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Effects of excess dietary iron and fat on glucose and lipid metabolism
  • 작성일2018-02-05
  • 최종수정일2018-02-05
  • 담당부서연구기획과
  • 연락처043-719-8033
  • 2,115
Journal of Nutritional Biochemistry, 2013, 01, 1634─1644

Effects of excess dietary iron and fat on glucose and lipid metabolism

JooSun Choi, InUk Koh, Hyo Jung Lee, Won Ho Kim, Jihyun Song

Abstract

    Purpose: Diets rich in fat and energy are associated with metabolic syndrome (MS). Increased body iron stores have been recognized as a feature of MS. High-fat diets (HFs), excess iron loading and MS are closely associated, but the mechanism linking them has not been clearly defined. We investigated the interaction between dietary fat and dietary Fe in the context of glucose and lipid metabolism in the body.
    Methods: C57BL6/J mice were divided into four groups and fed the modified AIN-93G low-fat diet (LF) and HF with adequate or excess Fe for 7 weeks. The Fe contents were increased by adding carbonyl iron (2% of diet weight) (LF+Fe and HF+Fe).
    Results: High iron levels increased blood glucose levels but decreased high-density lipoprotein cholesterol levels. The HF group showed increases in plasma levels of glucose and insulin and insulin resistance. HF+Fe mice showed greater changes. Representative indices of iron status, such hepatic and plasma Fe levels, were not altered further by the HF. However, both the HF and excess iron loading changed the hepatic expression of hepcidin and ferroportin. The LF+Fe, HF and HF+Fe groups showed greater hepatic fat accumulation compared with the LF group. These changes were paralleled by alterations in the levels of enzymes related to hepatic gluconeogenesis and lipid synthesis, which could be due to increases in mitochondrial dysfunction and oxidative stress.
    Conclusions: High-fat diets and iron overload are associated with insulin resistance, modified hepatic lipid and iron metabolism and increased mitochondrial dysfunction and oxidative stress.


  • ISBN or ISSN: 0955-2863

  • 본 연구는 질병관리본부 연구개발과제(과제번호 2012-NG64001-00) 연구비를 지원받아 수행되었습니다.
  • This research was supported by a fund(code 2012-NG64001-00) by Research of Korea Centers for Disease Control and Prevention.


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