Papel do canal TRPV1 no desenvolvimento de obesidade induzida por dieta rica em gordura em camundongos (Mus musculus)
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Data
2023-12
Tipo de documento
Artigo Científico
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Área do conhecimento
Modalidade de acesso
Acesso fechado
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Autores
BRAULINO, Julia dos Santos
Orientador
CASTRUCCI, Ana Maria de Lauro
Coorientador
SUA-CESPEDES, Cristhian David
Resumo
O canal TRPV1 regula o escurecimento dos adipócitos brancos e a ativação de moduladores metabólicos, tornando-o um alvo potencialmente relevante para estudos do metabolismo. A obesidade é caracterizada pelo acúmulo excessivo de tecido adiposo resultante de um gasto energético desequilibrado, e está associada a complicações como diabetes tipo 2 e desenvolvimento da síndrome metabólica. Embora o canal TRPV1 seja amplamente investigado em pesquisas metabólicas, os resultados na literatura são controversos devido às diferentes metodologias, principalmente a temperatura de manutenção dos animais que geralmente é fora da sua zona de termoneutralidade. Nosso objetivo foi avaliar o papel do canal TRPV1 no desenvolvimento da obesidade induzida por dieta rica em gordura (HFD), utilizando camundongos C57BL/6J e nocautes para Trpv1 na termoneutralidade (30°C) e desafiados a frio moderado (22°C). Foram avaliados o ganho de peso, ingestão alimentar, metabolismo glicêmico, determinação de lipídios no sangue, fígado e fezes e análises macroscópicas, além da expressão de genes hipotalâmicos que regulam o apetite. O protocolo foi eficaz no desenvolvimento da obesidade em ambos os genótipos e temperaturas, com os camundongos submetidos ao frio demonstrando níveis mais altos de colesterol e triglicérides séricos em relação aos seus controles na termoneutralidade. De forma interessante, os animais Trpv1-/- a 30°C eliminaram mais gordura nas fezes em relação aos outros grupos. Observou-se também uma expressão aumentada do receptor hipotalâmico da leptina nos animais WT a 22°C e nocautes a 30°C. Nossos resultados sugerem que a ausência do canal TRPV1 não afeta o ganho de peso em camundongos em termoneutralidade ou a 22°C, mas revela uma influência significativa em respostas metabólicas relacionadas à obesidade, especialmente em condições de frio moderado presente em biotérios.
The TRPV1 channel regulates white adipocyte browning and activates metabolic modulators, making it a potentially relevant target for metabolism studies. Obesity is characterized by the excessive accumulation of adipose tissue resulting from unbalanced energy expenditure and is associated with complications such as type 2 diabetes and the development of metabolic syndrome. Although the TRPV1 channel is widely investigated in metabolic research, the results in the literature are controversial due to different methodologies, especially the temperature at which the animals are kept, which is generally outside their thermoneutrality zone. We aimed to evaluate the role of the TRPV1 channel in the development of obesity induced by high-fat diet (HFD), using C57BL/6J and Trpv1 knockout mice in thermoneutrality (30°C) and subjected to moderate cold (22°C). Weight gain, food intake, glucose metabolism, determination of lipids in the blood, liver, and feces, macroscopic analyses, and the expression of hypothalamic genes that regulate appetite were evaluated. The protocol was effective in developing obesity in both genotypes and temperatures, with the mice subjected to cold showing higher levels of serum cholesterol and triglycerides compared to their controls in thermoneutrality. Interestingly, Trpv1-/- animals at 30°C eliminated more fat in the feces compared to the other groups. Increased expression of the hypothalamic leptin receptor was also observed in WT animals at 22°C and knockouts at 30°C. Our results suggest that the absence of the TRPV1 channel does not affect weight gain in mice in thermoneutrality or at 22°C, but reveals a significant influence on obesity-related metabolic responses, especially in the moderate cold conditions present in animal vivarium.
The TRPV1 channel regulates white adipocyte browning and activates metabolic modulators, making it a potentially relevant target for metabolism studies. Obesity is characterized by the excessive accumulation of adipose tissue resulting from unbalanced energy expenditure and is associated with complications such as type 2 diabetes and the development of metabolic syndrome. Although the TRPV1 channel is widely investigated in metabolic research, the results in the literature are controversial due to different methodologies, especially the temperature at which the animals are kept, which is generally outside their thermoneutrality zone. We aimed to evaluate the role of the TRPV1 channel in the development of obesity induced by high-fat diet (HFD), using C57BL/6J and Trpv1 knockout mice in thermoneutrality (30°C) and subjected to moderate cold (22°C). Weight gain, food intake, glucose metabolism, determination of lipids in the blood, liver, and feces, macroscopic analyses, and the expression of hypothalamic genes that regulate appetite were evaluated. The protocol was effective in developing obesity in both genotypes and temperatures, with the mice subjected to cold showing higher levels of serum cholesterol and triglycerides compared to their controls in thermoneutrality. Interestingly, Trpv1-/- animals at 30°C eliminated more fat in the feces compared to the other groups. Increased expression of the hypothalamic leptin receptor was also observed in WT animals at 22°C and knockouts at 30°C. Our results suggest that the absence of the TRPV1 channel does not affect weight gain in mice in thermoneutrality or at 22°C, but reveals a significant influence on obesity-related metabolic responses, especially in the moderate cold conditions present in animal vivarium.
Palavras-chave
TRPV1, obesidade, camundongos, tecido adiposo branco (WAT), tecido adiposo marrom (BAT)