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Vitamin C Inhibits Visceral Adipocyte Hypertrophy and Lowers Blood Glucose Levels in High-Fat-Diet-Induced Obese C57BL/6J Mice
Biomed Sci Letters 2018;24:311-318
Published online December 31, 2018;
© 2018 The Korean Society For Biomedical Laboratory Sciences.

Younghyun Park§,*, Joonseong Jang§,*, Dongju Lee** and Michung Yoon†,***

Department of Biomedical Engineering, Mokwon University, Daejeon 35349, Korea
Correspondence to: *Graduate student, **Undergraduate, ***Professor.
§These authors contributed equally: Younghyun Park, Joonseong Jang.
Michung Yoon. Department of Biomedical Engineering, Mokwon University, Daejeon 35349, Korea.
Tel: +82-42-829-7581, Fax: +82-42-829-7590, e-mail:
Received October 22, 2018; Revised December 3, 2018; Accepted December 4, 2018.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.
Keywords : Ascorbic acid, Hyperglycemia, Lipogenesis, Pancreas, Visceral obesity