Programa de Doctorado en Ciencias en Biología Molecular en Medicina, Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara. Guadalajara, Jalisco, México.
Instituto de Investigación de Enfermedades Crónico-Degenerativas del Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara. Guadalajara, Jalisco, México.
Exp Clin Endocrinol Diabetes. 2020 Nov;128(11):715-722. doi: 10.1055/a-0829-6324. Epub 2019 Feb 12.
The expansion of adipose tissue is regulated by insulin and leptin through sterol regulatory element-binding protein-1c (SREBP-1c), up-regulating lipogenesis in tissues by Stearoylcoenzyme A desaturase 1 (SCD1) enzyme, while adipose triglyceride lipase (ATGL) enzyme is key in lipolysis. The research objective was to evaluate the expression of Sterol Regulatory Element Binding Transcription Factor 1 (SREBF1), SCD1, Patatin Like Phospholipase Domain Containing 2 (PNPLA2), and leptin (LEP) genes in hepatic-adipose tissue, and related them with the increment and distribution of fat depots of individuals without insulin resistance. Thirty-eight subjects undergoing elective cholecystectomy with liver and adipose tissue biopsies (subcutaneous-omental) are included. Tissue gene expression was assessed by qPCR and biochemical parameters determined. Individuals are classified according to the body mass index, classified as lean (control group, n=12), overweight (n=11) and obesity (n=15). Abdominal adiposity was determined by anthropometric and histopathological study of the liver. Increased expression in omental adipose tissue (p=0.005) and in liver (p=0.01) were found in the obesity group. decreased expression in subcutaneous adipose tissue was significant in individuals with abdominal adiposity (p=0.017). Anthropometric parameters positively correlated with liver and the expression of liver with serum leptin. increased levels may represent lipid storage activity in omental adipose tissue. Liver increased expression could function as a primary compensatory event of visceral fat deposits associated to the leptin hormone related to the increase of adipose tissue.
脂肪组织的扩张受胰岛素和瘦素调节，通过固醇调节元件结合蛋白-1c（SREBP-1c）上调组织中的脂肪生成，Stearoylcoenzyme A 去饱和酶 1（SCD1）酶上调脂肪生成，而脂肪甘油三酯脂肪酶（ATGL）酶是脂肪分解的关键。研究目的是评估 Sterol Regulatory Element Binding Transcription Factor 1（SREBF1）、SCD1、Patatin Like Phospholipase Domain Containing 2（PNPLA2）和瘦素（LEP）基因在肝脂肪组织中的表达，并将其与无胰岛素抵抗个体脂肪蓄积的增量和分布相关联。共纳入 38 例行择期胆囊切除术并伴有肝和脂肪组织活检（皮下-网膜）的患者。通过 qPCR 评估组织基因表达，并测定生化参数。根据体重指数将患者分为瘦组（对照组，n=12）、超重组（n=11）和肥胖组（n=15）。通过人体测量学和肝脏组织病理学研究来确定腹部肥胖。发现肥胖组网膜脂肪组织中 表达增加（p=0.005），肝脏中 表达增加（p=0.01）。腹部肥胖患者皮下脂肪组织中 表达显著减少（p=0.017）。人体测量学参数与肝脏 表达呈正相关，而肝脏 表达与血清瘦素呈正相关。网膜脂肪组织中 水平升高可能代表脂质储存活性增加。肝脏 表达增加可能是与瘦素相关的内脏脂肪沉积的初级代偿事件，与脂肪组织增加有关。
