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아이스플랜트 추출물의 3T3-L1 지방세포 내 TNF-α 유도 염증 및 인슐린 저항성 개선 효과

Mesembryanthemum crystallinum extract ameliorates TNF-α-induced inflammation and insulin resistance in 3T3-L1 adipocytes

이효정|김승|정인선|박세은
한국식품저장유통학회 (The Korean Society of Food Preservation)|2022.10|Food Science and Preservation|제29권 제6호|pp. 1000-1011

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inflammationTNF-αinsulin resistanceadipocyteMesembryanthemum crystallinum
주제분류식품과학

초록

Obesity is classified as a low-grade chronic inflammatory disease. Obesity-induced inflammation is associated with the development of insulin resistance (IR). In this study, we investigated the effects of Mesembryanthemum crystallinum extract (MCE) on tumor necrosis factor-alpha (TNF-α)-induced inflammation and IR in 3T3-L1 adipocytes, as well as underlying mechanisms. Lipolysis was monitored by oil red O staining. Glucose uptake was measured by 2-deoxyglucose (2-DG). The production of cytokines and adiponectin was evaluated using enzyme-linked immunosorbent assay (ELISA). Protein expression was measured using western blotting. IR was induced in differentiated 3T3-L1 adipocytes by treatment with TNF-α. MCE treatment decreased lipolysis while increasing adiponectin production. MCE inhibited the production of pro- inflammatory cytokines such as interleukn (IL)-6 and monocyte chemoattractant protein (MCP)-1, as well as the Nuclear factor-κB (NF-κB) translocation. Additionally, MCE increased glucose uptake, prevented the protein expression of phosphorylated insulin receptor supstrate (IRS) and increased the protein expression of Glucose Transporter Type 4 (GLUT4) in a dose-dependent manner. These results demonstrate the potential of MCE in improving chronic inflammation and insulin sensitivity in obesity. Therefore, MCE can be used as a novel candidate for developing functional foods.

Abstract

Obesity is classified as a low-grade chronic inflammatory disease. Obesity-induced inflammation is associated with the development of insulin resistance (IR). In this study, we investigated the effects of Mesembryanthemum crystallinum extract (MCE) on tumor necrosis factor-alpha (TNF-α)-induced inflammation and IR in 3T3-L1 adipocytes, as well as underlying mechanisms. Lipolysis was monitored by oil red O staining. Glucose uptake was measured by 2-deoxyglucose (2-DG). The production of cytokines and adiponectin was evaluated using enzyme-linked immunosorbent assay (ELISA). Protein expression was measured using western blotting. IR was induced in differentiated 3T3-L1 adipocytes by treatment with TNF-α. MCE treatment decreased lipolysis while increasing adiponectin production. MCE inhibited the production of pro- inflammatory cytokines such as interleukn (IL)-6 and monocyte chemoattractant protein (MCP)-1, as well as the Nuclear factor-κB (NF-κB) translocation. Additionally, MCE increased glucose uptake, prevented the protein expression of phosphorylated insulin receptor supstrate (IRS) and increased the protein expression of Glucose Transporter Type 4 (GLUT4) in a dose-dependent manner. These results demonstrate the potential of MCE in improving chronic inflammation and insulin sensitivity in obesity. Therefore, MCE can be used as a novel candidate for developing functional foods.

참고문헌 (47)

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