ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
D-Glucose modulates intestinal Niemann-Pick C1-like 1 (NPC1L1) gene expression via transcriptional regulation.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- The biochemical effects of carotenoids in orange carrots on the colonic proteome in a mouse model of diet-induced obesity.Frontiers in nutrition · 2024Article
- Are We Using Ezetimibe As Much As We Should?Biomarker insights · 2024Review
- Relationship between Diabetes Mellitus and Serum Lathosterol and Campesterol Levels: The CACHE Study DM Analysis.Journal of atherosclerosis and thrombosis · 2023Article
- Intestinal Cholesterol Absorption in Diabetes Mellitus.Journal of atherosclerosis and thrombosis · 2023Article
- Intestinal lipid absorption and transport in type 2 diabetes.Diabetologia · 2022Review
- Updated Understanding of the Crosstalk Between Glucose/Insulin and Cholesterol Metabolism.Frontiers in cardiovascular medicine · 2022Review
- Review
- Mechanisms and regulation of cholesterol homeostasis.Nature reviews. Molecular cell biology · 2020Review
- The intestinal microbiota regulates host cholesterol homeostasis.BMC biology · 2019Article
- The Gastrointestinal Tract as Prime Site for Cardiometabolic Protection by Dietary Polyphenols.Advances in nutrition (Bethesda, Md.) · 2019Review
- Article
- Mechanisms of Niemann-Pick type C1 Like 1 protein degradation in intestinal epithelial cells.American journal of physiology. Cell physiology · 2019Article
- Small Heterodimer Partner and Fibroblast Growth Factor 19 Inhibit Expression of NPC1L1 in Mouse Intestine and Cholesterol Absorption.Gastroenterology · 2019Article
- Review
- Role of SHP2 protein tyrosine phosphatase in SERT inhibition by enteropathogenicAmerican journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Impact of a high-cholesterol diet on expression levels of Niemann-Pick C1-like 1 and intestinal transporters in rats and mice.European journal of drug metabolism and pharmacokinetics · 2016Article
- Dyslipidaemia of diabetes and the intestine.World journal of diabetes · 2015Review
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The expression of intestinal Niemann-Pick C1-like 1 (NPC1L1) cholesterol transporter has been shown to be elevated in patients with diseases associated with hypercholesterolemia such as diabetes mellitus. High levels of glucose were shown to directly increase the expression of NPC1L1 in intestinal epithelial cells, but the underlying mechanisms are not fully defined. The present studies were, therefore, undertaken to examine the transcriptional regulation of NPC1L1 expression in human intestinal Caco2 cells in response to glucose. Removal of glucose from the culture medium of Caco2 cells for 24 h significantly decreased the NPC1L1 mRNA, protein expression, as well as the promoter activity. Glucose replenishment significantly increased the promoter activity of NPC1L1 in a dose-dependent manner compared with control cells. Exposure of Caco2 cells to nonmetabolizable form of glucose, 3-O-methyl-d-glucopyranose (OMG) had no effect on NPC1L1 promoter activity, indicating that the observed effects are dependent on glucose metabolism. Furthermore, glucose-mediated increase in promoter activity was abrogated in the presence of okadaic acid, suggesting the involvement of protein phosphatases. Glucose effects on several deletion constructs of NPC1L1 promoter demonstrated that cis elements mediating the effects of glucose are located in the region between -291 and +56 of NPC1L1 promoter. Consistent with the effects of glucose removal on NPC1L1 expression in Caco2 cells, 24-h fasting resulted in a significant decrease in the relative expression of NPC1L1 in mouse jejunum. In conclusion, glucose appears to directly modulate NPC1L1 expression via transcriptional mechanisms and the involvement of phosphatase-dependent pathways.
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