Antagonistic effect of insulin on glucagon-evoked hyperpolarization. A correlation between changes in membrane potential and gluconeogenesis

Friedmann, Naomi; Dambach, George

doi:10.1016/0005-2736(80)90352-1

Cited by 57 publications

(11 citation statements)

References 15 publications

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“…Membrane hyperpolariz¬ ation has been shown to be important in energized solute accumulation by mouse Ehrlich ascites tumour cells (Gibb & Eddy, 1972) and human fibroblasts (Villereal & Cook, 1978). Interestingly, pancreatic glucagon evokes a hyperpolarization of the hepatocyte membrane (Friedmann & Dambach, 1980) and this hormone may therefore be involved in the starvation-induced increase in active solute entry into liver cells (Quinlan, Todderud, Kelley & Kletzein, 1982).…”

Section: Discussionmentioning

confidence: 98%

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Thompson¹,

Debnam²

1986

Journal of Endocrinology

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The effects of chronic (72 h) glucagon treatment on active nutrient uptake by the rat jejunum have been determined using in-vitro electrophysiological and autoradiographic methods together with an in-vivo technique which measures absorption across a cannulated segment of upper jejunum. Glucagon caused a marked increase in the potential difference across the brush border membrane from a mean value of -47.6 mV under control conditions to -54.2 mV following treatment with the hormone (P less than 0.025). A similar hyperpolarization was also noted after 24 h glucagon administration. The magnitude of the depolarization induced by the addition of D-galactose (4 mmol/l) to the mucosal fluid was increased from 6.0 to 14.3 mV following 72 h glucagon treatment (P less than 0.05). Phloridzin (0.1 mmol/l) abolished the galactose-induced depolarization in both control and treated animals. Glucagon induced significant increases of 49.9 and 61.0% respectively for glucose and galactose absorption measured under in-vivo conditions. Autoradiographic studies revealed that following glucagon treatment, L-valine uptake occurred earlier during enterocyte migration along the villus. This resulted in an enhanced accumulation of the amino acid at the villus tip. We conclude that glucagon increases nutrient transport across the small intestine. The raised electrical gradient for Na+- coupled nutrient entry into the enterocyte is likely to be a major factor in the transport response.

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Section: Discussionmentioning

confidence: 98%

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Thompson¹,

Debnam²

1986

Journal of Endocrinology

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“…Hormonally evoked ion redistribution has been mentioned. This redistribution is accompanied by a hyperpolarization of the plasma membrane [9], which is sensitive to ouabain [ 161. The data suggest the following sequence of events: a hormonal stimulus (e.g., glucagon) causes plasma membrane hyperpolarization by both an initial K' uptake by the electrogenic Na',K'-ATPase and a subsequent K' efflux via a different K' permeability.…”

Section: Resultsmentioning

confidence: 99%

Rapid stimulation of Na⁺,K⁺‐ATPase by glucagon, epinephrine, vasopressin and cAMP in perfused rat liver

et al. 1982

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“…Insertion of these vesicles into the plasma membrane is directly responsible for a 15‐fold increase in membrane conductance resulting from the opening of Cl − channels. Multiple lines of evidence suggest that Cl − channel activation modulates membrane potential and the intracellular pH, and these changes regulate a broad range of transport and metabolic processes in hepatocytes (Friedmann & Dambach, 1980; Boyer et al 1992; Li & Weinman, 2002). Thus, definition of the cellular mechanisms involved in modulation of the Cl − channel activity is critical for understanding regulation of the liver metabolism.…”

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confidence: 99%

Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

Puljak¹,

Pagliassotti²,

Wei³

et al. 2005

The Journal of Physiology

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The initial response of liver cells to insulin is mediated through exocytosis of Cl− channelcontaining vesicles and a subsequent opening of plasma membrane Cl − channels. Intracellular accumulation of fatty acids leads to profound defects in metabolism, and is closely associated with insulin resistance. It is not known whether the activity of Cl − channels is altered in insulin resistance and by which mechanisms. We studied the effects of fatty acid accumulation on Cl − channel opening in a model liver cell line. Overnight treatment with amiodarone increased the fat content by ∼2-fold, and the rates of gluconeogenesis by ∼5-fold. The ability of insulin to suppress gluconeogenesis was markedly reduced indicating that amiodarone treatment induces insulin resistance. Western blot analysis showed that these cells express the same number of insulin receptors as control cells. However, insulin failed to activate exocytosis and Cl − channel opening. These inhibitory effects were mimicked in control cells by exposures to arachidonic acid (15 µM). Further studies demonstrated that fatty acids stimulate the PKC activity, and inhibition of PKC partially restored exocytosis and Cl − channel opening in insulin-resistant cells. Accordingly, activation of PKC with PMA in control cells potently inhibited the insulin responses. These results suggest that stimulation of PKC activity in insulin resistance contributes to the inhibition of cellular responses to insulin in liver cells.

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Antagonistic effect of insulin on glucagon-evoked hyperpolarization. A correlation between changes in membrane potential and gluconeogenesis

Cited by 57 publications

References 15 publications

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Rapid stimulation of Na⁺,K⁺‐ATPase by glucagon, epinephrine, vasopressin and cAMP in perfused rat liver

Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

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Antagonistic effect of insulin on glucagon-evoked hyperpolarization. A correlation between changes in membrane potential and gluconeogenesis

Cited by 57 publications

References 15 publications

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Hyperglucagonaemia: effects on active nutrient uptake by the rat jejunum

Rapid stimulation of Na+,K+‐ATPase by glucagon, epinephrine, vasopressin and cAMP in perfused rat liver

Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

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Rapid stimulation of Na⁺,K⁺‐ATPase by glucagon, epinephrine, vasopressin and cAMP in perfused rat liver