Browsing by Author "Jancar, Sonia"
Now showing 1 - 2 of 2
- Results Per Page
- Sort Options
Item Eicosapentaenoic acid regulates inflammatory pathways through modulation of transcripts and mirna in adipose tissue of obese mice(2020) Ramalho, Theresa (TTU); Pahlavani, Mandana (TTU); Kalupahana, Nishan (TTU); Wijayatunga, Nadeeja (TTU); Ramalingam, Latha (TTU); Jancar, Sonia; Moustaid‐moussa, Naima (TTU)This study aims to investigate the global profiling of genes and miRNAs expression to explore the regulatory effects of eicosapentaenoic acid (EPA) in visceral adipose tissue (VAT) of obese mice. We used male mice, fed either a high‐fat diet (HF) or HF supplemented with EPA (HF‐ EPA), for 11 weeks. RNA, and small RNA profiling, were performed by RNAseq analysis. We conducted analyses using Ingenuity Pathway Analysis software (IPA®) and validated candidate genes and miRNAs related to lipid mediators and inflammatory pathways using qRT‐PCR. We identified 153 genes differentially downregulated, and 62 microRNAs differentially expressed in VAT from HF‐EPA compared to HF. Genes with a positive association with inflammation, chemotaxis, insulin resistance, and inflammatory cell death, such as Irf5, Alox5ap, Tlrs, Cd84, Ccr5, Ccl9, and Casp1, were downregulated by EPA. Moreover, EPA significantly reduced LTB4 levels, a lipid mediator with a central role in inflammation and insulin resistance in obesity. The pathways and mRNA/microRNA interactions identified in our study corroborated with data validated for inflammatory genes and miRNAs. Together, our results identified key VAT inflammatory targets and pathways, which are regulated by EPA. These targets merit further investigation to better understand the protective mechanisms of EPA in obesity‐associated inflammation.Item The role of captopril in leukotriene deficient type 1 diabetic mice(2023) Guimarães, João Pedro Tôrres (TTU); Queiroz, Luiz A.D.; Menikdiwela, Kalhara R. (TTU); Pereira, Nayara; Ramalho, Theresa; Jancar, Sonia; Moustaid-Moussa, Naima (TTU); Martins, Joilson O.T1D can be associated with metabolic disorders and several impaired pathways, including insulin signaling, and development of insulin resistance through the renin-angiotensin system (RAS). The main precursor of RAS is angiotensinogen (Agt) and this system is often linked to autophagy dysregulation. Dysregulated autophagy has been described in T1D and linked to impairments in both glucose metabolism, and leukotrienes (LTs) production. Here, we have investigated the role of RAS and LTs in both muscle and liver from T1D mice, and its effects on insulin and autophagy pathways. We have chemically induced T1D in 129sve and 129sve 5LO−/− mice (lacking LTs) with streptozotocin (STZ). To further inhibit ACE activity, mice were treated with captopril (Cap). In muscle of T1D mice, treatment with Cap increased the expression of RAS (angiotensinogen and angiotensin II receptor), insulin signaling, and autophagy markers, regardless of the genotype. In the liver of T1D mice, the treatment with Cap increased the expression of RAS and insulin signaling markers, mostly when LTs were absent. 5LO−/− T1D mice showed increased insulin sensitivity, and decreased NEFA, after the Cap treatment. Cap treatment impacted both insulin signaling and autophagy pathways at the mRNA levels in muscle and liver, indicating the potential role of ACE inhibition on insulin sensitivity and autophagy in T1D.