HFD, Metabolic inflammation, ARC, Altered POMC and AGRP functionality, Impaired metabolism
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Vol 142
Article 112012- octobre 2021 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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