Araújo Mizael C, Soczek Suzany H S, Pontes Jaqueline P, Pinto Bruno A S, França Lucas M, Soley Bruna da Silva, Santos Gabriela S, Saminez Warlison F de Silva, Fernandes Fernanda K M, Lima João L do Carmo, Maria-Ferreira Daniele, Rodrigues João F S, Quintão Nara L M, Monteiro-Neto Valério, Paes Antônio M A, Fernandes Elizabeth S
Programa de Pós-Graduação, Universidade CEUMA, São Luís 65075-120, MA, Brazil.
Programa de Pós-Graduação em Biotecnologia Aplicada à Saúde da Criança e do Adolescente, Faculdades Pequeno Príncipe, Curitiba 80230-020, PR, Brazil.
Pharmaceuticals (Basel). 2023 Aug 3;16(8):1100. doi: 10.3390/ph16081100.
Sugar-induced metabolic imbalances are a major health problem since an excessive consumption of saccharides has been linked to greater obesity rates at a global level. Sucrose, a disaccharide composed of 50% glucose and 50% fructose, is commonly used in the food industry and found in a range of fast, restaurant, and processed foods. Herein, we investigated the effects of a TRPC4/TRPC5 blocker, ML204, in the metabolic imbalances triggered by early exposure to sucrose-enriched diet in mice. TRPC4 and TRPC5 belong to the family of non-selective Ca channels known as transient receptor potential channels. High-sucrose (HS)-fed animals with hyperglycaemia and dyslipidaemia, were accompanied by increased body mass index. mesenteric adipose tissue accumulation with larger diameter cells and hepatic steatosis in comparison to those fed normal diet. HS mice also exhibited enhanced adipose, liver, and pancreas TNFα and VEGF levels. ML204 exacerbated hyperglycaemia, dyslipidaemia, fat tissue deposition, hepatic steatosis, and adipose tissue and liver TNFα in HS-fed mice. Normal mice treated with the blocker had greater hepatic steatosis and adipose tissue cell numbers/diameter than those receiving vehicle, but showed no significant changes in tissue inflammation, glucose, and lipid levels. The results indicate that TRPC4/TRPC5 protect against the metabolic imbalances caused by HS ingestion.
糖诱导的代谢失衡是一个主要的健康问题，因为全球范围内糖类的过量消费与更高的肥胖率相关。蔗糖是一种由50%葡萄糖和50%果糖组成的二糖，常用于食品工业，在一系列快餐、餐厅食品和加工食品中都有发现。在此，我们研究了TRPC4/TRPC5阻滞剂ML204对小鼠早期接触富含蔗糖饮食引发的代谢失衡的影响。TRPC4和TRPC5属于被称为瞬时受体电位通道的非选择性钙通道家族。与喂食正常饮食的动物相比，高蔗糖（HS）喂养的动物出现高血糖和血脂异常，伴有体重指数增加、肠系膜脂肪组织堆积，细胞直径更大，以及肝脂肪变性。HS小鼠还表现出脂肪组织、肝脏和胰腺中TNFα和VEGF水平升高。ML204加剧了HS喂养小鼠的高血糖、血脂异常、脂肪组织沉积、肝脂肪变性以及脂肪组织和肝脏中的TNFα。用该阻滞剂处理的正常小鼠比接受载体的小鼠有更严重的肝脂肪变性和脂肪组织细胞数量/直径，但在组织炎症、血糖和脂质水平上没有显著变化。结果表明，TRPC4/TRPC5可预防HS摄入引起的代谢失衡。
