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南极磷虾油对高脂饮食诱导肥胖小鼠肥胖及肥胖相关代谢综合征的预防和治疗作用。

Preventive and Therapeutic Effects of Krill Oil on Obesity and Obesity-Induced Metabolic Syndromes in High-Fat Diet-Fed Mice.

机构信息

Department of Veterinary Surgery, College of Veterinary Medicine, Kyungpook National University, Daegu 41566, Korea.

Department of Urology, College of Medicine, Yeungnam University, Daegu 42415, Korea.

出版信息

Mar Drugs. 2022 Jul 27;20(8):483. doi: 10.3390/md20080483.

DOI:10.3390/md20080483
PMID:36005486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9410137/
Abstract

Obesity increases the risks of metabolic syndromes including nonalcoholic fatty liver disease (NAFLD), diabetic dyslipidemia, and chronic kidney disease. Dietary krill oil (KO) has shown antioxidant and anti-inflammatory properties, thereby being a therapeutic potential for obesity-induced metabolic syndromes. Thus, the effects of KO on lipid metabolic alteration were examined in a high-fat diet (HFD)-fed mice model. The HFD model ( = 10 per group) received an oral gavage with distilled water as a control, metformin at 250 mg/kg, and KO at 400, 200, and 100 mg/kg for 12 weeks. The HFD-induced weight gain and fat deposition were significantly reduced in the KO treatments compared with the control. Blood levels were lower in parameters for NAFLD (e.g., alanine aminotransferase, and triglyceride), type 2 diabetes (e.g., glucose and insulin), and renal dysfunction (e.g., blood urea nitrogen and creatinine) by the KO treatments. The KO inhibited lipid synthesis through the modification of gene expressions in the liver and adipose tissues and adipokine-mediated pathways. Furthermore, KO showed hepatic antioxidant activities and glucose lowering effects. Histopathological analyses revealed that the KO ameliorated the hepatic steatosis, pancreatic endocrine/exocrine alteration, adipose tissue hypertrophy, and renal steatosis. These analyses suggest that KO may be promising for inhibiting obesity and metabolic syndromes.

摘要

肥胖增加了代谢综合征的风险,包括非酒精性脂肪肝(NAFLD)、糖尿病血脂异常和慢性肾脏病。膳食磷虾油(KO)具有抗氧化和抗炎特性,因此对肥胖引起的代谢综合征具有治疗潜力。因此,在高脂肪饮食(HFD)喂养的小鼠模型中检查了 KO 对脂质代谢改变的影响。HFD 模型(每组 10 只)接受口服灌胃蒸馏水作为对照,二甲双胍 250mg/kg,以及 KO 400、200 和 100mg/kg,持续 12 周。与对照组相比,KO 治疗显著减轻了 HFD 诱导的体重增加和脂肪沉积。KO 治疗降低了与 NAFLD(如丙氨酸转氨酶和甘油三酯)、2 型糖尿病(如葡萄糖和胰岛素)和肾功能障碍(如血尿素氮和肌酐)相关的血液参数。KO 通过肝脏和脂肪组织中基因表达的修饰和脂肪因子介导的途径抑制脂质合成。此外,KO 显示出肝脏抗氧化活性和降低血糖的作用。组织病理学分析显示,KO 改善了肝脂肪变性、胰腺内分泌/外分泌改变、脂肪组织肥大和肾脂肪变性。这些分析表明,KO 可能有望抑制肥胖和代谢综合征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/51bf1f8c8a8e/marinedrugs-20-00483-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/3019b2516841/marinedrugs-20-00483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/d5ec31b3cc6a/marinedrugs-20-00483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/e2c0dfdb1ea0/marinedrugs-20-00483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/977cc0615742/marinedrugs-20-00483-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/fa7c7a216bc8/marinedrugs-20-00483-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/4df67b598fa6/marinedrugs-20-00483-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/51bf1f8c8a8e/marinedrugs-20-00483-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/3019b2516841/marinedrugs-20-00483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/d5ec31b3cc6a/marinedrugs-20-00483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/e2c0dfdb1ea0/marinedrugs-20-00483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/977cc0615742/marinedrugs-20-00483-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/fa7c7a216bc8/marinedrugs-20-00483-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/4df67b598fa6/marinedrugs-20-00483-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a05f/9410137/51bf1f8c8a8e/marinedrugs-20-00483-g007.jpg

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