Hu Yuanyuan, Zeng Xiangbo, Luo Ying, Pei Xuechen, Zhou Dayong, Zhu Beiwei
Shenzhen Key Laboratory of Food Nutrition and Health, College of Chemistry and Environmental Engineering Shenzhen University Shenzhen China.
State Key Laboratory of Marine Food Processing & Safety Control, School of Food Science and Technology Dalian Polytechnic University Dalian China.
Food Sci Nutr. 2024 Jun 17;12(9):6398-6410. doi: 10.1002/fsn3.4273. eCollection 2024 Sep.
Peroxidation of polyunsaturated fatty acids results in the creation of numerous α, β-unsaturated aldehydes, many of which are complicated by the development of diabetes. Trans, trans-2,4-decadienal (DDE) is a dietary α, β-unsaturated aldehyde that is commonly found in food and the environment. However, it is unknown whether DDE exposure has some negative effects on glucose homeostasis and insulin sensitivity. This study investigated the biological effects of long-term DDE exposure in normal chow diet (NCD)-fed non-obese mice and high-fat diet (HFD)-fed obese mice. Results showed that oral administration of DDE for 14 weeks did not cause severe toxicity in NCD-fed non-obese mice but had significant adverse effects in HFD-fed obese mice. It was found that DDE exposure caused significant increases in LDL and ALT levels and aggravated glucose intolerance and insulin resistance in obese mice. Moreover, DDE robustly accumulated in adipose tissue and promoted the impairment of the insulin signaling pathway in the adipose tissue of obese mice while not affecting the skeletal muscle or liver. Mechanistically, DDE aggravated adipose tissue inflammation by promoting M1 macrophage accumulation and increasing proinflammatory cytokines in the adipocytes of obese mice, thus leading to impaired systemic insulin resistance. These findings provide crucial insights into the potential health impacts of long-term DDE exposure.
多不饱和脂肪酸的过氧化会产生大量α,β-不饱和醛，其中许多在糖尿病发展过程中会变得更加复杂。反,反-2,4-癸二烯醛（DDE）是一种饮食中的α,β-不饱和醛，常见于食物和环境中。然而，DDE暴露是否会对葡萄糖稳态和胰岛素敏感性产生负面影响尚不清楚。本研究调查了长期DDE暴露对正常饮食（NCD）喂养的非肥胖小鼠和高脂饮食（HFD）喂养的肥胖小鼠的生物学影响。结果表明，对NCD喂养的非肥胖小鼠口服DDE 14周不会引起严重毒性，但对HFD喂养的肥胖小鼠有显著的不良影响。研究发现，DDE暴露导致肥胖小鼠的低密度脂蛋白（LDL）和谷丙转氨酶（ALT）水平显著升高，并加重了葡萄糖不耐受和胰岛素抵抗。此外，DDE在脂肪组织中大量蓄积，并促进肥胖小鼠脂肪组织中胰岛素信号通路的损伤，而对骨骼肌或肝脏没有影响。从机制上讲，DDE通过促进M1巨噬细胞积累和增加肥胖小鼠脂肪细胞中的促炎细胞因子来加重脂肪组织炎症，从而导致全身胰岛素抵抗受损。这些发现为长期DDE暴露对健康的潜在影响提供了重要见解。
