Cytokine-induced metabolic effects in human adipocytes are independent of endogenous nitric oxide

Linscheid, Philippe; Seboek, Dalma; Zulewski, Henryk; Scherberich, Arnaud; Blau, Nenad; Keller, Ulrich; Müller, Beat

doi:10.1152/ajpendo.00374.2005

Cited by 11 publications

(7 citation statements)

References 49 publications

(76 reference statements)

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“…In contrast, in cultured human adipocytes, iNOS mRNA was activated only in a transient manner in response to inflammatory cytokines, but the protein was undetectable (although readily observable in 3T3-L1 adipocytes) (262). Consistently, iNOS inhibitors could not prevent the decrease in insulinstimulated glucose uptake that was induced by exposure to inflammatory agents (262). Regardless of this discrepancy between the two cell types, it appears based on in vitro experimental systems that inhibiting either mitochondrial or NADPH-derived ROS generation, and at least in muscle cells also iNOS-induced NO generation, can relieve insulin resistance.…”

Section: Preventing Ros/rns Generationmentioning

confidence: 87%

“…Metformin and troglitazone prevented these effects through their capacity to activate AMPK (both an activator of AMPK and a pharmacological inhibitor of iNOS prevented inflammation-induced insulin resistance) (337). In contrast, in cultured human adipocytes, iNOS mRNA was activated only in a transient manner in response to inflammatory cytokines, but the protein was undetectable (although readily observable in 3T3-L1 adipocytes) (262). Consistently, iNOS inhibitors could not prevent the decrease in insulinstimulated glucose uptake that was induced by exposure to inflammatory agents (262).…”

Section: Preventing Ros/rns Generationmentioning

confidence: 99%

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Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species

Bashan¹,

Kovsan²,

Kachko³

et al. 2009

Physiological Reviews

481

373

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Regulated production of reactive oxygen species (ROS)/reactive nitrogen species (RNS) adequately balanced by antioxidant systems is a prerequisite for the participation of these active substances in physiological processes, including insulin action. Yet, increasing evidence implicates ROS and RNS as negative regulators of insulin signaling, rendering them putative mediators in the development of insulin resistance, a common endocrine abnormality that accompanies obesity and is a risk factor of type 2 diabetes. This review deals with this dual, seemingly contradictory, function of ROS and RNS in regulating insulin action: the major processes for ROS and RNS generation and detoxification are presented, and a critical review of the evidence that they participate in the positive and negative regulation of insulin action is provided. The cellular and molecular mechanisms by which ROS and RNS are thought to participate in normal insulin action and in the induction of insulin resistance are then described. Finally, we explore the potential usefulness and the challenges in modulating the oxidant-antioxidant balance as a potentially promising, but currently disappointing, means of improving insulin action in insulin resistance-associated conditions, leading causes of human morbidity and mortality of our era.

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Section: Preventing Ros/rns Generationmentioning

confidence: 87%

Section: Preventing Ros/rns Generationmentioning

confidence: 99%

Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species

Bashan¹,

Kovsan²,

Kachko³

et al. 2009

Physiological Reviews

481

373

View full text Add to dashboard Cite

show abstract

“…IFN-c co-administration inhibited IL-1b-mediated PCT and CGRP secretion by 78 and 34%, respectively, but augmented IL-1b-mediated adrenomedullin secretion by 50% [4]. CALC-I and -II mRNAs were induced by exogenous CGRP and adrenomedullin, suggesting a positive autocrine feedback loop within the expression of the CT peptide superfamily [3][4][5]27]. Preliminary experimental evidence also suggests that this feedback loop is markedly enhanced by incubation with cycloheximide, an unspecific inhibitor of protein synthesis.…”

Section: Calcitonin Peptides Are Prototypes Of Hormokinesmentioning

confidence: 94%

“…However, at the highest concentration utilised (5 mg?L -1 ), PCT did not inhibit NO production and had no effect on unstimulated cells. Recent findings suggest a less prominent role of NO in human physiology and metabolism, as compared with rodents [27,130].…”

Section: The Central Role Of Hormokines In Host Defencementioning

confidence: 99%

Biomarkers in respiratory tract infections: diagnostic guides to antibiotic prescription, prognostic markers and mediators

Christ‐Crain¹,

Müller²

2007

Eur Respir J

225

149

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Used appropriately, biomarkers improve the assessment of respiratory tract infections and sepsis. Most prominently, circulating procalcitonin levels increase by a factor of several tens of thousands during sepsis. Using a sensitive assay, procalcitonin safely and markedly reduces antibiotic usage in respiratory tract infections and nonbacterial meningitis. Procalcitonin is the protopye of hormokine mediators. The term ''hormokine'' encompasses the cytokine-like behaviour of hormones during inflammation and infections. The concept is based on a ubiquitous expression of calcitonin peptides during sepsis. Adrenomedullin, another member of the calcitonin peptide superfamily, was shown to complement and improve the current prognostic assessment in lower respiratory tract infections. Other peptides share some features of hormokines, e.g. natriuretic peptide and copeptin. Hormokines are not only biomarkers of infection but are also pivotal inflammatory mediators. Like all mediators, their role during systemic infections is basically beneficial, possibly to combat invading microbes. However, at increased levels they can become harmful for their host. Multiple mechanisms of action were proposed. In several animal models the modulation and neutralisation of hormokines during infection was shown to improve survival, and thus might open new treatment options for severe infections, especially of the respiratory tract.

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“…This calcium- and inflammation-regulated peptide appears to have important immunomodulatory actions by 1) tempering inflammation through NFkB inhibition and 2) increasing endothelial production of PGI 2 , a prostaglandin with anti-inflammatory activities [61]. Interestingly, CGRP is expressed in rodent and human white adipose tissue (WAT), where Linscheid et al showed it can be induced by pro-inflammatory insults (e.g., [66, 67]). The peptide is also a powerful vasodilator, and CGRP has been proposed to contribute to the beneficial effects of dietary calcium/dairy in thwarting hypertension [68, 69].…”

Section: Dairy and Cardiometabolic Health: Potential Mechanismsmentioning

confidence: 99%

Associations between dairy foods, diabetes, and metabolic health: Potential mechanisms and future directions

Hirahatake¹,

Slavin²,

Maki³

et al. 2014

Metabolism

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Epidemiological evidence supports an inverse relationship between adequate intake of dairy foods and susceptibility to type 2 diabetes (T2D). The biological mechanisms responsible for this association remain to be established. This review provides a current perspective on proposed mechanisms that may underlie these effects, and highlights how randomized clinical trials can be applied to investigate these relationships. Results from epidemiological studies generally support that consumption of milk and dairy products is associated with a lower incidence of T2D or improvements in glucose homeostasis indices, and studies of animal and cell models support a positive effect of dairy-rich diets or components on metabolic and inflammation factors relevant to T2D and insulin resistance. Emerging evidence indicates that dairy components that alter mitochondrial function (e.g., leucine actions on silent information regulator transcript 1 (SIRT1)-associated pathways), promote gut microbial population shifts, or influence inflammation and cardiovascular function (e.g., Ca-regulated peptides calcitonin gene-related peptide [CGRP] or calcitonin) should be considered as possible mechanistic factors linking dairy intake with lower risk for T2D. The possibility that dairy-derived trans-palmitoleic acid (tC16:1) has metabolic bioactivities has also been proposed. Pre-clinical and clinical studies focusing specifically on these parameters are needed to validate hypotheses regarding the potential roles of dairy products and their components on the determinants of glucose tolerance, particularly insulin sensitivity, pancreatic endocrine function, and inflammation in individuals at-risk for T2D development. Such experiments would complement epidemiological studies and add to the evidence base for recommendations regarding consumption of dairy products and their individual components.

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Cytokine-induced metabolic effects in human adipocytes are independent of endogenous nitric oxide

Abstract: ller. Cytokine-induced metabolic effects in human adipocytes are independent of endogenous nitric oxide.

Cited by 11 publications

References 49 publications

Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species

Positive and Negative Regulation of Insulin Signaling by Reactive Oxygen and Nitrogen Species

Biomarkers in respiratory tract infections: diagnostic guides to antibiotic prescription, prognostic markers and mediators

Associations between dairy foods, diabetes, and metabolic health: Potential mechanisms and future directions

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