Cellular communication inside the liver. Binding, conversion and metabolic effect of prostaglandin D2 on parenchymal liver cells

Kuiper, Johan; Zijlstra, Freek J.; Kamps, Jan A. A. M.; Berkel, Theo J.C. Van

doi:10.1042/bj2620195

Cited by 42 publications

(20 citation statements)

References 38 publications

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“…Interestingly, in vitro studies have provided evidence that glucose production by hepatocytes is modulated by paracrine interaction with liver macrophages through production of adenosine, prostaglandins, and cytokines. [28][29][30][31] In vivo observations also provide support for the hypothesis that paracrine mechanisms are involved in hepatic glucose production. 32,33 We speculate that in GD the activity of liver macrophages is changed by the metabolic disorder, causing altered paracrine macrophage-hepatocyte interaction that results in increased glucose production.…”

Section: Discussionmentioning

confidence: 52%

Differential Effects of Enzyme Supplementation Therapy on Manifestations of Type 1 Gaucher Disease

Hollak

Corssmit

Aerts

et al. 1997

The American Journal of Medicine

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Differential effects of enzyme supplementation therapy on manifestations of type 1 gaucher disease Hollak, C.E.M.; Corssmit, E.P.M.; Aerts, J.M.F.G.; Endert, E.; Sauerwein, H.P.; Romijn, J.A.; van Oers, M.H.J. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. ) and hemoglobin and platelet count were obtained before and after 6 months of alglucerase therapy (15 U/kg per month). In 7 of the 12 patients hepatic glucose production was measured by infusing 3-3 H glucose. For comparison, REE and glucose metabolism were studied in 7 weight-and age-matched healthy subjects.RESULTS: REE and glucose production were increased in GD patients as compared with controls (REE: 29.8 kcal/kg/24 h { 3.6 and 23.1 { 2.3 kcal/kg/24 h, respectively, P õ 0.05; glucose production: 14.00 mmol/kg/min { 0.51 and 10.77 mmol/kg/min { 0.26, respectively, P õ 0.03). There were no differences in plasma glucose concentrations. Whereas the elevated REE decreased after 6 months of alglucerase therapy from 129% to 120% of predicted values (P õ 0.01), the increase in hepatic glucose production did not

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Section: Discussionmentioning

confidence: 52%

Differential Effects of Enzyme Supplementation Therapy on Manifestations of Type 1 Gaucher Disease

Hollak

Corssmit

Aerts

et al. 1997

The American Journal of Medicine

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“…Prostaglandin F2. [121], E2 [I221 and D, [123] stimulated glycogen phosphorylase activity or glucose release in hepatocyte suspensions, whereas the TXAz was inactive [121]. As in liver perfusions, half-maximal stimulation of glycogenolysis was observed in the concentration range 0.5 -5 pM for all three prostaglandins (Piischel, G. P., Schroder, A. and Jungermann, K., unpublished results).…”

Section: Metabolismmentioning

confidence: 99%

Nervous control of liver metabolism and hemodynamics

Gardemann

Püschel

Jungermann

1992

European Journal of Biochemistry

100

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Besides being a center of intermediary metabolism, a center of defense and a control center for the hormonal system, the liver acts as the glucose reservoir of the organism and, moreover, as an important blood reservoir, by taking up or releasing glucose and blood. The many diverse hepatic functions are controlled by the substrate concentrations in blood, the circulating hormone levels, the biomatrix and the autonomic hepatic nerves. In this review, the present knowledge on the metabolic and hemodynamic effects, the mechanism of action and the function of the hepatic nerves, as studied in the isolated perfused liver, are summarized. Effects of hepatic nerve stimulationIn perfused rat liver, activation of the sympathetic liver nervesincreases glucose and lactate release, urate and allantoin formation, decreases ketogenesis, urea release, ammonia uptake, xenobiotics conjugation, bile flow and bile acid secretion as well as oxygen utilization, and causes an overflow of noradrenaline into the hepatic vein. Furthermore, sympathetic stimulation decreases the flow and elicits an intrahepatic redistribution as well as a mobilization of blood by the closing of sinusoids. Activation of parasympathetic nerves enhances glucose utilization and causes re-opening of previously closed sinusoids. The actions of hepatic nerves are modulated by the hormones glucagon, insulin, adrenaline, noradrenaline, vasopressin and angiotensin. Extrahepatocellular signal chain of sympathetic nerve stimulationThe release of noradrenaline from the nerve endings and all effects of electrical nerve stimulation are strictly dependent on the presence of extracellular calcium. Sympathetic nerves regulate the hepatic metabolism of carbohydrates and ketone bodies and the conjugation of xenobiotics directly via interaction with non-parenchymal and parenchymal liver cells. However, sympathetic nerves regulate metabolism of nitrogenous compounds indirectly via reduction of blood flow. Studies with adrenergic and prostanoid agonists and antagonists support the following mechanism. Noradrenaline, released from the nerve endings via al-adrenergic receptors, directly interacts with periportal hepatocytes and also stimulates prostanoid formation in nearby non-parenchymal liver cells. Prostanoids, in turn, modulate metabolism in parenchymal cells. About 50% of the metabolic nerve effects in rat liver are mediated via signal propagation through gap junctions. By this mechanism, rat liver apparently compensates the scarce innervation of only a few parenchymal and non-parenchymal cells in the proximal periportal zone.

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“…In isolated rodent livers, infusion of PGF 2a but not thromboxane A 2 stimulates gluconeogenesis and glycogenolysis, and PGD 2 induces hepatic glycogenolysis (13), whereas PGE 2 inhibits glucagon-mediated gluconeogenesis from lactate (14). However, the relevance of these infusion experiments to the autocoidal role and concentrations of endogenous eicosanoids is unclear, and the potential importance of PGI 2 in regulating glucose metabolism in liver is unknown.…”

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confidence: 94%

I Prostanoid Receptor–Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT

et al. 2014

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Nonsteroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid (ASA), improve glucose metabolism in diabetic subjects, although the underlying mechanisms remain unclear. In this study, we observed dysregulated expression of cyclooxygenase-2, prostacyclin biosynthesis, and the I prostanoid receptor (IP) in the liver's response to diabetic stresses. High doses of ASA reduced hepatic prostaglandin generation and suppressed hepatic gluconeogenesis in mice during fasting, and the hypoglycemic effect of ASA could be restored by IP agonist treatment. IP deficiency inhibited starvationinduced hepatic gluconeogenesis, thus inhibiting the progression of diabetes, whereas hepatic overexpression of IP increased gluconeogenesis. IP deletion depressed cAMP-dependent CREB phosphorylation and elevated AKT phosphorylation by suppressing PI3K-g/PKC-z-mediated TRB3 expression, which subsequently downregulated the gluconeogenic genes for glucose-6-phosphatase (G6Pase) and phosphoenol pyruvate carboxykinase 1 in hepatocytes. We therefore conclude that suppression of IP modulation of hepatic gluconeogenesis through the PKA/CREB and PI3K-g/PKC-z/TRB3/AKT pathways contributes to the effects of NSAIDs in diabetes.Glucose is the major source of energy required by most mammalian cells to maintain normal physiological functions. Glucose homeostasis is tightly regulated within a relatively narrow range by hormones such as glucagon and insulin and through balancing of glucose output by the liver and its utilization by peripheral tissues such as skeletal muscle, heart, and adipocytes. Liver is the dominant organ in the maintenance of glucose homeostasis, which is regulated by way of glucose production through glycogenolysis and gluconeogenesis, glucose uptake by glycogenesis, and glycolytic conversion to pyruvate (1). Circulating insulin increases in response to feeding, leading to glycogenesis and lipogenesis and the suppression of hepatic glucose production (HGP). Conversely, during fasting conditions or in the case of untreated type 1 diabetes, insulin secretion drops and glucagon secretion rises, prompting hepatic glycogenolysis and gluconeogenesis. The key regulatory enzymes for hepatic gluconeogenesis include glucose 6 phosphatase (G6Pase), fructose-1, 6-bisphosphatase, and phosphoenolpyruvate carboxykinase 1 (PEPCK), also known as PCK1. However, in patients with type 2 diabetes, the rate of hepatic gluconeogenesis is considerably elevated, contributing to fasting hyperglycemia and to exaggerated postprandial hyperglycemia.Prostaglandins (PGs) play important roles in inflammation-mediated diseases, including diabetes (2).

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Cellular communication inside the liver. Binding, conversion and metabolic effect of prostaglandin D2 on parenchymal liver cells

Cited by 42 publications

References 38 publications

Differential Effects of Enzyme Supplementation Therapy on Manifestations of Type 1 Gaucher Disease

Differential Effects of Enzyme Supplementation Therapy on Manifestations of Type 1 Gaucher Disease

Nervous control of liver metabolism and hemodynamics

I Prostanoid Receptor–Mediated Inflammatory Pathway Promotes Hepatic Gluconeogenesis Through Activation of PKA and Inhibition of AKT

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