Journal
BIOLOGICAL TRACE ELEMENT RESEARCH
Volume 189, Issue 1, Pages 194-200Publisher
HUMANA PRESS INC
DOI: 10.1007/s12011-018-1446-3
Keywords
Dietary iron; Diabetic mice; Glycolipid metabolism; Type 2 diabetes mellitus; Obesity
Funding
- Natural Science Foundation of Zhejiang province of China [LR16C170001]
- National Natural Science Foundation of China [31572411]
- Major Science and Technology Project of Zhejiang province [2015C02022]
Ask authors/readers for more resources
Imbalance of iron homeostasis has been involved in clinical courses of metabolic diseases such as type 2 diabetes mellitus, obesity, and nonalcoholic fatty liver, through mechanisms not yet fully elucidated. Herein, we evaluated the effect of dietary iron on the development of diabetic syndromes in genetically obese db/db mice. Mice (aged 7weeks) were fed with high-iron (HI) diets (1000mg/kg chow) or low-iron (LI) diets (12mg/kg) for 9weeks. HI diets increased hepatic iron threefold and led to fourfold higher mRNA levels of hepcidin. HI also induced a 60% increase in fasting glucose due to insulin resistance, as confirmed by decreased hepatic glycogen deposition eightfold and a 21% decrease of serum adiponectin level. HI-fed mice had lower visceral adipose tissue mass estimated by epididymal and inguinal fat pad, associated with iron accumulation and smaller size of adipocytes. Gene expression analysis of liver showed that HI diet upregulated gluconeogenesis and downregulated lipogenesis. These results suggested that excess dietary iron leads to reduced mass, increased fasting glucose, decreased adiponectin level, and enhancement of insulin resistance, which indicated a multifactorial role of excess iron in the development of diabetes in the setting of obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available