Cyclic adenosine monophosphate differently affects the response of mouse pancreatic beta‐cells to various amino acids.

Henquin, Jean‐Claude; Meissner, Hp.

doi:10.1113/jphysiol.1986.sp016314

Cited by 25 publications

(24 citation statements)

References 36 publications

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“…Neither of these agents affect the membrane potential at 3.3 mmol/l glucose (34,35), and most likely, these effects of forskolin and TPA are mediated by lowering of the Ca 2+ requirement for insulin secretion through sensitization of the exocytotic machinery to even small changes in Ca 2+ influx in response to L-arginine (26). Thus glucose may sensitize L-arginine stimulation of insulin secretion by three mechanisms, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…Since L-arginine has previously been shown not to be metabolised in islets (3) and since L-NAME is most likely not metabolised in islets, the inhibitory effect of these agents on glucose metabolism may also be associated with membrane depolarization. Thus membrane depolarization by L-arginine is accompanied by a large stimulation of K + efflux through activation of delayed rectifying K + channels (4,34), which may lower cellular K + and inhibit pyruvate kinase (40). K + omission showed a similar ability to inhibit glucose oxidation, suggesting that L-arginine may inhibit glucose metabolism through lowering of cellular K + .…”

Section: Discussionmentioning

confidence: 99%

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L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide

Thams

Capito²

1999

European Journal of Endocrinology

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The mechanism of L-arginine stimulation of glucose-induced insulin secretion from mouse pancreatic islets was studied. At 16.7 mmol/l glucose, L-arginine (10 mmol/l) potentiated both phases 1 and 2 of glucose-induced insulin secretion. This potentiation of glucose-induced insulin secretion was mimicked by the membrane depolarizing agents tetraethylammonium (TEA, 20 mmol/l) and K + (60 mmol/l), which at 16.7 mmol/l glucose obliterated L-arginine (10 mmol/l) modulation of insulin secretion. Thus L-arginine may potentiate glucose-induced insulin secretion by stimulation of membrane depolarization. At 3.3 mmol/l glucose, L-arginine (10 mmol/l) failed to stimulate insulin secretion. In accordance with membrane depolarization by the electrogenic transport of L-arginine, however, L-arginine (10 mmol/l) stimulation of insulin secretion was enabled by the K + channel inhibitor TEA (20 mmol/l), which potentiates membrane depolarization by L-arginine. Furthermore, Larginine (10 mmol/l) stimulation of insulin secretion was permitted by forskolin (10 mmol/l) or tetradecanoylphorbol 13-acetate (0.16 mmol/l), which, by activation of protein kinases A and C respectively sensitize the exocytotic machinery to L-arginine-induced Ca 2+ influx. Thus glucose may sensitize L-arginine stimulation of insulin secretion by potentiation of membrane depolarization and by activation of protein kinase A or protein kinase C. Finally, L-arginine stimulation of glucose-induced insulin secretion was mimicked by N G -nitro-L-arginine methyl ester (10 mmol/l), which stimulates membrane depolarization but inhibits nitric oxide synthase, suggesting that L-arginine-derived nitric oxide neither inhibits nor stimulates insulin secretion. In conclusion, it is suggested that L-arginine potentiation of glucose-induced insulin secretion occurs independently of nitric oxide, but is mediated by membrane depolarization, which stimulates insulin secretion through protein kinase A-and Csensitive mechanisms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide

Thams

Capito²

1999

European Journal of Endocrinology

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“…More recently, using 13 C nuclear magnetic resonance, L-alanine was shown to undergo substantial metabolism in BRIN-BD11 cells (3), resulting in glutamate, aspartate, and lactate production. Additionally, by use of the respiratory poison oligomycin, the metabolism and oxidation of alanine was shown to be important for its ability to stimulate insulin secretion (58).…”

Section: Mechanisms Of Amino Acid-dependent Stimulation Of Insulin Sementioning

confidence: 99%

Amino Acid Metabolism, β-Cell Function, and Diabetes

2006

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Specific amino acids are known to acutely and chronically regulate insulin secretion from pancreatic ␤-cells in vivo and in vitro. Mitochondrial metabolism is crucial for the coupling of amino acid and glucose recognition to exocytosis of insulin granules. This is illustrated by in vitro and in vivo observations discussed in the present review. Mitochondria generate ATP, which is the main coupling messenger in insulin secretion, and other coupling factors, which serve as sensors for the control of the exocytotic process. Numerous studies have sought to identify the factors that mediate the key amplifying pathway over the Ca 2؉ signal in nutrient-stimulated insulin secretion. Predominantly, these factors are nucleotides (ATP, GTP, cAMP, and NADPH), although metabolites have also been proposed, such as long-chain acyl-CoA derivatives and glutamate. This scenario further highlights the importance of the key enzymes or transporters, e.g., glutamate dehydrogenase, the aspartate and alanine aminotransferases, and the malate-aspartate shuttle in the control of insulin secretion. In addition, after chronic exposure, amino acids may influence gene expression in the ␤-cell, which subsequently alters levels of insulin secretion. Therefore, amino acids may play a direct or indirect (via generation of putative messengers of mitochondrial origin) role in insulin secretion. Diabetes 55 (Suppl. 2)

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“…Arginine is also known as one of the nutrients which stimulates insulin secretion in humans [7,9,18], mouse [8,10] and cattle [24]. Also in cats, arginine induced a secretory response of insulin in perfused pancreas cells [5].…”

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confidence: 99%

“…In cats, insulin and glucagon responses were induced by highdose intravenous injection of arginine [12]. In other amino acids, alanine and leucine reportedly induced insulin secretion in mouse pancreatic -cells [8,10]. Other than amino acid, fatty acid induced a secretory response of insulin in humans [9].…”

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confidence: 99%

Insulin Responses to Administrations of Amino Acids and Fatty Acids in Healthy Cats

Yasuda

Takashima

Takagi

et al. 2011

The Journal of Veterinary Medical Science

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ABSTRACT. In order to compare the stimulation ability of insulin secretion, we determined changes in plasma glucose and insulin concentrations after intravenous administration of various amino acids and essential fatty acids in clinically healthy adult cats. Plasma glucose concentrations were within the normal ranges after injection of amino acids and fatty acids. Plasma insulin concentrations increased rapidly 2 to 4 min after injection of arginine, then decreased to the basal levels at 20 min in all five cats. Insulin peak responses were significantly greater in arginine injections than in normal saline (P<0.01). Areas under the curve (AUC) of plasma insulin concentrations from 0 to 10 min after injection of arginine were significantly larger than after injection of normal saline (P<0.01) and glucose (P<0.05). Increases in AUC of plasma insulin concentration from 0 to 60 min were observed after injection of arginine, leucine, alanine, and fat emulsion. Arginine had a strong insulinotropic effect, and leucine, alanine, and fatty acids had weak ones. Besides, valine, methionine, taurine and glutamine had no stimulant activity of insulin. Given the risk of glucose toxication and required time for testing, the intravenous arginine tolerance test may be useful for estimation of insulin responses in cats.KEY WORDS: amino acid, arginine, fatty acid, feline, insulin secretion.

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Cyclic adenosine monophosphate differently affects the response of mouse pancreatic beta‐cells to various amino acids.

Cited by 25 publications

References 36 publications

L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide

L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide

Amino Acid Metabolism, β-Cell Function, and Diabetes

Insulin Responses to Administrations of Amino Acids and Fatty Acids in Healthy Cats

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