| Grant number: | 17/06225-5 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Effective date (Start): | August 01, 2017 |
| Effective date (End): | December 31, 2019 |
| Field of knowledge: | Biological Sciences - Immunology |
| Principal Investigator: | Pedro Manoel Mendes de Moraes Vieira |
| Grantee: | Felipe Corrêa da Silva |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| Associated research grant: | 15/15626-8 - Macrophages and T lymphocytes immunometabolism in metabolic and inflammatory diseases, AP.JP |
| Associated scholarship(s): | 18/12257-0 - Hypothalamic neuropeptides as microglial immunoregulators, BE.EP.MS |
Abstract The comprehension of the molecular mechanisms involved in the genesis of obesity and the possibility reversing the obese phenotype is extremely relevant for the prevention and treatment of this pathology and its comorbidities. The global metabolic control, in mammals, is performed by the hypothalamus, a central nervous system structure. Neuronal populations in the hypothalamus are able to sense blood borne signals which indicate the organism nutrional status which involves insulin and leptin signaling. The feeding of diets rich in satureted fatty acids leads to hypothalamic inflammation and anorexigenic signaling impairment. This impairiment is a direct result of POMC (Pro-opiomelanocortin) + neurons death and its disfunction, which is triggered by tissue inflammation. ±-MSH (alpha-melanocyte stimulating hormone) is one of the peptides obtained from POMC cleavage. ±-MSH acts on membrane receptors called melanocortin receptors. In the central nervous system, the melanocortin receptor 3 4 are broadly expressed, and are the most relevant ±-MSH receptors for energy homeostasis. In addition to its function in metabolic control, ±-MSH also has a marked anti-inflammatory role directly on imune cells. Here, we hypothesize that the dysfunction of POMC+ neurons is required for the perpetuation and intensification of hypothalamic inflammation, which may be attributed to the diminished ±-MSH signaling in microglia. Our aim is to investigate the anti-inflammatory effects of ±-MSH on microglial. For this purpose, we will study the immune and metabolic phenotype of microglial cells. We expect that ±-MSH treatment will induce an anti-inflammatory phenotype in microglial cells, which may be dependent on the metabolic status of the microglia. This may result in attenuation of metabolic inflammation. (AU) | |
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