MicroRNAs as Potential Regulators of Glutathione Peroxidases Expression and Their Role in Obesity and Related Pathologies.

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obesity 59 endocrinologydiseases
rosiglitazone 1 endocrinologydiseasesdrugs
diabetes mellitus 4 endocrinologydiseases
diabetic retinopathy 1 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
type 2 diabetes mellitus 2 endocrinologydiseases
childhood obesity 3 endocrinologydiseases
dexamethasone 1 endocrinologydiseasesdrugs
hyperinsulinemia 2 endocrinologydiseases
metabolic syndrome 2 endocrinologydiseases

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dexamethasone 37988 glucocorticoid-induced central fat accumulation. The overexpression of miR-27b-3p had similar effect as dexamethasone treatment on inhibition of brown adipose differentiation [[130]]. miR-27-3p directly regulates lysyl
rosiglitazone 5263 of obese individuals, with its expression being restored in mice by treatment with antioxidants or rosiglitazone [[12]]. GPx7 loss resulted in enhanced oxidative stress and increased adipose tissue mass in mice [[10]].
Select Disease Character Offset Disease Term Instance
childhood obesity 5487 Certain single nucleotide polymorphisms for GPx4–6 genes were found to be associated with prepubertal childhood obesity in Spain [[13]]. Taking together, the importance of GPx in obesity and related pathologies is evident.
childhood obesity 28007 fertility, an association of the single nucleotide polymorphism (SNP) rs445870 within GPx5 with higher childhood obesity was found, with a minor allele of this genetic variant related to an increase in body mass index (BMI)
childhood obesity 30318 huntingtin [[92]]. In addition, the association of SNP rs406113 of GPx6 gene was linked to a higher childhood obesity risk, with the minor allele of this genetic variant related to an increase in BMI [[13]].In GPx6 regulation,
diabetes mellitus 1894 excessive fat accumulation, associated with increased risk of chronic diseases such as metabolic syndrome, diabetes mellitus , and cardiovascular disease is increasing worldwide. In general, the elucidation of the molecular mechanisms
diabetes mellitus 10652 thickness as well as a prevalence of cardiovascular and peripheral vascular disease in patients with type 2 diabetes mellitus [[20]].Because GPx1 is major antioxidant enzyme catalyzing the breakdown of H2O2, it is not surprising
diabetes mellitus 12119 identified by more than one program, there are several miRNAs with known relationships to obesity, diabetes mellitus , and/or oxidative stress. The serum miR-376a-3p was significantly diminished in obese serum and could
diabetes mellitus 18581 induction by cytokines [[50]]. The study of miRNAs abundance in the serum samples from people with type 2 diabetes mellitus (T2DM) as compared to that of healthy individuals revealed five significantly different miRNAs, including
diabetic retinopathy 21263 disease and diabetes, miR-146a-5p was suggested as a potential therapeutic target for the treatment of diabetic retinopathy [[57]]. miR-146a-5p gene polymorphism was related to the increased risk of atherosclerosis in diabetic
glucose intolerance 24813 and presented in obesity as well as in more severe cardio-metabolic diseases including dyslipidemia, glucose intolerance , liver steatosis, cardiac fibrosis, and hypertrophy. Katunga et al. [[72]] proposed a model of GPx4
hyperglycemia 9758 consequences. The overexpression of GPx1 was shown to protect mice from acute oxidative stress, however, later hyperglycemia , hyperinsulinemia, insulin resistance, obesity, as well as increased β-cell mass developed. The lack
hyperinsulinemia 9773 overexpression of GPx1 was shown to protect mice from acute oxidative stress, however, later hyperglycemia, hyperinsulinemia , insulin resistance, obesity, as well as increased β-cell mass developed. The lack of H2O2 caused by
hyperinsulinemia 9996 overexpressed GPx1 can inhibit insulin signaling and cause the overproduction of insulin. Incidences of hyperinsulinemia caused by GPx1-overexpression were not diminished by dietary limitation [[11]]. Conversely, a deficiency
metabolic syndrome 1874 IntroductionObesity, defined as excessive fat accumulation, associated with increased risk of chronic diseases such as metabolic syndrome , diabetes mellitus, and cardiovascular disease is increasing worldwide. In general, the elucidation
metabolic syndrome 18011 consumption of long-chain polyunsaturated fatty acids; this miRNA is connected with an improvement of metabolic syndrome markers [[48]]. Interestingly, miR-144-5p, identified by three programs, is the other strand of commonly
obesity 767 important selenoproteins. Dysregulated GPx expression is connected with severe pathologies, including obesity and diabetes. We performed a comprehensive bioinformatic analysis using the programs miRDB, miRanda,
obesity 1188 reports on identified microRNAs, with a special focus on the microRNAs related to oxidative stress, obesity , and related pathologies. We identified many microRNAs with an association with oxidative stress and
obesity 1297 and related pathologies. We identified many microRNAs with an association with oxidative stress and obesity as putative regulators of GPxs. In particular, miR-185-5p was predicted by a larger number of programs
obesity 1700 expression. Through the bioinformatics analysis we revealed the potential connection of microRNAs, GPxs, obesity , and other redox imbalance related diseases.1. IntroductionObesity, defined as excessive fat accumulation,
obesity 2043 increasing worldwide. In general, the elucidation of the molecular mechanisms involved in promoting obesity and adipogenesis is of utmost importance [[1]]. To date, various platforms for identification of novel
obesity 2472 radical, and superoxide radical, are involved in the etiology of a wide range of diseases, including obesity and obesity-related pathologies. Excess cellular ROS accumulation has been shown to induce DNA damage,
obesity 2484 superoxide radical, are involved in the etiology of a wide range of diseases, including obesity and obesity -related pathologies. Excess cellular ROS accumulation has been shown to induce DNA damage, from point
obesity 4579 consequences, and that dysregulated GPx expression is connected with severe pathologies, including obesity and diabetes [[8],[9]].The relationship between GPxs and obesity has been observed in animal models
obesity 4644 with severe pathologies, including obesity and diabetes [[8],[9]].The relationship between GPxs and obesity has been observed in animal models as well as in human studies. The changed expression/activities of
obesity 4866 found in the adipose tissues of obese individuals [[10]]. GPx1 is considered to play important role in obesity , insulin resistance, and atherosclerosis. Specifically, the action of intracellular ROS required for
obesity 5497 nucleotide polymorphisms for GPx4–6 genes were found to be associated with prepubertal childhood obesity in Spain [[13]]. Taking together, the importance of GPx in obesity and related pathologies is evident.
obesity 5564 associated with prepubertal childhood obesity in Spain [[13]]. Taking together, the importance of GPx in obesity and related pathologies is evident. For this reason, findings regarding regulatory mechanisms that control
obesity 6680 development to cell death [[14]]. A variety of metabolic processes, studied in the context of diabetes and obesity are as well affected by miRNAs [[17]]. It is not surprising that miRNAs have been also found to control
obesity 7482 1–8. Using literature searches, we cross-referenced these miRNAs and their links to oxidative stress, obesity , and related pathologies. Furthermore, in each section, we first discuss the literature dealing with
obesity 9811 mice from acute oxidative stress, however, later hyperglycemia, hyperinsulinemia, insulin resistance, obesity , as well as increased β-cell mass developed. The lack of H2O2 caused by overexpressed GPx1 can inhibit
obesity 10405 polymorphism at codon 198, which leads to a Pro198Leu substitution, a change associated with morbid obesity [[10]], coronary artery disease, intracerebral hemorrhage, diabetic associated atherosclerosis, and
obesity 12110 Among miRNAs identified by more than one program, there are several miRNAs with known relationships to obesity , diabetes mellitus, and/or oxidative stress. The serum miR-376a-3p was significantly diminished in obese
obesity 16711 miR-185-5p is silenced the expression of GPx2 rises [[38]]. miR-185-5p involvement in oxidative stress, obesity , and diabetes has been shown in many studies. Oxidative stress regulates the expression of miR-185-5p,
obesity 19791 reduce systematic oxidative stress and to maintain the bioavailability of vascular nitric oxide.As obesity is linked to oxidative stress and inflammation, the involvement of Gpx3 has been studied several times,
obesity 20256 subjects [[12]]. On the contrary, one study from central Mexico reported that patients with overweight or obesity had increased serum levels of GPx3 [[55]].miR-92a-3p has repeatedly been reported in connection to oxidative
obesity 21910 differentiation [[60]]. The up-regulation of miR-146b-5p was also observed during the development of obesity in mice fed a high-fat diet [[1]]. miR-146b-5p was downregulated in monocytes of obese persons, and
obesity 24519 structural abnormalities [[71]].Variants of GPx4 resulting in diminished activity have been associated with obesity inflammation and cardiovascular diseases [[13]]. In a model of GPx4 haplo-insufficiency, a causal role
obesity 24729 causing significantly increased lipid peroxide-derived aldehydes was demonstrated and presented in obesity as well as in more severe cardio-metabolic diseases including dyslipidemia, glucose intolerance, liver
obesity 24963 fibrosis, and hypertrophy. Katunga et al. [[72]] proposed a model of GPx4 as a protective adaptation to obesity . Obesity/nutrient overload is linked to permanent oxidative stress and increased peroxidation is followed
obesity 26054 liver cells [[75]]. miR-324-3p was among decreased circulating miRNAs downregulated in gestational obesity , and is also associated with pregnancy weight gain [[76]] as well as was previously reported as an inducer
obesity 26810 acids resulted in downregulation of this miRNA, which indicates its involvement in the regulation of obesity development [[80]]. Finally, the overexpression of miR-1908-5p inhibited differentiation and promoted
obesity 28017 association of the single nucleotide polymorphism (SNP) rs445870 within GPx5 with higher childhood obesity was found, with a minor allele of this genetic variant related to an increase in body mass index (BMI)
obesity 28461 expressed in epididymis. This miRNA has a role in adipogenic differentiation and is also closely related to obesity [[84]]. However, the expression of miR-143-3p is not essential for differentiation, as demonstrated
obesity 30328 [[92]]. In addition, the association of SNP rs406113 of GPx6 gene was linked to a higher childhood obesity risk, with the minor allele of this genetic variant related to an increase in BMI [[13]].In GPx6 regulation,
obesity 30574 miRNAs has been predicted by at least three software programs. Several of these are clearly connected to obesity and obesity related pathologies.Among the predicted GPx6-interacting miRNAs, miR-185-5p regulates GPx1
obesity 30586 predicted by at least three software programs. Several of these are clearly connected to obesity and obesity related pathologies.Among the predicted GPx6-interacting miRNAs, miR-185-5p regulates GPx1 and GPx2
obesity 30803 with miR-146a/b-5p was predicted as a GPx3 regulator. For this reason, the role of these miRNAs in obesity and related pathologies is discussed in previous sections of the present article. The up-regulation
obesity 33432 expression in abdominal fat and white adipose tissue, higher plasma malondialdehyde levels, weight gain, obesity , and higher BMI. The results of many studies showed a protective role of GPx7 against fat accumulation
obesity 33727 surprise that many of the identified putative miRNAs as GPx7 regulators have shown an association to obesity and diabetes. One of the two conserved miRNAs identified by TargetScan as a potential regulator of GPx7
obesity 34318 family, the three members a, b, and c of which share a seed sequence and are all implicated in diabetes, obesity , and cardiovascular diseases regulating glucose homeostasis [[105],[106],[107]]. Among all of the reported
obesity 35091 are involved in glucose homeostasis and insulin sensitivity, and are as well broadly associated with obesity [[111]]. A recent meta-analysis of adipocyte differentiation and obesity studies revealed the great
obesity 35164 well broadly associated with obesity [[111]]. A recent meta-analysis of adipocyte differentiation and obesity studies revealed the great importance of let-7 family in adipogenesis [[112]]. On the other hand, the
obesity 35779 brown adipocyte regeneration and was proposed as an important therapeutic target for the treatment of obesity [[114]]. miR-204-5p promoted the adipogenic differentiation of mesenchymal cells and inhibited the activation
obesity 36769 [[120],[121],[122],[123]]. The therapeutic silencing of miR-33-5p in a mouse model of diet-induced obesity promoted the notion of whole-body oxidative metabolism [[124]]. miRNAs from both arms of mir-138 were
obesity 36945 miRNAs from both arms of mir-138 were predicted by two programs. miR-138-5p was proposed as a potential obesity biomarker, since its expression in serum was significantly higher in obese subjects [[17]]; miR-138-5p
obesity 39763 GPx8 were mentioned above, e.g., miR-185-5p or miR-133a-3p. Other interesting miRNAs in relation to obesity include miR-26b-5p, which is upregulated in mature adipocytes and may play a role in the development
obesity 39875 include miR-26b-5p, which is upregulated in mature adipocytes and may play a role in the development of obesity [[137]]. miR-26b-5p regulates the proliferation of human preadipocytes via the arrest of the G1/S transition
obesity 42577 oxidative stress and inflammation. Intriguingly, as inflammation has been shown to have a distinct role in obesity , the involvement of GPxs variants in obesity has been reported repeatedly. The oxidative stress responsive
obesity 42622 inflammation has been shown to have a distinct role in obesity, the involvement of GPxs variants in obesity has been reported repeatedly. The oxidative stress responsive miRNAs play a role in altering the expression
obesity 43162 recent thorough review by Brandao et al. summarizes the involvement of miRNAs in adipocyte formation and obesity [[146]]. The intersection of identified miRNAs as putative GPxs regulators and obesity studies is summarized
obesity 43249 formation and obesity [[146]]. The intersection of identified miRNAs as putative GPxs regulators and obesity studies is summarized in Table 2. Several of the mentioned miRNAs could possibly regulate more than
obesity 46834 selenoproteins [[38]].Interestingly both mature miRNAs from pre-mir-125a were reported in connection to obesity . Three GPxs were predicted to be regulated by miR-125a-3p, which was upregulated in the adipose tissue
obesity 47231 [[48]].Among redoximiRs, miR-34a-5p and miR-34c-5p were predicted to regulate three GPxs. In terms of obesity , miR-34a-5p seems to be extremely important, as a significantly increased expression of miR-34a-5p has
obesity 47516 subjects [[158]]. A study by Fu et al. [[159]] identified miR-34a-5p as a potential target for treating obesity -related diseases due to inhibition of beige and brown fat formation [[159]]. An increased level of miR-34a
obesity 48514 number of miRNAs was predicted to regulate two or more GPxs. Some of these show a clear association with obesity and related pathologies. We identified the most interesting candidates that are worth exploring further
obesity 48674 interesting candidates that are worth exploring further to clarify the conjunction of GPxs, miRNAs, and obesity . These findings might contribute to the understanding of the mechanisms of the development of obesity-related
obesity 48776 obesity. These findings might contribute to the understanding of the mechanisms of the development of obesity -related pathologies.Figure 1Correlation between 3′UTR length (nt) of selected genes and the number
obesity 49174 by each program used. Identified microRNAs in boxes have reported connection to oxidative stress and obesity .ijms-19-01199-t001_Table 1Table 1In silico prediction of miRNAs targeting 3′UTR of GPxs employing
obesity 49873 application.ijms-19-01199-t002_Table 2Table 2List of identified miRNAs as putative regulators of respective GPxs with reported obesity association.GeneIdentified miRNAObserved Effect *NoteReferenceGpx1miR-376a-3p↓obese serum[[17]]miR-367b-3p↓peripheral
obesity 50504 subjects[[67]]miR-4269↓in obese donors[[68]]miR-24-3p↑liver high fat diet mice[[70]]Gpx4miR-324-3p↓gestational obesity associated with pregnancy weight gain[[76]]miR-1908-5pinvolvement in regulation of obesity development[[80]]Gpx5miR-143-3p↓in
obesity 50594 mice[[70]]Gpx4miR-324-3p↓gestational obesityassociated with pregnancy weight gain[[76]]miR-1908-5pinvolvement in regulation of obesity development[[80]]Gpx5miR-143-3p↓in obese human subject[[86]]miR-194-5p↓liver - High fat maternal
obesity 50878 diet[[1]]↓in monocytes of obese persons[[61]]miR-9↑adipose tissue in obese pigs[[95]]Gpx7miR-29 family obesity related [[105]]let-7 familyobesity related[[112]]mir-133b-3p↓ adipose tissue in micehigh fat diet[[1]]miR-204-5p↑
obesity 50913 persons[[61]]miR-9↑adipose tissue in obese pigs[[95]]Gpx7miR-29 familyobesity related [[105]]let-7 family obesity related[[112]]mir-133b-3p↓ adipose tissue in micehigh fat diet[[1]]miR-204-5p↑ adipose tissue in
obesity 51186 micegenetically fat mice/high fat diet[[118], [119]]miR-138-5p↑serum of obese subjectspotential biomarker of obesity [[17]]miR-27b-3p↑atria in micehigh fat diet[[127]]GPx8miR-486-5p↑plasma of obese children[[139]]miR-223-3p↓in
type 2 diabetes mellitus 10645 thickness as well as a prevalence of cardiovascular and peripheral vascular disease in patients with type 2 diabetes mellitus [[20]].Because GPx1 is major antioxidant enzyme catalyzing the breakdown of H2O2, it is not surprising
type 2 diabetes mellitus 18574 induction by cytokines [[50]]. The study of miRNAs abundance in the serum samples from people with type 2 diabetes mellitus (T2DM) as compared to that of healthy individuals revealed five significantly different miRNAs, including

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