Wang Lan, Zeng Fan, Huang Rong-Feng, Lin Shu, Zhang Zhi-Hui, Li Min-Dian
Department of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.
Yi Chuan. 2023 Feb 20;45(2):144-155. doi: 10.16288/j.yczz.22-302.
Neural regulation of adipose tissue is crucial in the homeostasis of energy metabolism. Adipose tissue neuropeptide Y (NPY) and its receptors contribute to the development of diet-induced obesity. NPY1R and NPY2R are major receptors for NPY in peripheral tissues including the adipose tissue. NPY receptor 4 () gene is expressed in adipose tissue. However, it is unknown whether is involved in the development of diet-induced obesity. Here, we established an immunofluorescence microscopy technique and generated an adipocyte-reconstituted gene knockout mouse. Among six adipose depots, we found that NPY is highly expressed around the vasculature in a dot-like fashion in interscapular brown fat and subcutaneous fat, and NPY receptors are expressed in a depot-specific manner. NPY1R is highly expressed in epidydimal fat, interscapular and peri-aortic brown fat, NPY2R in both interscapular and peri-aortic brown fat, and NPY4R in both brown fat and epidydimal fat. Next, we showed that adipocyte-reconstituted expression of promoted diet-induced obesity in mice ( < 0.0001). Overall, this study defines the abundance and distribution of NPY and its receptors 1, 2, and 4 in mouse adipose depots, and demonstrates in an adipocyte-reconstituted gene knockout model that adipocyte is sufficient to promote diet-induced obesity.
神经对脂肪组织的调节在能量代谢稳态中至关重要。脂肪组织神经肽Y(NPY)及其受体参与饮食诱导的肥胖症的发生发展。NPY1R和NPY2R是包括脂肪组织在内的外周组织中NPY的主要受体。NPY受体4()基因在脂肪组织中表达。然而,尚不清楚其是否参与饮食诱导的肥胖症的发生发展。在此,我们建立了一种免疫荧光显微镜技术,并构建了一种脂肪细胞重组的基因敲除小鼠。在六个脂肪库中,我们发现NPY在肩胛间棕色脂肪和皮下脂肪中以点状方式在血管周围高度表达,并且NPY受体以脂肪库特异性方式表达。NPY1R在附睾脂肪、肩胛间和主动脉周围棕色脂肪中高度表达,NPY2R在肩胛间和主动脉周围棕色脂肪中均有表达,NPY4R在棕色脂肪和附睾脂肪中均有表达。接下来,我们表明脂肪细胞重组表达可促进小鼠饮食诱导的肥胖症(<0.0001)。总体而言,本研究确定了NPY及其受体1、2和4在小鼠脂肪库中的丰度和分布,并在脂肪细胞重组的基因敲除模型中证明脂肪细胞足以促进饮食诱导的肥胖症。