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hyperinsulinism/proline
Veza se sprema u međuspremnik
Page 1 od 17 rezultati
Perspective of future drugs targeting sterile 20/SPS1-related proline/alanine-rich kinase for blood pressure control.
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According to a genome-wide association study, intronic SNPs within the human sterile 20/SPS1-related proline/alanine-rich kinase (SPAK) gene was linked to 20% of the general population and may be associated with elevated blood pressure. As cell volume changes, mammalian SPAK kinases respond to
Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism.
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The inwardly rectifying potassium channel Kir6.2 is the pore-forming subunit of the ATP-sensitive potassium (K(ATP)) channel, which controls insulin secretion by coupling glucose metabolism to membrane potential in beta-cells. Loss of channel function because of mutations in Kir6.2 or its associated
Insulin modulates rat intestinal glucose transport: effect of hypoinsulinemia and hyperinsulinemia.
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The current studies were designed to evaluate the role of plasma insulin and glucose as regulators of intestinal glucose transport in vivo. Initially, rats received either intravenous glucose infusion or intraperitoneal streptozotocin to induce sustained hyperglycemic hyperinsulinemia or
Hyperinsulinism in short-chain L-3-hydroxyacyl-CoA dehydrogenase deficiency reveals the importance of beta-oxidation in insulin secretion.
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A female infant of nonconsanguineous Indian parents presented at 4 months with a hypoglycemic convulsion. Further episodes of hypoketotic hypoglycemia were associated with inappropriately elevated plasma insulin concentrations. However, unlike other children with hyperinsulinism, this patient had a
First successful application of preimplantation genetic diagnosis and haplotyping for congenital hyperinsulinism.
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Congenital hyperinsulinism is the most common cause of persistent hypoglycaemia in infancy. Early surgical intervention is usually required to prevent brain damage. The prevention of the transmission to the offspring is important in families carrying the mutated gene. Preimplantation genetic
Insulin-mediated phosphorylation of the proline-rich Akt substrate PRAS40 is impaired in insulin target tissues of high-fat diet-fed rats.
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Clinical insulin resistance is associated with decreased activation of phosphatidylinositol 3'-kinase (PI3K) and its downstream substrate protein kinase B (PKB)/Akt. However, its physiological protein substrates remain poorly characterized. In the present study, the effect of in vivo insulin action
Transgenic mice overexpressing neuropeptide Y in noradrenergic neurons: a novel model of increased adiposity and impaired glucose tolerance.
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OBJECTIVE
A functional polymorphism leucine 7 proline in the human neuropeptide Y (NPY) gene leading to increased NPY release from sympathetic nerves is associated with traits of metabolic syndrome. Although hypothalamic NPY neurons play an established role in promoting positive energy balance, the
Over-expression of PRAS40 enhances insulin sensitivity in skeletal muscle.
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BACKGROUND
Silencing proline-rich Akt substrate of 40-kDa (PRAS40) impairs insulin signalling in skeletal muscle.
OBJECTIVE
This study assessed the effects of over-expressing wild type or mutant AAA-PRAS40, in which the major phosphorylation sites and mTORC1-binding site were mutated, on insulin
(Pro(3))GIP[mPEG]: novel, long-acting, mPEGylated antagonist of gastric inhibitory polypeptide for obesity-diabetes (diabesity) therapy.
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OBJECTIVE
Antagonism of the gastric inhibitory polypeptide (GIP) receptor with daily injection of proline-3 gastric inhibitory polypeptide ((Pro(3))GIP) can reverse or prevent many of the metabolic abnormalities associated with diet-induced obesity-diabetes (diabesity). This study has examined the
Essential role of protein kinase G and decreased cytoplasmic Ca2+ levels in NO-induced inhibition of rat aortic smooth muscle cell motility.
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Hyperinsulinemia is a major risk factor for the development of vascular disease. We have reported that insulin increases the motility of vascular smooth muscle cells via a hydrogen peroxide-mediated mechanism and that nitric oxide (NO) attenuates insulin-induced motility via a cGMP-mediated
Modulation of plasma glucose levels by thyrotropin-releasing hormone administered intracerebroventricularly in the rat.
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Thyrotropin-releasing hormone (TRH), but not histidyl-proline diketopiperazine (cyclo[His-Pro]), induced transient hyperglycemia associated with hyperglucagonemia and marked hyperinsulinemia when placed intracerebroventricularly (i.c.v.) in anesthetized rats. This TRH-induced hyperglycemia was
[WNK-SPAK-SLC12A signal cascade is a new therapeutic target for hypertension].
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WNK-oxidative stress-responsive 1 (OSR1) /STE20/SPS1-related proline-alanine-rich protein kinase(SPAK)-SLC12A transporters cascade regulates blood pressure through NaCl reabsorption in kidney and vasoconstriction. Furthermore, we recently reported that this cascade is positively regulated by
Effects of ammonia infusion on plasma glucagon, insulin, and amino acids in intact, pancreatectomized, and adrenalectomized dogs.
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Ammonium salts were infused in intact, pancreatectomized, and adrenalectomized dogs to produce coma-inducing amounts of plasma ammonia. Changes in intact dogs included hyperglycemia, hyperglucagonemia, hyperinsulinemia, and decreases in plasma concentrations of glutamine, alanine, threonine,
Regulation of with-no-lysine kinase signaling by Kelch-like proteins.
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In 2001, with-no-lysine (WNK) kinases were identified as the genes responsible for the human hereditary hypertensive disease pseudohypoaldosteronism type II (PHAII). It took a further 6 years to clarify that WNK kinases participate in a signaling cascade with oxidative stress-responsive gene 1
Phosphatidylinositol 3-kinase/Akt signaling pathway activates the WNK-OSR1/SPAK-NCC phosphorylation cascade in hyperinsulinemic db/db mice.
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Metabolic syndrome patients have insulin resistance, which causes hyperinsulinemia, which in turn causes aberrant increased renal sodium reabsorption. The precise mechanisms underlying this greater salt sensitivity of hyperinsulinemic patients remain unclear. Abnormal activation of the recently
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