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Correlation Between Resistin Level and Metabolic Syndrome Component: a Review

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Correlation Between Resistin Level and Metabolic Syndrome Component: a Review Review Mostafazadeh Mostafa et al. Correlation Between Resistin Level … Horm Metab Res 2018; 00: 00–00 Correlation Between Resistin Level and Metabolic Syndrome Component: A Review Authors Mostafa Mostafazadeh1, 2, Sanya Haiaty3, Ali Rastqar4, 5, Mahtab Keshvari6 Affiliations Isfahan University of medical Sciences 1 Immunology Research Center, Faculty of Medicine, Tabriz Isfahan University of Medical Sciences, Tabriz, Iran Iran 2 Department of Biochemistry and Clinical Laboratories, Tel.: + 98/311/36115 115, Fax: + 98/311/36115 115 Tabriz University of Medical Sciences, Tabriz, Iran [email protected] 3 Infectious and Tropical Diseases Research Center, Department of Clinical Biochemistry, Tabriz University of ABSTraCT Medical Sciences, Tabriz, Iran Metabolic syndrome (MetS) has a collection of some abnormal 4 Department de Psychiatry et Neuroscience, Université and pathological conditions that cause many critical diseases. Laval, Québec, QC, Canada Resistin is one of the possible candidates for these pathologies 5 Centre Hospitalier de l’Université Laval (CHUL), Québec, but there are not enough data to prove if resistin has positive, QC, Canada neutral, or negative effects on one or some components of 6 Isfahan Cardiovascular Research Center, Cardiovascular MetS. This review summarizes data about comparing the ef- Research Institute, Isfahan University of medical fects and contribution of resistin in initiation and progression Sciences, Isfahan, Iran of MetS components and also its different actions between human and other mammalians. This summarized data about Key words the relationship of resistin and MetS components have been correlation, resistin, metabolic syndrome obtained from clinical researches and in some cases even ani- received 01.02.2018 mal studies. To find the relevant studies, the search in PubMed, accepted 22.05.2018 Science Direct, and Scopus were performed. Human and ani- mal studies on relationships between resistin and MetS (initi- Bibliography ation and progression of components) were included in our DOI https://doi.org/10.1055/a-0637-1975 search. In experiments reported among different human ge- Horm Metab Res 2018; 50: 521–536 netic groups as well as the patients with various disease such © Georg Thieme Verlag KG Stuttgart · New York as diabetes, no significant correlation is shown between FBG ISSN 0018-5043 and resistin level. Furthermore, this review shows that the re- sults of correlation between resistin and TG, HDL, and central Correspondence or abdominal obesity were inconsistent. These inconsistencies Dr. Mahtab Keshvari can arise from different sample size or genetic groups, gender, Isfahan Cardiovascular Research Center and also from experimental studies. Therefore, to obtain pre- Cardiovascular Research Institute cise results systematic review and meta-analyses are required. Introduction proinflammatory and prothrombotic (thrombosis) states, and vis- The term of metabolic syndrome (MetS) is applied for a major and ceral adipose tissue play a key role in the initiation and future patho- escalating group of risk factors that raises risk for public health and genesis of it and also its complications [3]. Adipose tissue is an ac- clinical challenge worldwide. The term “metabolic” refers to the tive endocrine organ capable of producing several regulatory me- biochemical processes involved in the body’s normal functioning. diators that is called adipokines. Adipokines have been shown to Risk factors are traits, conditions, or habits that increase the chance be involved in several biological processes. Several adipokines have of developing a disease [1, 2]. been illustrated to exert regulatory roles on cardiovascular risk fac- There is a cluster of metabolic risk factors for cardiovascular dis- tors, for example, inflammation, adipogenesis, lipid metabolism, eases and type-2 diabetes mellitus (T2DM). In the major compo- and oxidative stress [4, 5]. nents of metabolic syndrome, excess abdominal fat, atherogenic Resistin is an adipokine with 114 amino acids, belonging to the dyslipidemia, hypertension, hyperglycemia, insulin resistance, resistin-like family of proteins [6]. In humans, resistin is an adipo- Mostafazadeh M et al. Resistin and Metabolic Syndrome... Horm Metab Res 2018; 50: 521–536 521 Review cyte- and monocyte-derived cytokine, which modulates insulin ac- tions are significantly higher in females versus males. It has been tion, energy, glucose, and lipid homeostasis [7]. It has been pro- reported that in obese and diabetic patients, the serum level of re- posed that resistin might serve as a molecular link between inflam- sistin is significantly increased [6, 22]. Resistin expression in rodent mation, metabolic parameters, and vascular dysfunction, and can adipocytes is stimulated by high levels of glucose but suppressed thus contribute to the risk for MetS, T2DM, and cardiovascular dis- by tumor necrosis factor α (TNF-α) while human resistin is strong- ease (CVD) [8, 9]. However, studies show controversial role of re- ly induced by various inflammatory stimuli, including interleukin 6 sistin in regulating insulin sensitivity and obesity [10, 11]. There- (IL-6), IL-1β, lipopolysaccharide (LPS), TNF-α, and resistin itself in fore, the present study was aimed to compare the effects and con- PBMCs and macrophages [23]. tribution of resistin in initiation and progression of MetS components and also its different actions among human and other mammalians. Resistin Receptors According to the data obtained from animal and human studies, the receptor or receptors of resistin especially in human is not fully Methods for Review understood. But, Toll-like receptor 4 (TLR4) and adenylyl cyclase-as- An extensive search was performed in PubMed, Science Direct, sociated protein 1 (CAP1) are accepted as putative candidates for Scopus, and Google scholar to identify clinical and animal studies its receptors [24]. TRL family is expressed in various organisms in- on the correlation between resistin level and MetS components cluding mammalians. Among the reported 13 TLR (TLR1–13), TLR1 published from inception up to November 15, 2017. Search terms to 9 are both in human and mice, TRL10 is not functional in mice were (“Resistin” OR” Adipokines”) AND (“Metabolic Syndrome” OR but in human is active, and the other ones do not express in human “metabolic”). The search was performed in titles and abstracts that but only in mice [25–27]. TLR1, 2, 4, 5, 6, and 10 are present on the were restricted to articles published in English and sometimes cell surface, whereas the others are endosomal or lysosomal recep- French languages. All titles, abstracts, and full texts of potentially tors [25, 26]. relevant studies were assessed for eligibility. Papers were excluded TLRs participate essentially in immunologic pathways and are if: 1) data on exposure (Resistin) or outcome (Metabolic Syndrome) divided in some groups while each group has own signaling path- were not reported and 2) no data were reported on the relation- way (for more details, see ref. [26]). Among TLRs, TLR4 is proposed ship between exposure and outcome. to be the one of resistin membrane receptors that mediates its in- tracellular functions [28, 29]. In fact, TLR4 is considered as an im- munoreceptor that promotes the production of inflammatory sub- Resistin and its Secretion stances in macrophages but, for example, it can also mediate the Resistin (or ‘resistance to insulin’), also known as the adipose tis- effects of resistin in hypothalamus for activating proinflammatory sue-specific secretory factor, C/EBP-epsilon-regulated myeloid-spe- pathways [25, 29]. cific secreted cysteine-rich protein (XCP1), found in inflammatory TLRs are found in macrophages, neutrophils, dendritic cells, nat- zone 3, was discovered in 2001 by Lazar’s group from the Univer- ural killer cells, and mast cells of the innate-immune system; in T- sity of Pennsylvania, who named resistin for its ability to interfere and B-lymphocytes of the adaptive-immune system, as well as in with insulin action and is identified as a link between obesity and some non-immune cells, such as epithelial and endothelial cells diabetes [6, 12]. [30]. According to some evidences, among TLRs, TLR4 is unique Resistin, encoded by the RETN gene, is a secretory protein that because after binding to appropriate ligand, this receptor can un- belongs to the resistin like molecules family with a distinct expres- dergo endocytosis and follow its action as an internal receptor [31]. sion patterns and biological functions [13]. The resistin expression Up to now, it was found that many endogenous ligands can ac- is identified in several cell types including adipocytes [6, 14], intes- tivate TLR4. These include HSP22, EDA fibronectin, low molecular tinal epithelium, adrenal gland, stomach, skeletal muscle cells [15], weight fragments of hyaluronic acid, fibrinogen, and tenascin-C, testis [16], and possibly astrocytes [17]. The main source of ro- whereas lipoteichoic acid, LPS, CpG motifs of bacterial DNA, and dent’s resistin is the white adipose tissue. Resistin in mouse has an viral RNA are exogenous ligands [26, 32]. After binding the ligands, 11 kDa cysteine-rich polypeptide, and its gene (RETN) is located on TLR4 usually exerts its effects via two classic models of signaling chromosome 8A1. It is synthesized as a 114 amino acid (aa) pre- pathways. They are MyD88 (myeloid differentiation primary re- cursor, with a signal peptide of 20 aa and a 94 aa mature segment. sponse gene 88) and Toll-interleukin
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