Expression of genes associated with inflammation and iron metabolism in 3T3-L1 cells induced with macrophages-conditioned medium, glucose and iron

Briones, Lautaro; Andrews, Mónica; Pizarro, Fernando; Arredondo, Miguel

doi:10.1007/s10534-018-0108-4

Cited by 4 publications

(4 citation statements)

References 58 publications

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“…This was confirmed by our previous study, which additionally revealed that HG did not affect the expression level of CBS (30). Several studies have also suggested that HG significantly increases the secretion of cytokines, including tumor necrosis factor-α (TNF-α), IL-6, monocyte chemoattractant protein-1 and adiponectin (31,32). However, the effect that this HG-induced reduction in CSE expression and H 2 S production has on the expression of the NLRP3 inflammasome remains unknown.…”

Section: Introductionsupporting

confidence: 83%

Hydrogen sulfide modulates high glucose‑induced NLRP3 inflammasome activation in 3T3‑L1 adipocytes

Zhang²,

Ruan

et al. 2019

Exp Ther Med

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Activation of the NACHT leucine rich repeat and pyd domains-containing 3 (NLRP3) inflammasome plays an important role in the initiation of inflammation in adipose tissue in diabetic patients. However, the mechanisms underlying this are not fully understood. Hydrogen sulfide (H 2 S) has been shown to have anti-inflammatory properties in various cell types. The present study aimed to investigate the effect of H 2 S on high glucose (HG)-induced NLRP3 inflammasome activation in adipocytes. Adipocytes were differentiated from 3T3-L1 cells and treated with low glucose (LG), HG, H 2 S donor sodium hydrosulfide (NaHS) or N-acetyl-tyrosyl-valyl-alanyl-aspartyl chloromethyl ketone, an inhibitor of the cysteine protease caspase-1. The expression levels of NLRP3, apoptosis-associated speck-like protein containing A CARD (ASC) and caspase-1, and the release of interleukin (IL)-1β and IL-18 were measured. The results of the present study indicated that HG increased the expression levels of NLRP3, ASC and cleaved caspase-1, and the release of IL-1β and IL-18 in adipocytes. Caspase-1 inhibition abolished HG-induced production of IL-1β and IL-18 in adipocytes. Furthermore, NaHS inhibited the expression of NLRP3, ASC and cleaved caspase-1, and the production of IL-1β and IL-18 in adipocytes treated with HG. In conclusion, HG may increase and exogenous H 2 S may inhibit HG-induced NLRP3 inflammasome activation in adipocytes.

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Section: Introductionsupporting

confidence: 83%

Hydrogen sulfide modulates high glucose‑induced NLRP3 inflammasome activation in 3T3‑L1 adipocytes

Zhang²,

Ruan

et al. 2019

Exp Ther Med

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“…In addition to the modulation by iron of adiponectin and leptin-important regulators in themselves of metabolism, appetite, and insulin signalingiron also regulates inflammatory cytokines produced by adipocytes. In cultured 3T3-L1 adipocytes, for example, iron increases interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) mRNA (86). Interestingly, iron accumulation in the absence of increased dietary exposure is seen in adipocytes in ob/ob (lep −/− ) mice, consistent with the effects of obesity on iron handling described in Section 4 (87).…”

Section: Other Inflammatory Adipokinessupporting

confidence: 56%

Iron and the Pathophysiology of Diabetes

Harrison

Lorenzo

McClain

2023

Annu. Rev. Physiol.

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High iron is a risk factor for type 2 diabetes mellitus (T2DM) and affects most of its cardinal features: decreased insulin secretion, insulin resistance, and increased hepatic gluconeogenesis. This is true across the normal range of tissue iron levels and in pathologic iron overload. Because of iron's central role in metabolic processes (e.g., fuel oxidation) and metabolic regulation (e.g., hypoxia sensing), iron levels participate in determining metabolic rates, gluconeogenesis, fuel choice, insulin action, and adipocyte phenotype. The risk of diabetes related to iron is evident in most or all tissues that determine diabetes phenotypes, with the adipocyte, beta cell, and liver playing central roles. Molecular mechanisms for these effects are diverse, although there may be integrative pathways at play. Elucidating these pathways has implications not only for diabetes prevention and treatment, but also for the pathogenesis of other diseases that are, like T2DM, associated with aging, nutrition, and iron. Expected final online publication date for the Annual Review of Physiology, Volume 85 is February 2023. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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“…Pan et al (2014) [ 10 ] demonstrated that a high-saccharide environment inhibits the expression of one of the H 2 S-producing enzymes, cystathionine-γ-lyase (CSE), in adipocytes. Several studies have also suggested that high glucose intake significantly increases the secretion of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), IL-6, and monocyte chemoattractant protein-1 [ 11 , 12 ], and the involved mechanism is partly related to inhibition of the CSE/H 2 S system.…”

Section: Introductionmentioning

confidence: 99%

Fructose Intake Impairs the Synergistic Vasomotor Manifestation of Nitric Oxide and Hydrogen Sulfide in Rat Aorta

Berenyiová

Golas

Drobna

et al. 2021

IJMS

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In this study, we evaluated the effect of eight weeks of administration of 10% fructose solution to adult Wistar Kyoto (WKY) rats on systolic blood pressure (SBP), plasma and biometric parameters, vasoactive properties of the thoracic aorta (TA), NO synthase (NOS) activity, and the expression of enzymes producing NO and H2S. Eight weeks of fructose administration did not affect SBP, glycaemia, or the plasma levels of total cholesterol or low-density and high-density lipoprotein; however, it significantly increased the plasma levels of γ-glutamyl transferase and alanine transaminase. Chronic fructose intake deteriorated endothelium-dependent vasorelaxation (EDVR) and increased the sensitivity of adrenergic receptors to noradrenaline. Acute NOS inhibition evoked a reduction in EDVR that was similar between groups; however, it increased adrenergic contraction more in fructose-fed rats. CSE inhibition decreased EDVR in WKY but not in fructose-fed rats. The application of a H2S scavenger evoked a reduction in the EDVR in WKY rats and normalized the sensitivity of adrenergic receptors in rats treated with fructose. Fructose intake did not change NOS activity but reduced the expression of eNOS and CBS in the TA and CSE and CBS in the left ventricle. Based on our results, we could assume that the impaired vascular function induced by increased fructose intake was probably not directly associated with a decreased production of NO, but rather with impairment of the NO–H2S interaction and its manifestation in vasoactive responses.

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Expression of genes associated with inflammation and iron metabolism in 3T3-L1 cells induced with macrophages-conditioned medium, glucose and iron

Cited by 4 publications

References 58 publications

Hydrogen sulfide modulates high glucose‑induced NLRP3 inflammasome activation in 3T3‑L1 adipocytes

Hydrogen sulfide modulates high glucose‑induced NLRP3 inflammasome activation in 3T3‑L1 adipocytes

Iron and the Pathophysiology of Diabetes

Fructose Intake Impairs the Synergistic Vasomotor Manifestation of Nitric Oxide and Hydrogen Sulfide in Rat Aorta

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