Evaluating the evidence for macrophage presence in skeletal muscle and its relation to insulin resistance in obese mice and humans: a systematic review protocol

Bhatt, Meha; Rudrapatna, Srikesh; Banfield, Laura; Bierbrier, Rachel; Wang, Pei‐Wen; Wang, Kuan Wen; Thabane, Lehana; Samaan, M. Constantine

doi:10.1186/s13104-017-2686-6

Cited by 5 publications

(4 citation statements)

References 37 publications

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“…As many studies have reported, lncRNAs showed tissue-specific expression patterns across various tissues with the regulatory specificity [45] and presented cell-type-specific expression patterns even in the same tissue [46]. Satellite cells [47], adult stem cells [47], macrophages [48], and vascular endothelial cells [49] reside in the skeletal muscle that possesses a three-dimensional microenvironment. Additionally, skeletal muscle fibers can be classified as fast oxidative-glycolytic, fast glycolytic, slow oxidative as well as various hybrid muscle fibers based on myosin heavy-chain (MHC) isoforms [50].…”

Section: Discussionmentioning

confidence: 95%

RNA-sequencing analysis reveals the potential contribution of lncRNAs in palmitic acid-induced insulin resistance of skeletal muscle cells

Han

You

et al. 2020

Bioscience Reports

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Insulin resistance (IR) has been considered as the common pathological basis and developmental driving force for most metabolic diseases. Long noncoding RNAs (lncRNAs) have emerged as pivotal regulators in modulation of glucose and lipid metabolism. However, the comprehensive profile of lncRNAs in skeletal muscle cells under the insulin resistant status and the possible biological effects of them were not fully studied. In this research, using C2C12 myotubes as cell models in vitro, deep RNA-sequencing was performed to profile lncRNAs and mRNAs between palmitic acid-induced IR C2C12 myotubes and control ones. The results revealed that a total of 144 lncRNAs including 70 up-regulated and 74 down-regulated (|fold change| > 2, q < 0.05) were significantly differentially expressed in palmitic acid-induced insulin resistant cells. In addition, functional annotation analysis based on the Gene Ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) databases revealed that the target genes of the differentially expressed lncRNAs were significantly enriched in fatty acid oxidation, lipid oxidation, PPAR signaling pathway, and insulin signaling pathway. Moreover, Via qPCR, most of selected lncRNAs in myotubes and db/db mice skeletal muscle showed the consistent expression trends with RNA-sequencing. Co-expression analysis also explicated the key lncRNA-mRNA interactions and pointed out a potential regulatory network of candidate lncRNA ENSMUST00000160839. In conclusion, the present study extended the skeletal muscle lncRNA database and provided novel potential regulators for future genetic and molecular studies on insulin resistance, which is helpful for prevention and treatment of the related metabolic diseases. sensitivity and whole-body metabolism. For example, perturbed heterogeneous nuclear ribonucleoprotein A1-induced turbulences in glucose homeostasis in the skeletal muscle could accelerate systemic IR under both basal and high-fat induced conditions [7]. Conversely, activating mTOR signaling, improved insulin sensitivity in the skeletal muscle, which could enhance whole-body metabolism via weight loss and an increased fatty acid oxidation capacity in the adipose tissue and liver [8,9]. Studies have shown that among the widely recognized mechanisms underlying IR in the skeletal muscle, quite a few studies displayed that accumulation of 'toxic' lipid metabolites was considered as an important contributor to IR in skeletal muscle [10][11][12][13][14]. Lipid-induced IR has been associated with different cellular events in skeletal muscle cells, including impaired insulin signaling transduction of IRS1-PI3K [15], activation of inflammatory and pro-inflammatory cytokines [16], abnormally accumulation of ceramides [17], and mitochondrial dysfunction [18]. Therefore, the factors or the mechanisms underlying IR in the skeletal muscle, which are induced by lipid overload, must be explored.Long noncoding RNAs (lncRNAs), transcribed by RNA polymerase II, is a kind of RNA molecules with lengths of more than 200 nucleot...

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Section: Discussionmentioning

confidence: 95%

RNA-sequencing analysis reveals the potential contribution of lncRNAs in palmitic acid-induced insulin resistance of skeletal muscle cells

Han

You

et al. 2020

Bioscience Reports

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“…This systematic review has been registered with PROSPERO (registration no. CRD42016033035), and the methods are available in a published protocol . This systematic review follows the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) guidelines, and the completed PRISMA checklist is available in Table S1 in the Supporting Information.…”

Section: Methodsmentioning

confidence: 99%

“…Additionally, we hand‐searched reference lists of included studies. A sample of the search strategy was included in the published protocol for this review …”

Section: Methodsmentioning

confidence: 99%

Obesity and muscle‐macrophage crosstalk in humans and mice: A systematic review

et al. 2019

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Obesity is associated with the production of inflammatory cytokines that are implicated in insulin resistance (IR), and if not addressed, can lead to type 2 diabetes (T2D). The role of the immune system in skeletal muscle (SM) inflammation and insulin sensitivity is not yet well characterized. As SM IR is an important determinant of glycaemia, it is critical that the muscle-immune phenotype is mapped to help design interventions to target T2D. This systematic review synthesized the evidence for SM macrophage content and phenotype in humans and murine models of obesity, and the association of muscle macrophage content and phenotype with IR. Results were synthesized narratively, as we were unable to conduct a meta-analysis. We included 28 studies (n=10 human, n=18 murine), and all studies detected macrophage markers in SM. Macrophage content was positively associated with IR. In humans and mice, there was variability in muscle macrophage content and phenotype in obesity.Overall certainty in the evidence was low due to heterogeneity in detection methods and incompleteness of data reporting. Macrophages are detected in human and murine SM in obesity and a positive association between macrophage content and IR is noted; however, the standardization of markers, detection methods, and reporting of study details is warranted to accurately characterize macrophages and improve the potential for creating specific and targeted immune-based therapies in obesity.

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“…All of these tissues have its own specific niche of macrophages having essential physiologic function that sustain integrity of tissues, adapting at every stage of T2D formation. [3][4][5]35,36 Tissue macrophages actions have been demonstrated to be markedly strong regulators of insulin signaling, their sensitivity as well as resistance Figure 4.…”

Section: Metabolic Physiology As Well As Pathology-role Of Tissue Macmentioning

confidence: 99%

Targeting macrophage polarization for therapy of diabesity–the feasibility of early improvement of insulin sensitivity and insulin resistance-a comprehensive systematic review

Kaur¹,

Allahbadia²,

Singh³

2021

JDMDC

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The incidence of obesity is increasing in mammoth proportions so much so that associated comorbidity T2DM incidence is increasing markedly that we had to coin a term "Diabesity" to target both together. Earlier trying to review etiopathogenesis of both obesity and type 2 DM we found that whatever drugs that are formulated usually do not work with some complications and till now other than bariatric surgery we have no permanent cure for long term maintenance. Further T2DM might be a disease of 2 etiopathogenesis, namely inflammatory, as well as metabolic. Although metabolic inflammation has the properties of being systemic, their common initiating point is tissue resident macrophages, whose successful physiological or abnormal pathological adaptation to its microenvironment dictates disease course as well as severity. Earlier we reviewed macrophage polarization in case of nonalcoholic fatty liver disease (NAFLD). Here we review it more comprehensively regarding crucial modes, of macrophage polarization, inflammatory, as well as non inflammatory which sees to the formation of insulin resistance (IR) as well as type 2 diabetes mellitus (T2DM). Details of macrophage polarization, bioenergetics macrophage adaptations in different scenario is discussed in detail along with role of transcription factors like interferon regulatory factor 5 (IRF5), nuclear factor kappa B (NFKB), toll like receptor 4 (TLR4), liver X receptor (LXR), activator protein 1(AP1), hypoxia inducible factor 1(HIF1), signal transducers and activators of transcription (STATS) in all these signaling besides peroxisome proliferator activated receptor (PPAR).

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Evaluating the evidence for macrophage presence in skeletal muscle and its relation to insulin resistance in obese mice and humans: a systematic review protocol

Cited by 5 publications

References 37 publications

RNA-sequencing analysis reveals the potential contribution of lncRNAs in palmitic acid-induced insulin resistance of skeletal muscle cells

RNA-sequencing analysis reveals the potential contribution of lncRNAs in palmitic acid-induced insulin resistance of skeletal muscle cells

Obesity and muscle‐macrophage crosstalk in humans and mice: A systematic review

Targeting macrophage polarization for therapy of diabesity–the feasibility of early improvement of insulin sensitivity and insulin resistance-a comprehensive systematic review

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