Glucose regulates clathrin adaptors at the<i>trans-</i>Golgi network and endosomes

Aoh, Quyen L.; Graves, Lee M.; Duncan, Mara C.

doi:10.1091/mbc.e11-04-0309

Cited by 25 publications

(45 citation statements)

References 43 publications

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“…Several physiological processes are altered by changes in the levels of glucose (5). Our present data indicate that NPC1L1 expression and the promoter activity are sensitive to alterations in the levels of glucose, as the withdrawal of glucose resulted in significant decreases in NPC1L1 expression.…”

Section: Resultsmentioning

confidence: 49%

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d-Glucose modulates intestinal Niemann-Pick C1-like 1 (NPC1L1) gene expression via transcriptional regulation

Malhotra

Boddy

Soni

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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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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Section: Resultsmentioning

confidence: 49%

“…Several biological processes are altered by increasing glucose levels or by removing glucose (5). NPC1L1 expression has been recently shown to be increased in intestinal epithelial cells by high levels of glucose (24).…”

Section: Resultsmentioning

confidence: 99%

d-Glucose modulates intestinal Niemann-Pick C1-like 1 (NPC1L1) gene expression via transcriptional regulation

Malhotra

Boddy

Soni

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Preparation of Cell Lysates and Immunoblotting-For analysis of GFP-Atg8, whole cell extracts were performed as described previously (10). Following extractions, immunoblotting was performed as described previously.…”

Section: Methodsmentioning

confidence: 99%

“…However, proteins involved in endocytosis remain membraneassociated (9,10). This could cause proteins endocytosed from the plasma membrane to be directed to intracellular compartments rather than getting recycled back to the membrane.…”

mentioning

confidence: 99%

Glucose Starvation Inhibits Autophagy via Vacuolar Hydrolysis and Induces Plasma Membrane Internalization by Down-regulating Recycling

Lang

Martínez-Márquez

Prosser

et al. 2014

Journal of Biological Chemistry

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107

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Background: During energy starvation, cells utilize intracellular resources for survival; however, the resources used during glucose starvation are unknown. Results: In glucose-starved yeast, vacuolar hydrolysis and endocytosis promote survival whereas autophagy is dispensable. Conclusion: Vacuolar hydrolysis blocks autophagy and provides resources for survival during glucose starvation. Significance: This new survival mechanism could protect cells from starvation in many situations.

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“…A transient inhibition of endosomal protein traffic likely contributes to energy conservation to counteract the energy deficit immediately after acute glucose starvation (Aoh et al ., 2011). In proliferating cells, membrane trafficking pathways consume large amounts of energy to maintain the steady-state localization of proteins within the endosomal system (reviewed in Luzio and Banting, 1993).…”

Section: Introductionmentioning

confidence: 99%

Energy metabolism regulates clathrin adaptors at thetrans-Golgi network and endosomes

Aoh

Hung

Duncan

2013

MBoC

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Glucose regulates clathrin adaptors at thetrans-Golgi network and endosomes

Cited by 25 publications

References 43 publications

d-Glucose modulates intestinal Niemann-Pick C1-like 1 (NPC1L1) gene expression via transcriptional regulation

d-Glucose modulates intestinal Niemann-Pick C1-like 1 (NPC1L1) gene expression via transcriptional regulation

Glucose Starvation Inhibits Autophagy via Vacuolar Hydrolysis and Induces Plasma Membrane Internalization by Down-regulating Recycling

Energy metabolism regulates clathrin adaptors at thetrans-Golgi network and endosomes

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