Biomedical Sciences Department, College of Health Sciences, QU Health, Qatar University, Doha 2713, Qatar.
Clinical Chemistry Laboratory, Hamad Medical Corporation, Doha 2713, Qatar.
Nutrients. 2022 Nov 1;14(21):4600. doi: 10.3390/nu14214600.
Hypoxia is caused by the excessive expansion of the white adipose tissue (AT) and is associated with obesity-related conditions such as insulin resistance, inflammation, and oxidative stress. Docosahexaenoic acid (DHA) is an omega-3 fatty acid reported to have beneficial health effects. However, the effects of DHA in AT against hypoxia-induced immune-metabolic perturbations in adipocytes exposed to low O tension are not well known. Consequently, this study aimed to evaluate the impact of DHA on markers of inflammation, metabolism, apoptosis, and oxidative stress in 3T3-L1 cell adipocytes exposed to low O tension (1% O) induced hypoxia.
The apoptosis and reactive oxygen species (ROS) rates were evaluated. Metabolic parameters such as lactate, FFA, glycerol release, glucose uptake, and ATP content were assessed by a fluorometer. The expression of HIF-1, GLUT1 and the secretion of adipocytokines such as leptin, adiponectin, and pro-inflammatory markers was evaluated.
DHA-treated hypoxic cells showed significantly decreased basal free fatty acid release, lactate production, and enhanced glucose consumption. In addition, DHA-treatment of hypoxic cells caused a significant reduction in the apoptosis rate and ROS production with decreased lipid peroxidation. Moreover, DHA-treatment of hypoxic cells caused a decreased secretion of pro-inflammatory markers (IL-6, MCP-1) and leptin and increased adiponectin secretion compared with hypoxic cells. Furthermore, DHA-treatment of hypoxic cells caused significant reductions in the expression of genes related to hypoxia (HIF-1, HIF-2), anaerobic metabolism (GLUT1 and Ldha), ATP production (ANT2), and fat metabolism (FASN and PPARY).
This study suggests that DHA can exert potential anti-obesity effects by reducing the secretion of inflammatory adipokines, oxidative stress, lipolysis, and apoptosis.
缺氧是由白色脂肪组织（AT）过度扩张引起的，与肥胖相关的疾病有关，如胰岛素抵抗、炎症和氧化应激。二十二碳六烯酸（DHA）是一种ω-3 脂肪酸，据报道具有有益的健康影响。然而，DHA 在 AT 中的作用在低氧张力下暴露于低氧张力的脂肪细胞中对缺氧诱导的免疫代谢紊乱的影响尚不清楚。因此，本研究旨在评估 DHA 对 3T3-L1 脂肪细胞中低氧张力（1% O）诱导的缺氧条件下炎症、代谢、细胞凋亡和氧化应激标志物的影响。
评估细胞凋亡和活性氧（ROS）的产生率。通过荧光计评估代谢参数，如乳酸、FFA、甘油释放、葡萄糖摄取和 ATP 含量。评估 HIF-1、GLUT1 的表达以及瘦素、脂联素和促炎标志物等脂肪细胞因子的分泌。
DHA 处理的缺氧细胞显示基础游离脂肪酸释放、乳酸产生和葡萄糖消耗明显减少。此外，DHA 处理的缺氧细胞导致凋亡率和 ROS 产生显著减少，脂质过氧化减少。此外，与缺氧细胞相比，DHA 处理的缺氧细胞的促炎标志物（IL-6、MCP-1）和瘦素分泌减少，脂联素分泌增加。此外，DHA 处理的缺氧细胞导致与缺氧相关的基因（HIF-1、HIF-2）、厌氧代谢（GLUT1 和 Ldha）、ATP 产生（ANT2）和脂肪代谢（FASN 和 PPARY）的表达显著降低。
本研究表明，DHA 通过减少促炎脂肪因子的分泌、氧化应激、脂肪分解和细胞凋亡，发挥潜在的抗肥胖作用。
