Apparent translocation of glucose transport activity in rat epididymal adipocytes by insulin-like effects of high pH or hyperosmolarity.

Toyoda, Nagayasu; Robinson, F W; Smith, M M; Flanagan, J E; Kôno, Tetsuro

doi:10.1016/s0021-9258(17)35905-7

Cited by 42 publications

(1 citation statement)

References 27 publications

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“…Sphingosine, although it partially inhibits insulin-activated glucose uptake in adipocytes, has a stimulatory insulin-like action increasing the basal rate of glucose uptake (Robertson et al, 1989). High concentrations of sorbitol increase glucose transport by inducing the translocation of glucose transporters to the cell surface (Toyoda et al, 1986). Diacylglycerols also stimulate glucose transport in adipocytes and may be a physiological activator of this process by a mechanism independent of protein kinase C (StrSIfors, 1988).…”

Section: Discussionmentioning

confidence: 99%

Action of insulin in rat adipocytes and membrane properties

Epand

Stafford²,

Debanne³

1991

Biochemistry

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Several small peptides inhibit insulin-promoted glucose uptake in rat adipocytes. At 10 microM peptide concentration, the extent of their inhibition of the insulin effect is related to the ability of these peptides to raise the bilayer- to hexagonal-phase transition temperature in model membranes. Hexane and DL-threo-dihydrosphingosine lower this phase transition temperature in model membranes, and they promote glucose uptake in adipocytes. There is thus an empirical relationship between the action of membrane additives on glucose uptake in adipocytes and their effect on the hexagonal-phase-forming tendency in model membranes. The most potent of the bilayer-stabilizing peptides tested in this work is carbobenzoxy-D-Phe-L-Phe-Gly. This peptide also inhibits insulin-stimulated protein synthesis in adipocytes. In contrast, DL-threo-dihydrosphingosine stimulates protein synthesis. The uptake of [125I]iodoinsulin by adipocytes is inhibited by carbobenzoxy-D-Phe-L-Phe-Gly. The mechanism of action of the bilayer-stabilizing peptides includes inhibition of insulin-dependent protein phosphorylation in adipocytes. The peptides are not specific inhibitors of a single function but are suggested to cause their effects by altering the physical properties of the membrane in a nonspecific manner. These results demonstrate that insulin-dependent functions of rat adipocytes can be modified by membrane additives in a manner predictable from the properties of these additives in model membranes.

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Section: Discussionmentioning

confidence: 99%

Action of insulin in rat adipocytes and membrane properties

Epand

Stafford²,

Debanne³

1991

Biochemistry

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Regulation of cell volume via microvillar ion channels

Lange¹

2000

J. Cell. Physiol.

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A novel mechanism of cellular volume regulation is presented, which ensues from the recently introduced concept of transport and ion channel regulation via microvillar structures (Lange K, 1999, J Cell Physiol 180:19-35). According to this notion, the activity of ion channels and transporter proteins located on microvilli of differentiated cells is regulated by changes in the structural organization of the bundle of actin filaments in the microvillar shaft region. Cells with microvillar surfaces represent two-compartment systems consisting of the cytoplasm on the one side and the sum of the microvillar tip (or, entrance) compartments on the other side. The two compartments are separated by the microvillar actin filament bundle acting as diffusion barrier ions and other solutes. The specific organization of ion and water channels on the surface of microvillar cell types enables this two-compartment system to respond to hypo- and hyperosmotic conditions by activation of ionic fluxes along electrochemical gradients. Hypotonic exposure results in swelling of the cytoplasmic compartment accompanied by a corresponding reduction in the length of the microvillar diffusion barrier, allowing osmolyte efflux and regulatory volume decrease (RVD). Hypertonic conditions, which cause shortening of the diffusion barrier via swelling of the entrance compartment, allow osmolyte influx for regulatory volume increase (RVI). Swelling of either the cytoplasmic or the entrance compartment, by using membrane portions of the microvillar shafts for surface enlargement, activates ion fluxes between the cytoplasm and the entrance compartment by shortening of microvilli. The pool of available membrane lipids used for cell swelling, which is proportional to length and number of microvilli per cell, represents the sensor system that directly translates surface enlargements into activation of ion channels. Thus, the use of additional membrane components for osmotic swelling or other types of surface-expanding shape changes (such as the volume-invariant cell spreading or stretching) directly regulates influx and efflux activities of microvillar ion channels. The proposed mechanism of ion flux regulation also applies to the physiological main functions of epithelial cells and the auxiliary action of swelling-induced ATP release. Furthermore, the microvillar entrance compartment, as a finely dispersed ion-accessible peripheral space, represents a cellular sensor for environmental ionic/osmotic conditions able to detect concentration gradients with high lateral resolution. Volume regulation via microvillar surfaces is only one special aspect of the general property of mechanosensitivity of microvillar ionic pathways.

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Effect of hypertonicity on hexose transporter regulation in chicken embryo fibroblasts

Tillotson

Isselbacher

1987

Journal Cellular Physiology

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The regulation of hexose transporters of cultured fibroblasts was investigated by exposing chicken embryo fibroblasts (CEF) to hypertonic culture medium, a condition known to enhance hexose transport activity. The effects of hypertonicity and the role of protein synthesis were examined with CEF in the basal (glucose fed) and transport enhanced (glucose starved) states. Glucose-fed CEF exposed to hypertonic conditions developed four-fold enhancement of hexose transport activity within 4 hrs; this declined in the following 20 hrs to a level slightly higher than the fed control. Protein synthesis was required in part for this effect, since the presence of cycloheximide during hypertonic exposure of fed CEF blocked the increase in of transport by almost 50%. Although the increased transport produced by glucose starvation was not further enhanced by hypertonicity, hypertonic treatment of starved CEF during glucose refeeding largely prevented the loss of transport activity to the basal, fed state. The hypertonic effects were concentration dependent (240mOsm optimal) and could be elicited with NaCl, KCl, or sucrose. Hypertonic treatment typically led to a greater than 50% decline in the incorporation of [3H]leucine into acid-insoluble fractions. The changes in transport were evident at the plasma membrane level, and studies of membrane vesicles prepared from hypertonically treated fed CEF showed a doubling of both [3H]cytochalasin B binding and the Vmax of D-glucose transport. These findings indicate that exposure of CEF to hypertonic conditions has some effects similar to those produced by glucose starvation and suggest that protein synthesis is to some extent involved in the regulation of hexose transporters in CEF.

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Apparent translocation of glucose transport activity in rat epididymal adipocytes by insulin-like effects of high pH or hyperosmolarity.

Cited by 42 publications

References 27 publications

Action of insulin in rat adipocytes and membrane properties

Action of insulin in rat adipocytes and membrane properties

Regulation of cell volume via microvillar ion channels

Effect of hypertonicity on hexose transporter regulation in chicken embryo fibroblasts

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