Effects of Catecholamines and Glucagon on Amino Acid Transport in the Liver

Chambers, John W.; Georg, Ralph H.; Bass, Allan D.

doi:10.1210/endo-83-6-1185

Cited by 46 publications

(14 citation statements)

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“…1.8%. These stimulations of AIB uptake by the perfused liver following the in vitro administration of glucagon and insulin are in accord with the earlier work of Chambers et al (2).…”

Section: Jss: 193supporting

confidence: 92%

Hormonal regulation of hepatic amino acid transport

Kilberg

Neuhaus

1977

J Supramol Struct

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The transport of 2-aminoisobutyric acid (AIB) into liver tissue was increased by both insulin and glucagon. We have now shown that these hormones do not stimulate the same transport system. Glucagon, possibly via cAMP, increased the hepatic uptake of AIB by a mechanism which resembled system A. This glucagon-sensitive system could be monitored by the use of the model amino acid MeAIB. In contrast, the insulin-stimulated system exhibited little or no affinity for MeAIB and will be referred to as system B. On the basis of other reports that the hepatic transport of AIB is almost entirely Na+ dependent and the present finding that the uptake of 2-aminobicyclo [2,2]heptane-2-carboxylic acid (BCH) was not stimulated by either hormone, we conclude that system B is Na+ dependent. Furthermore, insulin added to the perfusate of livers from glucagon-pretreated donors suppressed the increase in AIB or MeAIB uptake. Depending upon the specificities of systems A and B, both of which are unknown for liver tissue, the insulin/glucagon ratio may alter the composition of the intracellular pool of amino acids.

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“…1.8%. These stimulations of AIB uptake by the perfused liver following the in vitro administration of glucagon and insulin are in accord with the earlier work of Chambers et al (2).…”

Section: Jss: 193supporting

confidence: 92%

Hormonal regulation of hepatic amino acid transport

Kilberg

Neuhaus

1977

J Supramol Struct

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“…Amino acids are substrates for hepatic gluconeogenesis and their availability, particularly during fasting, could limit the rate of gluconeogenesis. Although several hormones have been shown to regulate the transport of amino acids in perfused liver (4)(5)(6), liver slices (7), or isolated hepatocytes (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18), the mechanisms for the hormonal regulation of amino acid transport are poorly understood. The present studies were undertaken to examine the hormonal regulation (by glucagon, epinephrine, norepinephrine, dexamethasone, and insulin) of amino acid transport in hepatocyte monolayers under three different culture conditions involving cellular calcium.…”

mentioning

confidence: 99%

Calcium-dependent hormonal regulation of amino acid transport and cyclic AMP accumulation in rat hepatocyte monolayer cultures.

Kelley¹,

Evanson²,

Potter³

1980

Proc. Natl. Acad. Sci. U.S.A.

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The effect of glucagon, epinephrine, norepinephrine, dexamethasone, insulin, and. dexamethasone plus glucagon on the transport of 2-aminoisobutyric acid (AIB) and that of glucagon on the production of cyclic AMP were examined in rat hepatocyte monolayer cultures under three different culture conditions involving calcium. The hepatocytes were studied in calcium-containing medium after treatment with or without 0.033% dimethyl sulfoxide, the solvent for the calcium ionophore A23187 (calcium controls) calcium-free medium after treatment with A23187 (calciumdepleted); and calcium-containing medium after treatment with ionophore (calcium-restored). The basal and hormonally regulated rates of AIB transport for hepatocytes in calcium control and calcium-depleted cultures were comparable. The restoration of calcium in calcium-restored cultures increased the basal and the hormonally stimulated transport of AIB when compared to the other conditions. Calcium markedly enhanced the stimulation of AIB transport in cultures treated with glucagon, catecholamines, and Nexamethasone plus glucagon. The level of cyclic AMP production in response to glucagon in calcium control and calcium-depleted cultures was the same and it was conspicuously higher than the level in calcium-restored cultures. Varying the concentration of calcium in the medium used to maintain the hepatocytes in calcium control cultures did not affect the stimulation of AIB transport or cyclic AMP production by glucagon. However, in calcium-restored cultures, increasing the calcium concentration of the medium resulted in increased stimulation of AIB transport and decreased production of cyclic AMP by glucagon. In the calcium-restored cultures, calcium in the absence of glucagon enhanced AIB transport but had no effect on cyclic AMP production. Cultures maintained for 6 hr in calcium-free medium after the depletion of calcium showed a 6-to 7-fold increase in the production of cyclic AMP in response to glucagon, but no stimulation of AIB transport. We suggest that mobilization of cellular calcium by glucagon either directly or through cyclic AMP mediates its stimulation of amino acid transport.Calcium regulates a variety of cellular functions, including the hormonal regulation of gluconeogenesis (1-3). Amino acids are substrates for hepatic gluconeogenesis and their availability, particularly during fasting, could limit the rate of gluconeogenesis. Although several hormones have been shown to regulate the transport of amino acids in perfused liver (4-6), liver slices (7), or isolated hepatocytes (8-18), the mechanisms for the hormonal regulation of amino acid transport are poorly understood. The present studies were undertaken to examine the hormonal regulation (by glucagon, epinephrine, norepinephrine, dexamethasone, and insulin) of amino acid transport in hepatocyte monolayers under three different culture conditions involving cellular calcium. Because it has been suggested that glucagon effects result from alterations in the level of intracellular cyclic A...

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“…45 Excess glucagon or increased adrenergic stimulation could produce a state of increased amino acid uptake by these transport systems and also stimulate increased amino acid catabolism in gluconeogenic and urea cycle pathways. 40,[44][45][46][47] The plasma amino acid profiles of dogs with SND are very similar to those observed in association with glucagonoma in dogs 4,14,15 and humans. 40 Seven dogs with SND associated with a pancreatic glucagonoma have been described.…”

Section: 23mentioning

confidence: 71%

Superficial Necrolytic Dermatitis in 11 Dogs with a History of Phenobarbital Administration (1995–2002)

March

Hillier

Weisbrode

et al. 2004

Veterinary Internal Medicne

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The clinical records of 11 dogs with histologically confirmed superficial necrolytic dermatitis (SND) and a history of phenobarbital (PB) administration (SND/PB) were evaluated retrospectively (1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002). Historical, clinical, clinicopathologic, ultrasonographic, and pathologic findings were compared with those in dogs with SND without prior PB exposure (SND/No PB; n ϭ 9) and with those dogs with PB-associated hepatotoxicity without skin disease (PB/hepatotoxicity). Dogs in the SND/PB group accounted for 44% of all histologically confirmed cases of SND that were evaluated at The Ohio State University Veterinary Teaching Hospital between 1995 and 2002. Median age of dogs in the SND/PB group was 10 years, and median duration of PB therapy was 6 years. Mean alanine aminotransferase (ALT) activity was 239 U/L, and median duration of abnormally high ALT activity was 6.25 months before SND diagnosis. Plasma amino acid concentrations measured in 1 dog were severely decreased. Ultrasonographic findings of hypoechoic nodules with hyperechoic borders corresponded to pathologic findings of nodular areas of normal hepatic tissue surrounded by zones of collapsed parenchyma with vacuolated hepatocytes. Clinical, clinicopathologic, ultrasonographic, and pathologic features of SND/PB and SND/No PB were similar. PB-associated cirrhosis and overt hepatic failure were not features of SND/PB. Different pathogenic mechanisms might induce SND in dogs. Chronic administration of PB requires further examination as a potential risk factor for the development of SND.

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Effects of Catecholamines and Glucagon on Amino Acid Transport in the Liver

Cited by 46 publications

References 0 publications

Hormonal regulation of hepatic amino acid transport

Hormonal regulation of hepatic amino acid transport

Calcium-dependent hormonal regulation of amino acid transport and cyclic AMP accumulation in rat hepatocyte monolayer cultures.

Superficial Necrolytic Dermatitis in 11 Dogs with a History of Phenobarbital Administration (1995–2002)

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