Priyanka Ariyapalli, Anusree Sasidharan Suseela, Nisha Vijayakumar Marykutty, Raghu Kozhiparambil Gopalan
Agroprocessing and Natural Products Division, Council of Scientific and Industrial Research-National Institute for Interdisciplinary Science and Technology (CSIR-NIIST), Thiruvananthapuram, 695019, Kerala, India.
Biofactors. 2014 Sep-Oct;40(5):513-23. doi: 10.1002/biof.1175. Epub 2014 Aug 11.
Obesity induced metabolic syndrome is increasing worldwide at an alarming rate. It is characterized by excessive expansion of white adipose tissue which leads to hypoxia and impairs normal metabolism. Recent studies reveal that hypoxia could be one of the factors for inflammation, insulin resistance and other obesity related complications. There is a high demand for anti-obese phytoceuticals to control and manage the complications resulting from obesity. In this study, we investigated how hypoxia affect the physiological functions of 3T3-L1 adipocytes emphasizing on oxidative stress, inflammation, and mitochondrial functions. We also evaluated the protective role of various doses of curcumin, a well-known dietary antioxidant, on hypoxia induced alterations. The results revealed that hypoxia significantly altered the vital parameters of adipocyte biology like HIF 1α expression (103.47% ↑), lactate, and glycerol release (184.34% and 69.1% ↑, respectively), reactive oxygen species production (432.53% ↑), lipid and protein oxidation (376.6% and 566.6% ↑, respectively), reduction in antioxidant enzymes (superoxide dismutase and catalase) status, secretion of inflammatory markers (TNF α, IL 6, IL 1β, and IFN γ), and mitochondrial functions (mitochondrial mass, membrane potential, permeability transition pore integrity, and superoxide generation). Curcumin substantially protected adipocytes from toxic effects of hypoxia in a dose dependent manner by protecting mitochondria and down regulating inflammation. Acriflavine is used as a positive control. A detailed investigation is required for the development of curcumin as an effective nutraceutical against obesity.
肥胖诱导的代谢综合征在全球范围内正以惊人的速度增长。其特征是白色脂肪组织过度扩张，导致缺氧并损害正常代谢。最近的研究表明，缺氧可能是炎症、胰岛素抵抗和其他肥胖相关并发症的因素之一。对控制和管理肥胖引起的并发症的抗肥胖植物药有很高的需求。在本研究中，我们研究了缺氧如何影响3T3-L1脂肪细胞的生理功能，重点是氧化应激、炎症和线粒体功能。我们还评估了不同剂量的姜黄素（一种著名的膳食抗氧化剂）对缺氧诱导的改变的保护作用。结果表明，缺氧显著改变了脂肪细胞生物学的重要参数，如HIF 1α表达（升高103.47%）、乳酸和甘油释放（分别升高184.34%和69.1%）、活性氧产生（升高432.53%）、脂质和蛋白质氧化（分别升高376.6%和566.6%）、抗氧化酶（超氧化物歧化酶和过氧化氢酶）状态降低、炎症标志物（TNFα、IL 6、IL 1β和IFNγ）分泌以及线粒体功能（线粒体质量、膜电位、通透性转换孔完整性和超氧化物产生）。姜黄素通过保护线粒体和下调炎症，以剂量依赖的方式显著保护脂肪细胞免受缺氧的毒性作用。吖啶黄用作阳性对照。需要对姜黄素作为一种有效的抗肥胖营养保健品进行详细研究。
