Effect of hyperosmolality on basal and hormone‐stimulated hepatic glucose metabolism <i>in vitro</i>

Komjati, M.; Kastner, Gerhard; Waldhäusl, W.; Bratusch-Marrain, P.

doi:10.1111/j.1365-2362.1989.tb00206.x

Cited by 25 publications

(18 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This was recently supported using 3T3-L1 adipocytes: insulinstimulated glucose uptake and GLUT4 translocation were completely abolished in presence of hyperosmolarity [29]. Interestingly, GLUT4-independent glucose uptake of rat hepatocytes is suppressed by increases in osmolarity as little as 10 mosmol/l [30]. Hyperosmolarity during insulin infusion in rat liver reverses proteolysis inhibition by insulin in a dominant fashion [10].…”

Section: Cell Hydration and Insulin Resistancementioning

confidence: 65%

Cell Hydration and Insulin Signalling

Schliess

Häussinger²

2000

Cell Physiol Biochem

View full text Add to dashboard Cite

Changes in cell hydration are critically important for the signalling towards metabolic responses to hormones, substrates and reactive oxygen intermediates. In liver insulin-induced cell swelling is due to a net K⁺-uptake resulting from the concerted activation of Na⁺/K⁺/2Cl^- cotransport, Na⁺/H⁺ exchange and the Na⁺/K⁺-ATPase. Insulin-induced swelling is essential for generating the antiproteolytic response to the hormone, which depends on activation of the MAP-kinase p38. Recent investigations show, that cell swelling induced by either hypoosmolarity or insulin triggers the activation of signalling cascades. Cell swelling by insulin is Ptdins-3-kinase mediated and contributes to the activation of Erk- and p38-type MAP-kinases. Conditions dehydrating insulin target tissues such as hyperosmolarity or amino acid deprivation are frequently associated with insulin resistance. In liver, hyperosmolarity impairs the Ptdins-3-kinase-dependent K⁺ uptake and cell swelling in response to insulin, leading to resistance of MAP-kinases and proteolysis to regulation by insulin. Likewise, a reduction of insulin-induced swelling by the loop diuretics furosemide and bumetanide cause insulin resistance shown by the levels of cell swelling, MAP-kinase activation and proteolysis control. Blockage of the cell volume response to insulin may be the common denominator in dehydration-induced insulin resistance found in clinical settings such as sepsis, burn injury and diabetes mellitus.

show abstract

Section: Cell Hydration and Insulin Resistancementioning

confidence: 65%

Cell Hydration and Insulin Signalling

Schliess

Häussinger²

2000

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Th ese changes were also seen with only mild deviations of serum sodium from the normal range. By contrast, complications of hypernatraemia and consequent hyperosmolality are manifold, and include decrease in cardiac contractility, decreased glucose utilization, insulin resistance, cognitive impairment and cerebral shrinkage leading to vascular rupture [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 89%

Dysnatraemias in the emergency room: Undetected, untreated, unknown?

Arampatzis

Exadaktylos

Buhl

et al. 2011

Wien Klin Wochenschr

View full text Add to dashboard Cite

Dysnatraemias are present in almost 1 in 5 patients who presented to the emergency department. Contrarily to patients who are already hospitalized, hypernatraemia was by far more common than hyponatraemia in patients at the emergency department. Surprisingly, patients with hyponatraemia were significantly older than normonatraemic patients while there was no age difference in hypernatraemic patients. Dysnatraemias are common in the emergency room and further studies are indicated to evaluate the causes and the impact on outcome of patients.

show abstract

“…This effect involves insulin-induced NKCC1 activation with subsequent hepatocyte swelling, which in turn activates osmosensing and osmosignaling cascades towards proteolysis [9]. Prevention of insulin-induced hepatocyte swelling by loop diuretics or hyperosmolarity abolishes the antiproteolytic effect, indicating that the disturbances of insulin-induced hepatocyte swelling can produce insulin resistance, as it is observed in clinical settings [12][13][14][15][16].…”

Section: Liver Cell Hydration and Liver Functionmentioning

confidence: 87%

Osmosensing and osmosignaling in the liver

Häussinger

2008

Wien Med Wochenschr

View full text Add to dashboard Cite

Alterations of hepatocyte volume induced by either anisoosmotic environments or under the influence of hormones, concentrative amino acid uptake and oxidative stress are now recognized as an independent signal which contributes to the regulation of liver cell function and gene expression. Several long-known but mechanistically poorly understood effects of amino acids, which could not be related to their metabolism, such as the stimulation of glycogen synthesis or the inhibition of proteolysis are due to their effects on hepatocyte hydration, because they are quantitatively mimicked by swelling the cells in hypoosmotic media to the extent as the amino acids do. Likewise, transmembrane ion movements under the influence of hormones are an integral part of hormonal signal transduction mechanisms with alterations of cellular hydration acting as another "second messenger" of hormone action. Integrins act as osmosensors for hepatocyte swelling and trigger activation of mitogen- activated protein kinase systems as osmosignaling cascades towards choleresis and autophagy inhibition. On the contrary, hepatocyte shrinkage triggers endosomal acidification as a signal for a ceramide-dependent activation of NADPH oxidase isoenzymes, which results in an oxidative stress signal with proapoptotic effects. Disturbances of osmosignaling and osmosensing are involved in a variety of pathophysiological conditions such as insulin resistance, protein catabolic states and cholestatic liver injury. This article briefly summarizes some aspects of our own work on osmosignaling and osmosensing; for indepth surveys the reader is refered to recent reviews [1-6].

show abstract

Effect of hyperosmolality on basal and hormone‐stimulated hepatic glucose metabolism in vitro

Cited by 25 publications

References 20 publications

Cell Hydration and Insulin Signalling

Cell Hydration and Insulin Signalling

Dysnatraemias in the emergency room: Undetected, untreated, unknown?

Osmosensing and osmosignaling in the liver

Contact Info

Product

Resources

About