Endocrine regulations最新文献

{"title":"Role of medicinal plants in ameliorating the lipid and glucose levels in diabetes: A systematic literature review.","authors":"Phaik Har Yong, Tan Yee Qing, Meram Azzani, Deepa Anbazhagan, Zhi Xiang Ng","doi":"10.2478/enr-2025-0008","DOIUrl":"https://doi.org/10.2478/enr-2025-0008","url":null,"abstract":"<p><p><b>Objective.</b> Diabetes is a chronic disease that causes insulin resistance and destruction of β-cells in pancreas. It is highly associated with hyperglycemia and hyperlipidemia, which can cause microvascular and macrovascular complications. The aim of this systematic review was to evaluate the beneficial effects of medicinal plant extracts on ameliorating glucose levels and lipid profile in diabetic rats. <b>Methods.</b> A systematic review search was conducted using PubMed, Scopus, Google Scholar and ScienceDirect databases using combined terms. The data were extracted and selected by two reviewers under the PRISMA guidelines, which included 25 articles. These 25 articles were selected by the inclusion and exclusion criteria. The quality assessments of the articles were carried out by using the Risk of Bias tool and animal intervention studies. <b>Results.</b> A total of 4651 articles were identified by searching the databases. Articles in the amount of 4505 were then excluded after screening the title and abstract. The remaining 146 articles proceeded to eligibility analysis and finally 25 articles were included into systemic review studies. From the 25 articles reviewed, <i>Clerodendrum volubile</i> showed the highest reducing effect on the blood glucose levels and lipid profile in diabetic rats. <i>Solena amplexicaulis</i> showed the lowest effect on ameliorating glucose levels, while <i>Myrtus communis</i> demonstrated the lowest effect on improving lipid profile in diabetic rats. <b>Conclusion.</b> The reviewed medicinal plant extracts reviewed demonstrated promising efficacy in ameliorating the blood glucose and lipid levels in diabetic rats.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"57-77"},"PeriodicalIF":0.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of FTO protein with hyperandrogenism metabolic disturbances in women with polycystic ovary syndrome.","authors":"Sadaf Parveen, Saba Khan, Shagufta Moin, Asma Nigar, Mohammad Mustufa Khan, Roshan Alam","doi":"10.2478/enr-2025-0005","DOIUrl":"https://doi.org/10.2478/enr-2025-0005","url":null,"abstract":"<p><p><b>Objective.</b> Polycystic ovary syndrome (PCOS) is one of the commonest endocrinopathies in women characterized by hyperandrogenism, ovulatory dysfunction, and insulin resistance affecting 5-20% of reproductive-aged women worldwide. Recent studies have emphasized the role of the fat mass and obesity-associated (FTO) gene in the development of PCOS, specifically the rs9939609 A/T polymorphism, which is linked to an increased risk of PCOS. The study aimed to investigate the levels of FTO protein and its association with luteinizing hormone (LH), follicle-stimulating hormone (FSH) and anthropometric parameters in patients with PCOS compared to healthy controls. <b>Materials.</b> A total of 298 women, comprising 149 patients and 149 healthy controls, enrolled in the study. Anthropometric parameters (body mass index, BMI; waist circumference, WC; hip circumference, HC; waist-to-hip ratio, WHR), and hormonal assays (LH, FSH, LH/FSH ratio) were performed. FTO protein levels were measured by ELISA kit and their association with these parameters was analyzed. A receiver operator characteristic (ROC) curve analysis was performed to evaluate the discriminatory power of FTO protein levels in distinguishing PCOS cases and controls. A value p<0.05 was considered statistically significant. <b>Results.</b> FTO protein levels were significantly elevated in PCOS women with increased BMI, WC, HC, and WHR (p=<0.05). The mean of BMI showed a positive correlation with both WC (r=0.367, p<0.001) and HC (r=0.395, p<0.001). WC strongly correlated with HC (r=0.780, p<0.001) and WHR (r=0.465, p<0.001). LH significantly correlated with FSH (r=0.543, p<.001), and LH/FSH (r=0.553, p<.001). FTO protein showed a positive correlation with LH (r=0.364, p<0.001), and FSH (r=0.166, p<0.001). Additionally, a negative correlation of FTO protein with BMI (r=-0.190, p<0.05), WC (r=-0.277, p<0.05), and WHR (r=-0.408 p<0.001) was observed. The levels of FTO protein were significantly higher in PCOS patients compared to controls. Significant correlations were also found between FTO protein levels and the anthropometric or hormonal parameters. The AUC for FTO protein levels was 0.624 (p=0.550), indicating moderate discriminatory power, but lacking statistical significance. <b>Conclusion.</b> The study found that FTO protein levels are significantly higher in PCOS women correlating with anthropometric and hormonal parameters (increased LH, decreased FSH). This highlights potential involvement of FTO protein in the hormonal and metabolic disturbances characteristics of the syndrome indicating its biomarker character for the condition.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"33-41"},"PeriodicalIF":0.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hydrocortisone interacts with endoplasmic reticulum stress in hypoxic regulation of phosphoserine aminotransferase 1 gene expression differently in normal human astrocytes and glioblastoma cells.","authors":"Oleksandr H Minchenko, Anastasiia I Abramchuk, Yevgen P Khikhlo, Myroslava Y Sliusar, Oleh V Halkin, Olha Y Luzina, Serhiy V Danilovsryi, Yuliia M Viletska, Dmytro O Minchenko","doi":"10.2478/enr-2025-0007","DOIUrl":"https://doi.org/10.2478/enr-2025-0007","url":null,"abstract":"<p><p><b>Objective.</b> Endoplasmic reticulum (ER) stress and hypoxia are key factors for the effective growth of malignant tumors, including glioblastoma. The phosphoserine aminotransferase 1 (PSAT1) is an ER stress-responsive enzyme responsible for serine synthesis and necessary for tumor cell proliferation. The present study aims to investigate the regulation of the <i>PSAT1</i> gene expression in U87MG glioblastoma cells and normal human astrocytes by ER stress and hypoxia depending on hydrocortisone, a native stress hormone used for co-treatment of glioblastoma and other malignant tumors. <b>Methods.</b> The U87MG glioblastoma cells and normal human astrocytes were used. Hypoxia was introduced by dimethyloxalylglycine. Tunicamycin was used for the induction of ER stress. Further, the cells were treated with hydrocortisone. RNA was extracted from cells after 4 h exposure to hydrocortisone, tunicamycin, and hypoxia. The expression level of the <i>PSAT1</i> gene was studied by quantitative RT-PCR and normalized to ACTB mRNA. <b>Results.</b> We found that treatment of normal human astrocytes with hydrocortisone resulted in a decreased expression of the <i>PSAT1</i> gene, but its expression in glioblastoma cells was resistant to this hormone action. However, hypoxia did not significantly change the expression of the <i>PSAT1</i> gene in normal astrocytes, but strongly modified the effect of hydrocortisone on this gene expression. At the same time, hypoxia increased the expression of the <i>PSAT1</i> gene in glioblastoma cells independently of hydrocortisone. Tunicamycin decreased the expression of this gene in normal astrocytes, but increased it in glioblastoma cells. In addition, the impact of tunicamycin on <i>PSAT1</i> gene expression was suppressed by hypoxia in both normal astrocytes and glioblastoma cells and by hydrocortisone only in normal astrocytes. At the same time, the combined effect of hypoxia and hydrocortisone greatly enhanced the expression of the <i>PSAT1</i> gene in tunicamycin-treated normal astrocytes and especially glioblastoma cells. <b>Conclusion.</b> The results of this study showed that hydrocortisone differentially controls the regulation of <i>PSAT1</i> gene expression by ER stress and hypoxia in normal astrocytes and glioblastoma cells and that the combined effect of hydrocortisone and hypoxia greatly enhanced <i>PSAT1</i> gene expression in tunicamycin-treated cells.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"48-56"},"PeriodicalIF":0.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin degludec/insulin aspart (IDegAsp) treatment on glycemic control and weight in patients with insulin experienced uncontrolled type 2 diabetes mellitus: A retrospective observational study.","authors":"Ramazan Cakmak, Ozge Telci Caklili, Caner Kapar, Yunus Catma, Osman Faruk Bayramlar, Fulya Calikoglu, Kubilay Karsidag, Nevin Dinccag","doi":"10.2478/enr-2025-0006","DOIUrl":"https://doi.org/10.2478/enr-2025-0006","url":null,"abstract":"<p><p><b>Objective.</b> In this retrospective observational study, we aimed to evaluate the impact of insulin degludec/insulin aspart (IDegAsp) treatment on glycemic status, metabolic parameters, and weight/body mass index (BMI) change at a single tertiary diabetes center in Turkey. <b>Methods.</b> We conducted a retrospective cohort study of patients with type 2 diabetes who received IDegAsp treatment between October 2018 and November 2019 at the diabetes outpatient clinic. The patients who had inadequate responses (HbA1c ≥8%) to at least 3 months of experienced insulin (± oral antidiabetic drug [OAD]) treatment were included into the study. <b>Results.</b> One hundred patients (61% females) with a mean age of 61.7±10.0 years (range; 39-88 years) were analyzed. Mean fasting plasma glucose and HbA1c levels decreased by 3rd, 6th, 9th, and 12th months (p=0.010, p=0.007, p=0.027, and p=0.090, respectively and p<0.001, p<0.001, p<0.001, and p=0.001, respectively). Mean body weight and BMI values increased in the 3rd (83.1±15.6 kg and 31.6±5.7 kg/m2, repecitvely) and 6th (87.0±15.4 kg and 32.3±5.3 kg/m2, resepctively) months, although the changes were not statistically significant (p=0.10 and p=0.08, respectively). However, mean body weight returned to baseline levels by the 9th (80.8±17.0 kg and 30.5±6.4 kg/m2, respectively) and 12th (79.5±13.5 kg and 30.5±5.7 kg/m2, respectively) months (p=0.074 and p=0.400, respectively). <b>Conclusions.</b> IDegAsp can provide a significant decrease in HbA1c in a real-life setting. Although weight gain was observed in the first months of the treatment, this effect disappeared over time and decreased to the baseline levels.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"42-47"},"PeriodicalIF":0.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143988132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ectopic dopamine agonist-resistant macroprolactinoma to the clivus masquerading as a chordoma - A case report.","authors":"Ines Bayar, Atef Ben Nsir, Sana Abid, Bilel Ben Amor, Hela Marmouch, Asma Ben Mabrouk, Kais Maamri, Jamel Saad, Mehdi Darmoul, Ines Khochtali","doi":"10.2478/enr-2025-0002","DOIUrl":"10.2478/enr-2025-0002","url":null,"abstract":"<p><p><b>Objective.</b> Pituitary neuroendocrine tumors (PitNETS) are common intracranial tumors, but extrasellar or ectopic PitNETS are very rare and supposed to originate from some pituitary remnants. They are mostly found in sphenoidal sinus. But particularly, ectopic clival PitNETS are highly aggressive and can cause bone invasion and can be misdiagnosed as other lesions of the skull base such as chordomas. <b>Case Report.</b> We report a challenging case of an ectopic prolactin-secreting PitNET arising in the clivus in a young female presenting with secondary amenorrhea and sellar mass effect symptoms. On magnetic resonance imaging (MRI), the tumor showed osteolytic features that firstly oriented towards chordoma. Regarding the very high levels of prolactin that constantly exceeded 200 ng/mL, prolactinoma was indeed very presumable. Dopamine agonist treatment was progressively introduced to its maximal tolerated dose, but with neither hormonal response nor size reduction. Hence, surgical resection was decided and the patient underwent an endoscopic transsphenoidal resection of the tumor that was purely ectopic to the clivus. The diagnosis of prolactinoma was confirmed by pathological examination and immunohistochemical staining was intensely and diffusely positive for prolactin and focally for follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The surgery succeeded to normalize prolactin level, but with residual tumor on the fourth month MRI control. <b>Conclusion.</b> Management of these rare tumors should be individualized with multidisciplinary collaboration.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"10-16"},"PeriodicalIF":0.0,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of ERN1 endoribonuclease activity inhibition on <i>TOB1</i>, <i>HBEGF</i>, and <i>TWIST1</i> genes expression in U87MG glioblastoma cells.","authors":"Oleksandr H Minchenko, Myroslava Y Sliusar, Yuliia M Viletska, Olha V Rudnytska, Denys V Kolybo","doi":"10.2478/enr-2025-0004","DOIUrl":"10.2478/enr-2025-0004","url":null,"abstract":"<p><p><b>Objective.</b> It is known that inhibition of the endoplasmic reticulum transmembrane signaling protein (ERN1) suppresses the glioblastoma cells proliferation. The present study aims to investigate the impact of inhibition of ERN1 endoribonuclease and protein kinase activities on the <i>TOB1</i>, <i>HBEGF</i>, and <i>TWIST1</i> gene expression in U87MG glioblastoma cells with an intent to reveal the role of ERN1 signaling in the regulation of expression of these genes. <b>Methods.</b> The U87MG glioblastoma cells with inhibited ERN1 endoribonuclease (dnrERN1) or both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used. Cells transfected with empty vector served as controls. Wild-type glioblastoma cells were used for mRNA silencing. The expression level of the <i>TOB1</i>, <i>HBEGF</i>, and <i>TWIST1</i> genes and microRNA were studied by quantitative RT-PCR. <b>Results.</b> We found that inhibition of ERN1 endoribonuclease activity led to a strong down-regulation of <i>HBEGF</i> gene expression in glioblastoma cells and did not significantly change the expression of <i>TOB1</i> and <i>TWIST1</i> genes. At the same time, inhibition of both enzymatic activities of ERN1 strongly increased the expression of the <i>TOB1</i> gene and down-regulated <i>HBEGF</i> and <i>TWIST1</i> genes in glioblastoma cells. The expression of <i>TWIST1</i> gene increased, but <i>HBEGF</i> and <i>TOB1</i> genes significantly decreased in cells with silencing of ERN1 mRNA by specific siRNA. At the same time, silencing of XBP1 mRNA reduced the expression of <i>HBEGF</i> gene only. In addition, in glioblastoma cells with ERN1 knockdown, the level of miR-96-5p was suppressed, but miR-182-5p was increased and could promote post-transcriptional expression of <i>TWIST1</i>, <i>HBEGF</i>, and <i>TOB1</i> mRNAs. <b>Conclusion.</b> The results of the present study demonstrate that inhibition of ERN1 strongly up-regulated the expression of the anti-proliferative <i>TWIST1</i> gene through protein kinase activity of ERN1 and that decreased <i>HBEGF</i> and <i>TOB1</i> genes expression was also controlled preferentially by ERN1 protein kinase activity. These changes in the expression level of <i>TWIST1</i>, <i>HBEGF</i>, and <i>TOB1</i> genes may also contribute to ERN1 knockdown-mediated suppression of glioblastoma cells proliferation.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"24-32"},"PeriodicalIF":0.0,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipokine levels and T786C polymorphism of eNOS gene promoter correlation in patients with arterial hypertension.","authors":"Svitlana Pidruchna, Uliana Zakharchuk, Olga Svan, Bohdan Zablotskyi, Oleksandr Tokarskyy","doi":"10.2478/enr-2025-0003","DOIUrl":"10.2478/enr-2025-0003","url":null,"abstract":"<p><p><b>Objective.</b> Genetic factors contribute to the development of metabolic syndrome and subsequent arterial hypertension (AH). The study of the T786C polymorphism of the endothelial nitric oxide synthase (eNOS) gene in arterial hypertension is important as its correlation with adipokine imbalance is a novelty area to find associations between hypertension development, obesity, and heredity. The purpose of the current study was to investigate serum adipokines levels, depending on the T786C polymorphism of the eNOS in patients with arterial hypertension. <b>Methods.</b> We examined 86 patients with arterial hypertension who underwent the determination of the T786C-gene promoter eNOS allelic polymorphism by PCR with electrophoretic detection. Additionally, the serum adipokines (resistin, leptin, adipoleptin, and ghrelin) levels were determined using enzyme-linked immunosorbent assay. <b>Results.</b> In the patients with arterial hypertension, a significant increase in resistin level was found only in TC and CC genotype carriers of T786C, while adiponectin and leptin levels were significantly higher in all three genotypes (TT, TC, CC) compared to control healthy group. The most severe increase in the adipokine levels was observed in CC genotype, followed by TC geno-type. The antianorexic hormone ghrelin had an opposite trend, with the lowest levels found in CC, followed by TC, and TT genotypes of T786C promoter eNOS gene. Interestingly, ghrelin level in TT genotype patients was not statistically different from control healthy group. <b>Conclusions.</b> We demonstrated that CC and TC, compared with TT genotype carriers of the T786C polymorphism of the promoter eNOS gene, had significantly higher levels of all adipokines, except ghrelin, where an opposite trend was observed, which suggests their higher risk in development of more severe arterial hypertension with concomitant obesity, and other associated disorders.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"17-23"},"PeriodicalIF":0.0,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ERN1 signaling pathway of unfolded protein controls the expression of EDEM1 and its hypoxic regulation in glioblastoma cells.","authors":"Oleksandr H Minchenko, Vita O Hrebennykova, Yuliia M Viletska, Oksana S Hnatiuk, Myroslava Y Sliusar, Halyna E Kozynkevych, Dmytro O Minchenko","doi":"10.2478/enr-2025-0001","DOIUrl":"10.2478/enr-2025-0001","url":null,"abstract":"<p><p><b>Objective.</b> For the effective growth of malignant tumors, including glioblastoma, the necessary factors involve endoplasmic reticulum (ER) stress, hypoxia, and the availability of nutrients, particularly glucose. The ER degradation enhancing alpha-mannosidase like protein 1 (EDEM1) is involved in ER-associated degradation (ERAD) targeting misfolded glycoproteins for degradation in an N-glycan-independent manner. EDEM1 was also identified as a new modulator of insulin synthesis and secretion. The present study aims to investigate the regulation of the <i>EDEM1</i> gene expression in U87MG glioblastoma cells by hypoxia and glucose or glutamine deprivations depending on the knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1) with the intent to reveal the role of ERN1 signaling in the regulation of this gene expression and function in tumorigenesis. <b>Methods.</b> The U87MG glioblastoma cells (transfected by an empty vector; control) and ERN1 knockdown cells with inhibited ERN1 endoribonuclease and protein kinase (dnERN1) or only ERN1 endoribonuclease (dnrERN1) were used. Hypoxia was introduced by dimethyloxalylglycine (4 h). For glucose and glutamine deprivations, the cells were exposed to DMEM medium without glucose and glutamine, respectively, for 16 h. The expression level of the <i>EDEM1</i> gene was studied by quantitative RT-PCR and normalized to the ACTB mRNA. <b>Results.</b> It was found that inhibition of endoribonuclease and protein kinase activities of ERN1 led to down-regulation of <i>EDEM1</i> gene expression in glioblastoma cells. Moreover, the expression of this gene was also decreased after silencing ERN1 in glioblastoma cells. At the same time, the expression of <i>EDEM1</i> gene did not significantly change in cells with inhibited ERN1 endoribonuclease only. The expression of the <i>EDEM1</i> gene was increased under hypoxia in control U87MG cells, but resistant to hypoxia in cells with ERN1 knockdown. Furthermore, the expression of this gene was up-regulated under glucose and glutamine deprivations in control glioblastoma cells. However, the ERN1 knockdown increased the sensitivity of <i>EDEM1</i> gene expression to glucose and decreased to glutamine deprivations. <b>Conclusion.</b> The results of the present study demonstrate that inhibition of ERN1 down-regulated the expression of the <i>EDEM1</i> gene through protein kinase activity of ERN1 and that the regulation of this gene expression by hypoxia and nutrient supply, especially glucose, is differently controlled by ERN1 in glioblastoma cells.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between breast cancer and thyroid autoimmune disorders in southeast Iran: A case-control study.","authors":"Shahin Nosratzehi, Seyed Mehdi Hashemi, Abolfazl Payandeh, Ahmad Bolouri, Fahimeh Okati","doi":"10.2478/enr-2024-0030","DOIUrl":"https://doi.org/10.2478/enr-2024-0030","url":null,"abstract":"<p><p><b>Objective.</b> To better understand the role of thyroid hormones in regulating the growth of breast epithelial cells and the estrogen-like effects of these hormones, the present study was conducted to investigate the relationship between breast cancer and thyroid autoimmune disorders in southeast Iran women. <b>Methods.</b> In this case-control study, in the case group, all newly diagnosed breast cancer pa-tients referred to the oncology clinics in Zahedan city in years 2021‒2022 were studied. The num-ber of participants in each group was represented by 40 breast cancer patients. The control group was represented by women without breast cancer. The sampling method was simple or available using the nonprobability method. The presence or absence of thyroid dysfunction was checked using thyroid-stimulating hormone (TSH), free thyroxin (FT4), free triiodothyronine (FT3), anti-thyroid peroxidase (TPO), and anti-thyroglobulin (Tg) tests. <b>Results.</b> The mean age of participants was 47±11 years. The risk of subclinical hyperthyroid-ism was higher in subjects with breast cancer and about 8 times higher than in the healthy ones (OR=8.27). According to the value of OR=1, the risk of developing autoimmune thyroid disease was the same in individuals with breast cancer as in healthy individuals. The odds ratio of hypothy-roidism could not be calculated because the value in the control group was zero. <b>Conclusion.</b> The results of this study show that there are abnormal characteristics of the thy-roid gland in breast cancer patients compared to the control group. The incidence of subclinical hyperthyroidism was significantly increased in the breast cancer patients. However, there was no difference in the incidence of autoimmune thyroid disease between the two groups.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between serum thyroid hormone levels and symptoms severity in young children with autism.","authors":"Maria Kopcikova, Barbara Raskova, Ivan Belica, Jan Bakos, Hana Celusakova, Zuzana Chladna, Jana Zibolenova, Daniela Ostatnikova","doi":"10.2478/enr-2024-0031","DOIUrl":"https://doi.org/10.2478/enr-2024-0031","url":null,"abstract":"<p><p><b>Objective.</b> Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by impaired social interaction and communication, restrictive and repetitive patterns of behavior, interests and activities. The aim of this study was to determine the postnatal levels of thyroid hor-mones and investigate their association with the severity of ASD symptoms. <b>Methods.</b> The study included 56 children (46 boys and 10 girls) with ASD aged 24-42 months. For ASD diagnostics the Autism Diagnostic Observation Schedule - second version (ADOS-2) and the Autism Diagnostic Interview-Revised (ADI-R) - interview with the child's parents or guard-ians were used. Venous blood was drawn right after the diagnostic procedures to analyze serum thyroid-stimulating hormone (s-TSH), free triiodothyronine (s-fT3), and free thyroxine (s-fT4) levels. Linear regression analysis was conducted to assess the relationship between the concentra-tions of thyroid hormones and ASD symptoms severity. <b>Results.</b> Serum concentrations of measured hormones were within normal reference ranges in almost all children. Decline of s-TSH was significantly associated with an increase in the severity of impaired social interaction and impaired communication as rated by parents (ADI-R) and with a higher prevalence of stereotyped behavior as observed in the diagnostic examination (ADOS-2). A decrease in s-fT3 was associated with higher frequency of stereotyped behavior as assessed by parents (ADI-R). Neither sex nor age were significant predictors. <b>Conclusion.</b> Although thyroid hormone levels were normal, we demonstrated an association of thyroid hormones with ASD symptoms.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}