Epidermal growth factor and 12-O-tetradecanoylphorbol 13-acetate stimulate lactate production and the pentose phosphate pathway in freshly isolated rat hepatocytes.

Conricode, Kevin M.; Ochs, Raymond S.

doi:10.1016/s0021-9258(17)45306-3

Cited by 25 publications

(2 citation statements)

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“…Abolition of membrane-limitation can be induced as well by metabolic stress, e.g. by 2,4-dinitrophenol-induced reduction of cellular ATP (40), receptor-mediated stimulation (63)(64)(65)(66). The reverse process is observed in cell cultures reaching confluence or by cultivation under differentiating conditions (5).…”

Section: Energy Metabolism In the Membrane-limited Statementioning

confidence: 99%

“…Loss of membrane-limitation is characterized by two experimental criteria: First, the steady state content of free intracellular glucose increased up to the extracellular level (41,42) and second, the aerobic lactate production is elevated (49,67). Increased aerobic lactate production, most obvious after oncogenic transformation, also occurs under other experimental conditions such as inhibition of respiration (ATP depletion) (68) and stimulation by growth factors (64,65). Both effects indicate that the loss of membrane limitation is accompanied by the reestablishment of competition between respiration and glycolysis for adenine nucleotides.…”

Section: Energy Metabolism In the Membrane-limited Statementioning

confidence: 99%

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Regulation of glucose uptake in differentiated cells

Lange¹

2001

Front Biosci

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Glucose uptake into the cell is mediated by a family of glycosylated membrane proteins, called glucose transporters (GTs) that are able to facilitate passive hexose transfer across the lipid plasma membrane. The tissue-specific transporter isoforms generally differ in their affinity to the natural substrate D-glucose according to the specific functions of the respective organ. The mechanisms by which external and internal signals regulate glucose uptake into the cells belong to one of the most extensively studied fields of cell physiology. However, in spite of significant progress in identifying the involved molecular components and signaling pathways, the final cellular mechanism responsible for the short-term regulation of glucose uptake is still a matter of intense debate. The widely accepted translocation hypothesis, which explains transport regulation by exo- and endocytic modulation of the number of GTs in the plasma membrane, insufficiently accounts for the whole insulin-induced transport stimulation and is insufficient to integrate the wide variety of different transport-modulating signals in differentiated tissue cells into a common mechanistic concept. Some time ago, a novel type of glucose transport regulation has been proposed prevailing in differentiated tissue cells. This mechanism depends on the presence of glucose transporters on microvilli of differentiated cells. The basic framework for this theory was provided by a recently presented novel concept of ion channel regulation via microvillar structures [Lange, K. (1999): Microvillar Ca++ signaling: A new view on an old problem. J. Cell. Physiol. 180, 19-35; Lange, K. (2000): Regulation of cell volume via microvillar ion channels. J. Cell. Physiol. 185, 21-35; Lange, K. (2000): Microvillar ion channels - Cytoskeletal regulation of ion fluxes. J. Theor. Biol. 206, 561-584], earlier studies on glucose transport regulation and a number actual biochemical findings. Here, a survey on both concepts is given and the ability of the novel mechanism of microvillar transport regulation to integrate a large body of experimental data into the common concept of cellular regulation via microvillar pathways is discussed.

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Section: Energy Metabolism In the Membrane-limited Statementioning

confidence: 99%

Section: Energy Metabolism In the Membrane-limited Statementioning

confidence: 99%

Regulation of glucose uptake in differentiated cells

Lange¹

2001

Front Biosci

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Understanding the dynamics of cellular responsiveness to modifications of metabolic substrates in perifusion

Brand

Lyons

Midgley

1994

Journal Cellular Physiology

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A novel microperifusion system with capabilities for continuous, real‐time, potentiometric monitoring of extracellular hydrogen ion concentration has been used to define the response of HeLa cells to abrupt changes in extracellular energy sources or introduction of an inhibitor of glycolysis. Glycolytic inhibition, induced by removal of glucose or introduction of iodoacetate, each led to a rapid, continuous decrease in acid release. The response to iodoacetate took longer than removal of glucose, perhaps due to the time required for binding and activation. Once inhibition began, however, the rate of change was greater than following glucose removal. Conversely, recovery time following iodoacetate inhibition was much slower than with glucose removal. Unlike the response to short‐term glucose depletion, a second pulse of iodoacetate resulted in a faster response followed by an even longer recovery time. The response to switching between glucose and glutamine began almost without evident delay. The response patterns revealed that HeLa cells prefer glutamine to glucose, but, in the presence of both energy sources, some glucose continues to be used. In summary, these results indicate that continuous, real‐time monitoring of the kinetics of hydrogen‐ion release can be used to gain new insights into the dynamics of cellular response to perturbations of extracellular energy sources. © 1994 Wiley‐Liss, Inc.

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