Regulation of insulin secretion and reactive oxygen species production by free fatty acids in pancreatic islets

Graciano, Maria Fernanda Rodrigues; Valle, Maíra Mello Rezende; Kowluru, Anjaneyulu; Curi, Rui; Carpinelli, Ângelo Rafael

doi:10.4161/isl.3.5.15935

Cited by 63 publications

(45 citation statements)

References 149 publications

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“…Production of ROS for short periods is associated with an increase in GSIS, but excessive or sustained production of ROS is negatively correlated with the insulin secretory process [6]. For example, fatty acid modulation of ROS production by pancreatic β-cells can occur by one or more of several possible mechanisms, such as the control of mitochondrial respiratory complexes and electron transport, induction of uncoupling proteins and NOX activation [65]. Indeed, NOX is physiologically activated by several secretagogues such as glucose, L-arginine, fatty acids and KCl [66].…”

Section: The Role Of Nox In Pancreatic Islet Dysfunction and Possiblementioning

confidence: 98%

The regulatory roles of NADPH oxidase, intra- and extra-cellular HSP70 in pancreatic islet function, dysfunction and diabetes

et al. 2015

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The 70 kDa heat-shock protein (HSP70) family is important for a dynamic range of cellular processes that include protection against cell stress, modulation of cell signalling, gene expression, protein synthesis, protein folding and inflammation. Within this family, the inducible 72 kDa and the cognate 73 kDa forms are found at the highest level. HSP70 has dual functions depending on location. For example, intracellular HSP70 (iHSP70) is anti-inflammatory whereas extracellular HSP70 (eHSP70) has a pro-inflammatory function, resulting in local and systemic inflammation. We have recently identified a divergence in the levels of eHSP70 and iHSP70 in subjects with diabetes compared with healthy subjects and also reported that eHSP70 was correlated with insulin resistance and pancreatic β-cell dysfunction/death. In the present review, we describe possible mechanisms by which HSP70 participates in cell function/dysfunction, including the activation of NADPH oxidase isoforms leading to oxidative stress, focusing on the possible role of HSPs and signalling in pancreatic islet α- and β-cell physiological function in health and Type 2 diabetes mellitus.

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Section: The Role Of Nox In Pancreatic Islet Dysfunction and Possiblementioning

confidence: 98%

The regulatory roles of NADPH oxidase, intra- and extra-cellular HSP70 in pancreatic islet function, dysfunction and diabetes

et al. 2015

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“…However, accumulated evidence has proved the crucial effect of FFAs in the pathogenesis of atherosclerotic diseases. Excess of serum FFAs can induce reactive oxygen species production,5 endoplasmic reticulum stress,6 apoptosis,7 inflammation and thrombosis 8. Finally, all these disadvantageous impacts may result in impaired cardiovascular functions.…”

Section: Discussionmentioning

confidence: 99%

Free fatty acids as a marker for predicting periprocedural myocardial injury after coronary intervention

Wang

Zhang

Guo

et al. 2019

Postgraduate Medical Journal

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BackgroundPrevious studies have revealed that plasma levels of free fatty acids (FFAs) are related to cardiovascular risk. However, whether FFAs could predict periprocedural myocardial injury (PMI) following percutaneous coronary intervention (PCI) in patients with stable coronary artery disease (CAD) remains unclear.PurposeThis study aimed to investigate the relationship of FFAs to PMI in untreated patients with CAD who underwent PCI.MethodsA total of 374 consecutive patients with CAD without lipid-lowering treatment on admission and with normal preprocedural cardiac troponin I (cTnI) levels who underwent PCI were prospectively enrolled. The baseline characteristics were collected and PMI was evaluated by cTnI analysis within 24 hours. The relation of preprocedural FFA levels to peak cTnI values after PCI was examined.ResultsPreprocedural FFAs were positively correlated with peak cTnI values after PCI in both simple regression model (β=0.119, p=0.021) and multiple regression model (β=0.198, p=0.001). Patients with higher FFA levels had higher postprocedural cTnI levels compared with those with normal FFA levels (0.27±0.68 ng/mL vs 0.66±0.31 ng/mL, p=0.014). In the multivariable model, preprocedural FFA levels were associated with an increased risk of postprocedural cTnI elevation above 1× upper limit of normal (ULN, OR: 1.185, 95% CI 0.997 to 1.223, p=0.019) up to 10× ULN (OR: 1.132, 95% CI 1.005 to 1.192, p=0.003) .ConclusionsThe present study first suggested that elevated FFA levels were associated with an increased risk of PMI in untreated patients with CAD. Further study with large sample size may be needed to confirm our findings.

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“…through modulation of the redox state of signalling molecules [38,118]. Thus, in physiological levels, ROS might function as signalling molecules in numerous cellular processes, including differentiation [89], proliferation [128], apoptosis [156], migration [148], secretion [64], regulation of transcription factor expression [30] and adaptation processes, such as HPV [190,202,203]. Pathological excess in ROS production or disproportionate removal of ROS by the cellular antioxidant system causes development of different pathologies [146], including PH [128,179].…”

Section: The Mechanism Of Hpv and Pulmonary Vascular Remodellingmentioning

confidence: 99%

NADPH oxidases—do they play a role in TRPC regulation under hypoxia?

Malczyk

Veith

Schermuly

et al. 2015

Pflugers Arch - Eur J Physiol

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In the lung, acute alveolar hypoxia causes hypoxic pulmonary vasoconstriction (HPV) to maintain ventilation perfusion matching and thus optimal oxygenation of blood. In contrast, global chronic hypoxia triggers a pathological thickening of pulmonary arterial walls, called pulmonary vascular remodelling, leading to persistence of pulmonary hypertension (PH). Moreover, ischaemia or hypoxia can lead to a damage of pulmonary endothelial cells with subsequent oedema formation. Alterations in reactive oxygen species (ROS) have been suggested as a crucial mediator of such responses. Among the various sources of cellular ROS production, NADPH oxidases (NOXs) have been found to contribute to these physiological and pathophysiological signalling processes. NOXs are the only known examples that generate ROS as the primary function of the enzyme system. However, the downstream targets of NOX-derived ROS signalling in hypoxia are still not known. Canonical transient receptor potential (TRPC) channels recently have been recognised as directly or indirectly ROS-activated channels and have been shown to be essential for hypoxia-dependent vascular regulatory processes in the lung. Against this background, we here summarise the current knowledge on NOX-mediated TRPC channel signalling during hypoxia in the pulmonary circulation.

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Regulation of insulin secretion and reactive oxygen species production by free fatty acids in pancreatic islets

Cited by 63 publications

References 149 publications

The regulatory roles of NADPH oxidase, intra- and extra-cellular HSP70 in pancreatic islet function, dysfunction and diabetes

The regulatory roles of NADPH oxidase, intra- and extra-cellular HSP70 in pancreatic islet function, dysfunction and diabetes

Free fatty acids as a marker for predicting periprocedural myocardial injury after coronary intervention

NADPH oxidases—do they play a role in TRPC regulation under hypoxia?

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