The deletion of T-type Ca_v3.1 channels may reduce high-fat diet (HFD)-induced weight gain, which correlates positively with obesity and endothelial dysfunction. Therefore, experiments were designed to study the involvement of T-type Ca_v3.1 channels in HFD-induced endothelial dysfunction in mice. Wildtype (WT) and Ca_v3.1^−/− mice were fed either a normal diet (ND) or an HFD for 8 weeks. Body composition was assessed, and thoracic aortae and mesenteric arteries were harvested for myography to assess endothelium-dependent responses. Changes in intracellular calcium were measured by fluorescence imaging, and behavior was assessed with the open-field test. Ca_v3.1^−/− mice had attenuated HFD-induced weight gain and lower total fat mass compared with WT mice. Ca_v3.1^−/− mice on an HFD had reduced plasma cholesterol levels compared with WT mice on the same diet. Increased feeding efficiency, independent of food intake, was observed in WT mice on an HFD compared with an ND, but no difference in feeding efficiency between diets was observed for Ca_v3.1^−/− mice. Nitric oxide-dependent dilatation was increased in mesenteric arteries of Ca_v3.1^−/− mice compared with WT mice on an HFD, with no difference observed in aortae. No differences in mouse locomotor activity were observed between the experimental groups. Mice on an HFD lacking T-type channels have reduced weight gain, lower total cholesterol levels, and increased dilatation of resistance vessels compared with WT mice on an HFD, suggesting that Ca_v3.1 deletion protects against endothelial dysfunction in resistance vessels but not in large conduit vessels.

中文翻译：

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T型电压门控钙通道的缺乏导致小鼠高脂饮食诱导的体重增加减弱和内皮细胞对阻力血管的内皮依赖性扩张的改善。

T型Ca _v 3.1通道的缺失可能会减少高脂饮食（HFD）引起的体重增加，这与肥胖症和内皮功能障碍呈正相关。因此，设计了实验来研究T型Ca _v 3.1通道在HFD诱导的小鼠内皮功能障碍中的作用。给野生型（WT）和Ca _v 3.1 ^-/-小鼠喂食正常饮食（ND）或HFD，持续8周。评估身体成分，并收集胸主动脉和肠系膜动脉进行肌成像检查，以评估内皮依赖性反应。通过荧光成像测量细胞内钙的变化，并通过开放视野测试评估行为。Ca _v 3.1 ^-/-与野生型小鼠相比，小鼠的HFD诱导的体重增加减弱，总脂肪量降低。与相同饮食的WT小鼠相比，HFD的Ca _v 3.1 ^-/-小鼠血浆胆固醇水平降低。与ND相比，在HFD上的WT小鼠中观察到饲喂效率增加，而与食物摄入量无关，但是对于Ca _v 3.1 ^-/-小鼠，在日粮之间没有观察到饲喂效率的差异。一氧化氮依赖性扩张在Ca _v 3.1 ^-/-的肠系膜动脉中增加在HFD上与WT小鼠相比，主动脉中没有观察到差异。实验组之间没有观察到小鼠运动活动的差异。与在HFD上的WT小鼠相比，在缺乏T型通道的HFD上的小鼠体重减轻，总胆固醇水平降低，并且耐药血管的扩张增加，这表明Ca _v 3.1缺失可防止耐药血管中的内皮功能障碍导管容器。