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J Nutr Biochem. 2019 May 14;70:75-81. doi: 10.1016/j.jnutbio.2019.04.011. [Epub ahead of print]

Riboflavin deficiency affects lipid metabolism partly by reducing apolipoprotein B100 synthesis in rats.

Author information

1
College of Food Science and Technology, Shanghai Ocean University, Shanghai 201306, People's Republic of China; Department of Nutrition and Food Hygiene, Institute of Environmental and Operational Medicine, Tianjin 300050, People's Republic of China.
2
Department of Nutrition and Food Hygiene, Institute of Environmental and Operational Medicine, Tianjin 300050, People's Republic of China.
3
Department of Nutrition and Food Hygiene, Institute of Environmental and Operational Medicine, Tianjin 300050, People's Republic of China. Electronic address: guocjtj@126.com.
4
College of Food Science and Technology, Shanghai Ocean University, Shanghai 201306, People's Republic of China. Electronic address: blli@shou.edu.cn.

Abstract

Lipid metabolism is dependent on riboflavin status. Apolipoprotein B100 plays an important role in lipids transportation. This study was aimed to investigate the effect of riboflavin status on lipid metabolism and explore its association with apolipoprotein B100 synthesis in vivo. Riboflavin deficiency was developed in rats by feeding riboflavin-deficient diets. Compared to the control rats, the mRNA and protein expressions of apolipoprotein B100 were significantly reduced in riboflavin-deficient rats. Endoplasmic reticulum oxidoreductin 1 (ERO1) and protein disulfide isomerase (PDI), two enzymes involved in the oxidative folding of apolipoprotein B100, were also lowered remarkably in expression at protein level. Meanwhile, total cholesterol and triglyceride levels were decreased in the plasma and increased in the liver of riboflavin-deficient rats. The plasma very low-density lipoprotein cholesterol (VLDL-c) and low-density lipoprotein cholesterol (LDL-c) were also reduced in riboflavin-deficient rats. Our findings demonstrate that riboflavin deficiency affects lipid metabolism partly by reducing apolipoprotein B100 synthesis.

KEYWORDS:

Apolipoprotein B100; Endoplasmic reticulum stress; Lipid metabolism; Lipid transport; Riboflavin deficiency

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