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Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice.
Nutrients. 2015 Sep 08; 7(9):7543-61.N

Abstract

Niacin is a popular nutritional supplement known to reduce the risk of cardiovascular diseases by enhancing high-density lipoprotein levels. Despite such health benefits, niacin impairs fasting blood glucose. In type 2 diabetes (T2DM), an increase in jejunal glucose transport has been well documented; however, this is intriguingly decreased during niacin deficient state. In this regard, the role of the niacin receptor GPR109a in T2DM jejunal glucose transport remains unknown. Therefore, the effects of diabetes and high-glucose conditions on GPR109a expression were studied using jejunal enterocytes of 10-week-old m+/db and db/db mice, as well as Caco-2 cells cultured in 5.6 or 25.2 mM glucose concentrations. Expression of the target genes and proteins were quantified using real-time polymerase chain reaction (RT-PCR) and Western blotting. Glucose uptake in Caco-2 cells and everted mouse jejunum was measured using liquid scintillation counting. 10-week T2DM increased mRNA and protein expression levels of GPR109a in jejunum by 195.0% and 75.9%, respectively, as compared with the respective m+/db control; high-glucose concentrations increased mRNA and protein expression of GPR109a in Caco-2 cells by 130.2% and 69.0%, respectively, which was also confirmed by immunohistochemistry. In conclusion, the enhanced GPR109a expression in jejunal enterocytes of T2DM mice and high-glucose treated Caco-2 cells suggests that GPR109a is involved in elevating intestinal glucose transport observed in diabetes.

Authors+Show Affiliations

School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China. wongtp@cuhk.edu.hk.School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China. leokychan@link.cuhk.edu.hk.School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China. psleung@cuhk.edu.hk.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26371038

Citation

Wong, Tung Po, et al. "Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice." Nutrients, vol. 7, no. 9, 2015, pp. 7543-61.
Wong TP, Chan LK, Leung PS. Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice. Nutrients. 2015;7(9):7543-61.
Wong, T. P., Chan, L. K., & Leung, P. S. (2015). Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice. Nutrients, 7(9), 7543-61. https://doi.org/10.3390/nu7095352
Wong TP, Chan LK, Leung PS. Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice. Nutrients. 2015 Sep 8;7(9):7543-61. PubMed PMID: 26371038.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of the Niacin Receptor GPR109a in the LocalControl of Glucose Uptake in Small Intestine of Type 2Diabetic Mice. AU - Wong,Tung Po, AU - Chan,Leo Ka Yu, AU - Leung,Po Sing, Y1 - 2015/09/08/ PY - 2015/08/03/received PY - 2015/08/18/revised PY - 2015/08/26/accepted PY - 2015/9/16/entrez PY - 2015/9/16/pubmed PY - 2016/6/30/medline KW - Caco-2 KW - GLUT2 KW - SGLT1 KW - enterocytes KW - glucose transport KW - hyperglycemia KW - hyperlipidemia KW - jejunum SP - 7543 EP - 61 JF - Nutrients JO - Nutrients VL - 7 IS - 9 N2 - Niacin is a popular nutritional supplement known to reduce the risk of cardiovascular diseases by enhancing high-density lipoprotein levels. Despite such health benefits, niacin impairs fasting blood glucose. In type 2 diabetes (T2DM), an increase in jejunal glucose transport has been well documented; however, this is intriguingly decreased during niacin deficient state. In this regard, the role of the niacin receptor GPR109a in T2DM jejunal glucose transport remains unknown. Therefore, the effects of diabetes and high-glucose conditions on GPR109a expression were studied using jejunal enterocytes of 10-week-old m+/db and db/db mice, as well as Caco-2 cells cultured in 5.6 or 25.2 mM glucose concentrations. Expression of the target genes and proteins were quantified using real-time polymerase chain reaction (RT-PCR) and Western blotting. Glucose uptake in Caco-2 cells and everted mouse jejunum was measured using liquid scintillation counting. 10-week T2DM increased mRNA and protein expression levels of GPR109a in jejunum by 195.0% and 75.9%, respectively, as compared with the respective m+/db control; high-glucose concentrations increased mRNA and protein expression of GPR109a in Caco-2 cells by 130.2% and 69.0%, respectively, which was also confirmed by immunohistochemistry. In conclusion, the enhanced GPR109a expression in jejunal enterocytes of T2DM mice and high-glucose treated Caco-2 cells suggests that GPR109a is involved in elevating intestinal glucose transport observed in diabetes. SN - 2072-6643 UR - https://www.unboundmedicine.com/medline/citation/26371038/Involvement_of_the_Niacin_Receptor_GPR109a_in_the_LocalControl_of_Glucose_Uptake_in_Small_Intestine_of_Type_2Diabetic_Mice_ L2 - https://www.mdpi.com/resolver?pii=nu7095352 DB - PRIME DP - Unbound Medicine ER -