STAT5 ablation in AgRP neurons increases female adiposity and blunts food restriction adaptations

Autor(es)

Furigo, Isadora C. ^[1] ; Teixeira, Pryscila D. S. ^[1] ; Quaresma, Paula G. F. ^[1] ; Mansano, Naira S. ^[2] ; Frazao, Renata ^[2] ; Donato Jr, Jose

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Ciencias Biomed, Dept Fisiol & Biofis, Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Inst Ciencias Biomed, Dept Anat, Sao Paulo, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF MOLECULAR ENDOCRINOLOGY; v. 64, n. 1, p. 13-27, JAN 2020.
• Citações Web of Science: 0

Resumo

AgRP neurons are important players in the control of energy homeostasis and are responsive to several hormones. In addition, STAT5 signalling in the brain, which is activated by metabolic hormones and growth factors, modulates food intake, body fat and glucose homeostasis. Given that, and the absence of studies that describe STAT5 function in AgRP cells, the present study investigated the metabolic effects of Stat5a/b gene ablation in these neurons. We observed that STAT5 signalling in AgRP neurons regulates body fat in female mice. However, male and female STAT5-knockout mice did not exhibit altered food intake, energy expenditure or glucose homeostasis compared to control mice. The counter-regulatory response or glucoprivic hyperphagia induced by 2-deoxy-D-glucose treatment were also not affected by AgRP-specific STAT5 ablation. However, under 60% food restriction, AgRP STAT5-knockout mice had a blunted upregulation of hypothalamic Agrp mRNA expression and corticosterone serum levels compared to control mice, suggesting a possible role for STAT5 in AgRP neurons for neuroendocrine adaptations to food restriction. Interestingly, ad libitum fed knockout male mice had reduced Pomc and Ucp-1 mRNA expression compared to control group. Taken together, these results suggest that STAT5 signalling in AgRP neurons regulates body adiposity in female mice, as well as some neuroendocrine adaptations to food restriction. (AU)

• Processo FAPESP: 17/22189-9 - Fatores que alteram a ingestão alimentar modulam a atividade de neurônios Kiss1?
• Beneficiário: Naira da Silva Mansano
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/02983-2 - Ação do hormônio do crescimento no sistema nervoso: relevância para as funções neurais e na doença
• Beneficiário: Jose Donato Junior
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 17/25281-3 - Efeitos do hormônio do crescimento sobre os neurônios POMC, colinérgicos e do núcleo paraventricular do hipotálamo: implicações no controle do metabolismo energético e glicêmico
• Beneficiário: Paula Gabriele Fernandes Quaresma Bergonsi
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 16/09679-4 - Estudo dos efeitos centrais do hormônio do crescimento sobre o metabolismo energético e controle glicêmico
• Beneficiário: Isadora Clivatti Furigo
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 17/21840-8 - Sinalização do hormônio do crescimento no sistema nervoso central como mediador da puberdade e fertilidade
• Beneficiário: Renata Frazão
• Modalidade de apoio: Auxílio à Pesquisa - Regular