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红小豆 MY59 提取物通过下调脂联素 2 减轻高脂肪喂养小鼠的胰岛素抵抗和肝脂肪变性。

Adzuki Bean MY59 Extract Reduces Insulin Resistance and Hepatic Steatosis in High-Fat-Fed Mice via the Downregulation of Lipocalin-2.

机构信息

Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Republic of Korea.

Department of Southern Area Crop Science, National Institute of Crop Science, Rural Development Administration, Miryang 50424, Republic of Korea.

出版信息

Nutrients. 2022 Nov 27;14(23):5049. doi: 10.3390/nu14235049.

DOI:10.3390/nu14235049
PMID:36501079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9739659/
Abstract

Adzuki bean is well known as a potential functional food that improves metabolic complications from obesity and diabetes. Lipocalin-2 (LCN2) has been implicated to have an important role in obesity and diabetes. However, the protective roles of adzuki bean MY59 extract (ABE) on insulin resistance and hepatic steatosis are not fully understood. In the present study, we investigated the effects of ABE on LCN2 expression in high-fat diet (HFD)-fed mice. ABE reduced HFD-induced fat mass and improved insulin resistance. In addition to hepatic steatosis, HFD-fed mice showed many apoptotic cells and neutrophils in the epididymal fat pads. However, these findings were significantly reduced by ABE supplementation. In particular, we found that increased LCN2 proteins from serum, epididymal fat pads, and liver in HFD-fed mice are significantly reduced by ABE. Furthermore, ABE reduced increased heme oxygenase-1 and superoxide dismutase-1 expressions in adipose tissue and liver in HFD-fed mice. We found that hepatic nuclear factor-kappa B (NF-κB) p65 expression in HFD-fed mice was also reduced by ABE. Thus, these findings indicate that ABE feeding could improve insulin resistance and hepatic steatosis by decreasing LCN2-mediated inflammation and oxidative stress in HFD-fed mice.

摘要

小豆是一种众所周知的潜在功能性食品,可改善肥胖和糖尿病引起的代谢并发症。脂联素 2(LCN2)在肥胖和糖尿病中具有重要作用。然而,小豆 MY59 提取物(ABE)对胰岛素抵抗和肝脂肪变性的保护作用尚不完全清楚。在本研究中,我们研究了 ABE 对高脂肪饮食(HFD)喂养小鼠中 LCN2 表达的影响。ABE 可减少 HFD 诱导的脂肪量并改善胰岛素抵抗。除了肝脂肪变性外,HFD 喂养的小鼠在附睾脂肪垫中显示出许多凋亡细胞和中性粒细胞。然而,ABE 的补充可明显减少这些发现。特别是,我们发现 HFD 喂养的小鼠的血清,附睾脂肪垫和肝脏中的 LCN2 蛋白含量显着降低。此外,ABE 可降低 HFD 喂养的小鼠脂肪组织和肝脏中血红素加氧酶-1 和超氧化物歧化酶-1 的表达增加。我们发现 HFD 喂养的小鼠肝核因子-κB(NF-κB)p65 的表达也被 ABE 降低。因此,这些发现表明 ABE 喂养可通过减少 LCN2 介导的炎症和氧化应激来改善 HFD 喂养的小鼠的胰岛素抵抗和肝脂肪变性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/9e94461d59d3/nutrients-14-05049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/1509000c9326/nutrients-14-05049-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/7679a55de0f2/nutrients-14-05049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/d4f1c2f5b605/nutrients-14-05049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/f8372f42adc5/nutrients-14-05049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/c5ddafeb9fda/nutrients-14-05049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/9e94461d59d3/nutrients-14-05049-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/1509000c9326/nutrients-14-05049-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/7679a55de0f2/nutrients-14-05049-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/d4f1c2f5b605/nutrients-14-05049-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/f8372f42adc5/nutrients-14-05049-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/c5ddafeb9fda/nutrients-14-05049-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0388/9739659/9e94461d59d3/nutrients-14-05049-g006.jpg

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