Autoregulation of Glucose Transport: Effects of Glucose on Glucose Transporter Expression and Cellular Location in Muscle

Glucose transporter isoform-1 (GLUT-1) expression is stimulated in response to stressful conditions. Here we examined the mechanisms mediating the enhanced expression of GLUT-1 by hyperosmolarity. GLUT-1 mRNA, GLUT-1 protein, and glucose transport increased after exposure of Clone 9 cells to 600 mosmol/l (produced by addition of mannitol). The stimulation of glucose transport was biphasic: in the early phase (0–6 h) a ∼2.5-fold stimulation of glucose uptake was associated with no change in the content of GLUT-1 mRNA, GLUT-1 protein, or GLUT-1 in the plasma membrane, whereas the ∼17-fold stimulation of glucose transport during the late phase (12–24 h) was associated with increases in both GLUT-1 mRNA (∼7.5-fold) and GLUT-1 protein content. Cell sorbitol increased after 3 h of exposure to hyperosmolarity. The increase in GLUT-1 mRNA content was associated with an increase in the half-life of the mRNA from 2 to 8 h. A 44-bp region in the proximal GLUT-1 promoter was necessary for basal activity and for the two- to threefold increases in expression by hyperosmolarity. It is concluded that the increase in GLUT-1 mRNA content is mediated by both enhanced transcription and stabilization of GLUT-1 mRNA and is associated with increases in GLUT-1 content and glucose transport activity.

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Vagal involvement in dietary regulation of nutrient transport

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1998.274.3.g552 ◽

1998 ◽

Vol 274 (3) ◽

pp. G552-G560 ◽

Cited By ~ 4

Author(s):

Sarah L. Bates ◽

Keith A. Sharkey ◽

Jon B. Meddings

Keyword(s):

Vagus Nerve ◽

Glucose Transport ◽

Glucose Transporter ◽

Intestinal Transport ◽

Membrane Vesicles ◽

Vagal Afferents ◽

Carbohydrate Diet ◽

Adaptive Process ◽

Low Carbohydrate Diet ◽

Transporter Expression

In omnivores, gradual alterations in dietary nutrient composition are observed. To efficiently absorb dietary nutrients these animals alter intestinal nutrient transporter expression to match the pattern of nutrient intake. This often involves reprogramming the crypt cell to express greater numbers of the relevant transport system. The aim of this study was to determine whether vagal afferents are involved in this adaptive process. Guinea pigs were habituated to a low-carbohydrate diet and then switched to a high-carbohydrate diet. The resultant increase in glucose transporter expression was assessed by determining rates of glucose transport in jejunal brush-border membrane vesicles. Ablation of vagal afferents was accomplished by application of capsaicin to exposed cervical vagi and confirmed using Fast blue tracer studies. We found that animals in which vagal afferents were ablated with capsaicin were unable to alter rates of glucose transport in response to an increase in dietary carbohydrate. This suggests that vagal afferents are involved in this adaptive process. These findings support a role for the vagus nerve in regulating intestinal transport function, which may be important to consider in clinical disease that involves the vagus nerve.

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Glucose transporter expression in rat mammary gland

Biochemical Journal ◽

10.1042/bj2700277 ◽

1990 ◽

Vol 270 (1) ◽

pp. 277-279 ◽

Cited By ~ 35

Author(s):

A F Burnol ◽

A Leturque ◽

M Loizeau ◽

C Postic ◽

J Girard

Keyword(s):

Mammary Gland ◽

Glucose Transport ◽

Glucose Transporter ◽

Glut 1 ◽

Glut 4 ◽

Lactating Mammary Gland ◽

Development And Differentiation ◽

Rat Mammary Gland ◽

High Level ◽

Transporter Expression

The expression of different glucose transporter isoforms was measured during the development and differentiation of the rat mammary gland. Before conception, when the mammary gland is mainly composed of adipocytes, Glut 4 and Glut 1 mRNAs and proteins were present. During pregnancy, the expression of Glut 4 decreased progressively, whereas that of Glut 1 increased. In the lactating mammary gland only Glut 1 was present, and was expressed at a high level. The absence of Glut 4 suggests that glucose transport is not regulated by insulin in the lactating rat mammary gland.

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Hypoxia induces glucose transporter expression in endothelial cells

AJP Cell Physiology ◽

10.1152/ajpcell.1992.263.2.c326 ◽

1992 ◽

Vol 263 (2) ◽

pp. C326-C333 ◽

Cited By ~ 123

Author(s):

J. D. Loike ◽

L. Cao ◽

J. Brett ◽

S. Ogawa ◽

S. C. Silverstein ◽

...

Keyword(s):

Endothelial Cells ◽

Energy Metabolism ◽

Glucose Transport ◽

Glucose Transporter ◽

Umbilical Vein ◽

The Body ◽

Prolonged Treatment ◽

Transport Activity ◽

Low Oxygen ◽

Transporter Expression

Endothelial cells in various tissues of the body are often exposed to hypoxic conditions. To examine the effects of sustained hypoxia on energy metabolism in endothelial cells, we have maintained bovine aortic and human umbilical vein endothelial cells in an atmosphere containing low oxygen concentrations (14 mmHg) for up to 96 h. We report here that endothelial cells maintained under these conditions upregulate their glucose transport activity, consume more glucose, and produce greater amounts of lactic acid than normoxic cells. Upregulation of glucose transport activity by hypoxic endothelial cells required several hours to occur, was associated with increased expression of mRNA and protein for the erythroid/brain form of the facilitative glucose transporter, and was not due to depletion of glucose from the medium. Prolonged treatment of endothelial cells with inhibitors or uncouplers of oxidative phosphorylation (antimycin, azide, dinitrophenol) under normoxic conditions also upregulated glucose transporter expression. These results suggest that reduced rates of oxidative metabolism may represent an important signal for cells to adapt metabolically to hypoxia. Furthermore, in our examination of endothelial cell energy metabolism, we discovered that endothelial cells contain phosphocreatine and express both the brain and muscle isozymes of creatine kinase.

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