Resistin increases islet blood flow and decreases subcutaneous adipose tissue blood flow in anaesthetized rats

Danielsson, Tom; Fredriksson, Lennart; Jansson, Leif; Henriksnäs, Johanna

doi:10.1111/j.1748-1716.2008.01891.x

Cited by 7 publications

(4 citation statements)

References 46 publications

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“…In studies of fixed human pancreata, resistin was shown to be expressed in human beta cells, but not alpha cells, and its expression increased with T2D (AlSalam et al 2011). Finally, another potential mechanism by which resistin may impact on beta cell function is by enhancing blood flow to the pancreas (Danielsson et al 2009). Beta cell function is negatively impacted by hypoxia (Cantley et al , 2013 and hypoxia-inducible factor 1a activation (Cantley et al 2009); therefore, as nutrient stimulation can lead to a transient decrease in oxygen tension (Bensellam et al 2012), resistin may help to sustain adequate islet perfusion and oxygenation during times of high-metabolic demand.…”

Section: Resistinmentioning

confidence: 98%

The control of insulin secretion by adipokines: current evidence for adipocyte-beta cell endocrine signalling in metabolic homeostasis

Cantley

2014

Mamm Genome

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Metabolic homeostasis is maintained by the coordinated action of multiple organ systems. Insulin secretion is often enhanced during obesity or insulin resistance to maintain glucose and lipid homeostasis, whereas a loss of insulin secretion is associated with type 2 diabetes. Adipocytes secrete hormones known as adipokines which act on multiple cell types to regulate metabolism. Many adipokines have been shown to influence beta cell function by enhancing or inhibiting insulin release or by influencing beta cell survival. Insulin, in turn, regulates lipolysis and promotes glucose uptake and lipid storage in adipocytes. As adipokine secretion and action is strongly influenced by obesity, this provides a potential route by which beta cell function is coordinated with adiposity, independently of alterations in blood glucose or lipid levels. In this review, I assess the evidence for the direct regulation of beta cell function by the adipokines leptin, adiponectin, extracellular nicotinamide phosphoribosyltransferase, apelin, resistin, retinol binding protein 4, fibroblast growth factor 21, nesfatin-1 and fatty acid binding protein 4. I summarise in vitro and in vivo data and discuss the influence of obesity and diabetes on circulating adipokine concentrations, along with the potential for influencing beta cell function in human physiology. Finally, I highlight future research questions that are likely to yield new insights into the exciting field of insulinotropic adipokines.

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Section: Resistinmentioning

confidence: 98%

The control of insulin secretion by adipokines: current evidence for adipocyte-beta cell endocrine signalling in metabolic homeostasis

Cantley

2014

Mamm Genome

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“…Auch Resistin wird von Fettzellen proportional zur Fettmasse synthetisiert. Bei Normalgewichtigen führt es zu einem vermehrten Blutfluss zum Pankreas, bei adipösen Patienten fördert es jedoch die Insulinresistenz und Glukoseintoleranz (15,16). Von Hepatozyten wird das o.g.…”

Section: Nafld Und Adipositasunclassified

Die nicht-alkoholische Fettlebererkrankung: Eine Systemerkrankung

Leven¹,

Fingas²,

Canbay³

2017

Adipositas - Ursachen, Folgeerkrankungen, Therapie

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ZusammenfassungDie nicht-alkoholische Fettlebererkrankung (NAFLD) ist die führende Lebererkrankung in der westlichen Welt und zeitgleich zentraler Bestandteil des metabolischen Syndroms. Ihr Spektrum reicht von der simplen Steatose über die nicht-alkoholische Fettleberhepatitis (NASH) und führt nicht selten in eine Fibrose mit anschließender Leberzirrhose, welche im hepatozellulären Karzinom enden kann. Dieser Progress verdeutlicht, dass die NAFLD nicht wie lange Zeit angenommen als „benigne” oder triviale Begleiterscheinung verkannt werden darf. Im Gegenteil, die NAFLD zeigt sich als eigenständiger Risikofaktor hinsichtlich der Entwicklung eines Diabetes mellitus Typ 2, Herzkreislauferkrankungen, chronischer Nephropathie und extrahepatischer Karzinome. Aufgrund dieser Zusammenhänge bedürfen NAFLD-Patienten umfassender Screeninguntersuchungen, um etwaige Entwicklungen frühzeitig zu detektieren.

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“…An ability to reduce expression levels of insulin receptor in pancreatic beta-cells has been reported, 28 as has a role in islet blood flow. 29 As resistin is expressed in pancreatic beta-cells, it remains to be shown whether these effects are due to locally secreted resistin or an endocrine effect of the fat-secreted form.…”

Section: Adipokines and Glucose Homeostasis – Regulation Of Insulin Smentioning

confidence: 99%

Dysregulated adipokines in the pathogenesis of type 2 diabetes and vascular disease

Brown¹

2012

Diabetes & Vascular Disease

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O besity is commonly associated with type 2 diabetes and vascular disease. Changes in body composition in the obese state lead to a dysregulation of secretion of adipocyte-secreted hormones known as adipokines. Adipokines such as leptin and adiponectin are known to be involved in many physiological and pathological processes. Current knowledge suggests that adipokines provide potential therapeutic targets against type 2 diabetes and vascular disease. Br J Diabetes Vasc Dis 2012;12:249-254.

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Resistin increases islet blood flow and decreases subcutaneous adipose tissue blood flow in anaesthetized rats

Cited by 7 publications

References 46 publications

The control of insulin secretion by adipokines: current evidence for adipocyte-beta cell endocrine signalling in metabolic homeostasis

The control of insulin secretion by adipokines: current evidence for adipocyte-beta cell endocrine signalling in metabolic homeostasis

Die nicht-alkoholische Fettlebererkrankung: Eine Systemerkrankung

Dysregulated adipokines in the pathogenesis of type 2 diabetes and vascular disease

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