Endocrine regulations最新文献

{"title":"ERN1 dependent impact of glutamine and glucose deprivations on the pyruvate dehydrogenase genes expression in glioma cells.","authors":"Hanna O Shatokhina,&nbsp;Olena O Khita,&nbsp;Dmytro O Minchenko,&nbsp;Dariia O Tsymbal,&nbsp;Olha R Luzina,&nbsp;Serhiy V Danilovskyi,&nbsp;Myroslava Y Sliusar,&nbsp;Liudmyla O Levadna,&nbsp;Oleksandr H Minchenko","doi":"10.2478/enr-2022-0027","DOIUrl":"https://doi.org/10.2478/enr-2022-0027","url":null,"abstract":"<p><p><b>Objective.</b> The aim of the present study was to investigate the expression of pyruvate dehydrogenase genes such as PDHA1, PDHB, DLAT, DLD, and PDHX in U87 glioma cells in response to glutamine and glucose deprivations in control glioma cells and endoplasmic reticulum to nucleus signaling 1 (ERN1) knockdown cells, the major endoplasmic reticulum (ER) stress signaling pathway, to find out whether there exists a possible dependence of these important regulatory genes expression on both glutamine and glucose supply as well as ERN1 signaling. <b>Methods.</b> The expression level of PDHA1, PDHB, DLAT, DLD, and PDHX genes was studied by real-time quantitative polymerase chain reaction in control U87 glioma cells (transfected by empty vector) and cells with inhibition of ERN1(transfected by dnERN1) after cells exposure to glucose and glutamine deprivations. <b>Results.</b> The data showed that the expression level of PDHA1, PDHB, DLAT, and DLD genes was down-regulated (more profound in PDHB gene) in control glioma cells treated with glutamine deprivation. At the same time, ERN1 knockdown modified the impact of glutamine deprivation on the expression level of all these genes in glioma cells: suppressed the sensitivity of PDHB and DLD genes expression and removed the impact of glutamine deprivation on the expression of PDHA1 and DLAT genes. Glucose deprivation did not significantly change the expression level of all studied genes in control glioma cells, but ERN1 knockdown is suppressed the impact of glucose deprivation on PDHX and DLD genes expression and significantly enhanced the expression of PDHA1 and PDHB genes. No significant changes were observed in the sensitivity of PDHX gene expression to glutamine deprivation neither in control nor ERN1 knock-down glioma cells. The knock-down of ERN1 removed the sensitivity of DLAT gene expression to glucose deprivation. <b>Conclusion.</b> The results of this investigation demonstrate that the exposure of control U87 glioma cells under glutamine deprivation significantly affected the expression of PDHA1, PDHB, DLAT, and DLD genes in a gene specific manner and that impact of glutamine deprivation was modified by inhibition of the ER stress signaling mediated by ERN1. At the same time, glucose deprivation affected the expression of PDHA1, PDHB, PDHX, and DLD genes in ERN1 knockdown glioma cells only. Thus, the expression of pyruvate dehydrogenase genes under glutamine and glucose deprivation conditions appears to be controlled by the ER stress signaling through ERN1.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 4","pages":"254-264"},"PeriodicalIF":0.0,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40563320","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":"Assessment of the diagnostic performance of the 1 mg dexamethasone suppression test in class 3 obese patients.","authors":"Suleyman Baldane,&nbsp;M Celik,&nbsp;Levent Kebapcilar,&nbsp;Suleyman Hilmi Ipekci,&nbsp;Sedat Abusoglu,&nbsp;Huseyin Yilmaz,&nbsp;Husnu Alptekin","doi":"10.2478/enr-2022-0028","DOIUrl":"https://doi.org/10.2478/enr-2022-0028","url":null,"abstract":"<p><p><b>Objective.</b> This study was aimed to evaluate the prevalence of Cushing's syndrome and the diagnostic performance of the 1 mg dexamethasone suppression test in class 3 obese patients. <b>Methods.</b> Anthropometric measurements and other laboratory data, including 1 mg dexamethasone suppression test of 753 class 3 obese patients, who applied to the Endocrinology and Metabolism Outpatient Clinic for the pre-bariatric surgery evaluation between 2011 and 2020, were evaluated retrospectively. <b>Results.</b> An abnormal response to the 1 mg dexamethasone suppression test (cortisol ≥1.8 mcg/dl) was observed in 24 patients and the presence of Cushing's syndrome was confirmed by additional tests in 6 patients. The prevalence of abnormal dexamethasone suppression test was 3.18% and the prevalence of Cushing's syndrome 0.79%. The specificity value was determined as 97.5% for 1 mg dexamethasone suppression test with cortisol threshold value ≥1.8 mcg/dl. <b>Conclusions.</b> The prevalence of Cushing's syndrome was found to be low in class 3 obese patients and 1 mg of dexamethasone suppression test had a very sufficient performance for Cushing's syndrome screening in this patient group.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 4","pages":"265-270"},"PeriodicalIF":0.0,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40563322","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":"A rare case of poorly differentiated mixed neuroendocrine-nonneuroendocrine tumor of the caecum with long term survival: A case report.","authors":"Antonis Polymeris,&nbsp;Christina Kogia,&nbsp;Paraskevi Kazakou,&nbsp;Stavroula Psachna,&nbsp;Dimitrios Lilis,&nbsp;Maria Drakou,&nbsp;Konstantinos Michalakis,&nbsp;Dimitrios Ioannidis","doi":"10.2478/enr-2022-0026","DOIUrl":"https://doi.org/10.2478/enr-2022-0026","url":null,"abstract":"<p><p>A 59-year-old woman presented with flushing attacks accompanied by tachycardia and hypotension, which lasted approximately 30 to 60 minutes, underwent 18 years ago a gastrointestinal tumor resection. The histologic examination revealed a poorly differentiated mixed neuroendocrine/adenocarcinoma located in the caecum with regional metastases. Postoperatively, the patient received combined chemotherapy of 5-fluorouracil with interferon for six months and since has remained asymptomatic. Her examination revealed positivity for chromogranin A (CgA) and a-Fetoprotein (aFP) (580 ng/24 h, normal range 27-94, and 10 IU/mL, normal range 0-6, respectively). Urinary 5-hydroxy indole acetic acid excretion was remarkably high (41.8 mg/24 h, normal range 2-10 mg/24 h). An abdominal Magnetic Resonance Imaging scan revealed multiple focal loci in the liver whose histological examination revealed a carcinoid tumor confirmed by an Octreoscan. Additional uptake was noted on the right shoulder and the right sternum-clavicle joint confirmed by Tc-99m MDP scan. The patient received somatostatin analogue therapy followed by long-acting release octreotide analogue therapy (30 mg/month) showing a partial improvement of relevant biomarkers. Two years later, carcinoid syndrome symptoms reappeared and due to the tumors expression of somatostatin receptors the patient received peptide receptor radionuclide therapy with 177Lu-DOTATATE that resulted in both clinical and biochemical improvements.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 4","pages":"249-253"},"PeriodicalIF":0.0,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40578384","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":"Prolactinoma - which patients react favorably to cabergoline medication?","authors":"Savas Karatas,&nbsp;Yalcin Hacioglu,&nbsp;Taskin Rakicioglu","doi":"10.2478/enr-2022-0030","DOIUrl":"https://doi.org/10.2478/enr-2022-0030","url":null,"abstract":"<p><p><b>Objective.</b> Prolactinoma, as a common endocrine disorder and the most frequent type of pituitary tumor, acts primarily as a suppressor on the gonadal functions. It is generally successfully treated with dopamine agonists; however, treatment resistance still remains in an unneglectable ratio. In this study, we aimed to identify factors, which may play a role in the treatment response. <b>Methods.</b> Seventy-six patients with prolactinoma, who have been routinely followed between 2018 and 2022 in Istanbul Research and Educational Hospital Endocrinology Outpatient Clinic, were included into the study. Initial prolactin level, adenoma size, baseline weight, body mass index (BMI), glucose, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride levels were obtained from the patient's medical records. The patients were divided into two groups: treatment respondent and non-respondent (refractory) ones, according to treatment response in the duration as suggested by the guidelines. The treatment respondent and non-respondent groups were compared according to the initial and the 3rd month prolactin levels, adenoma size, weight, BMI, and metabolic values. <b>Results.</b> The initial tumor diameter was 15.27±10.62 mm in the refractory and 7.42±4.42 mm in the treatment respondent groups (p=0.01). The refractory group had higher prolactin baseline level 269.96±275.78 µg/l vs. 124.55±67.35 µg/l of the respondent group (p=0.01). The refractory group had higher the 3rd month prolactin level 50.97±52.55 µg/l vs. 29.70±27.31 µg/l of the respondent group (p=0.04). The refractory group had higher frequency of cystic/hemorrhagic adenoma (47.6%, n=11/21) (p=0.01), baseline pituitary failure (33.3%, n=7/21) (p=0.01), and baseline cavernous sinus invasion (25.8, n=5/21) (p=0.01). The treatment respondent group had lower initial body weight (69.54±17.51 kg vs. 83.29±16.21 kg) (p<0.01), and lower BMI (25.98±5.47 kg/m² vs. 27.69±6.42 kg/m²) (p=0.02). <b>Conclusions.</b> In this study, initial tumor size, male gender, weight, BMI, the 3rd month prolactin level, initial pituitary deficiency, and cystic/hemorrhagic component in pituitary imaging in patients with prolactinoma were associated with a lower treatment response.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 4","pages":"279-283"},"PeriodicalIF":0.0,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40563319","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 association between mental health and obesity in postmenopausal women: A systematic review.","authors":"Mona Mohamed Ibrahim Abdalla,&nbsp;Meram Azzani,&nbsp;Wahib Atroosh,&nbsp;Deepa Anbazhagan,&nbsp;Vinoth Kumarasamy","doi":"10.2478/enr-2022-0032","DOIUrl":"https://doi.org/10.2478/enr-2022-0032","url":null,"abstract":"<p><p>Postmenopausal women are at great risk of mental health deterioration, which may lead to morbidity and mortality. The decrement of mental health with aging is attributed to hormonal changes, lowered physical activity, sleep disturbances, economic factors, as well as modifiable variables such as smoking and obesity. Studies have shown controversial results on the association between obesity and mental health in postmenopausal women. This study is a systematic review of the evidence available on the association between obesity and mental health in postmenopausal women with the aim to identify the most reliable obesity measure that has been shown in association with mental health as well as the effective measures that have been practiced for improving mental health in postmenopausal obese women. CINAHL, Scopus, Science Direct and PubMed including Medline databases were searched. Out of 3,766 articles, 23 studies of average to good quality were included, out of which 17 were cross-sectional and 6 interventional. Out of the 17 studies, 12 showed a positive association between obesity and deterioration of mental health, 3 showed a negative association and two showed no association. From the interventional studies, 4 showed positive and two not significant impact of the intervention used on obesity and mental health. In conclusion, more studies showed a positive association between obesity, especially visceral obesity, and mental health issues particularly depression, anxiety, and sleep disorders. Combination of caloric restriction and exercise seems to have a better impact on the mental health of the postmenopausal in comparison with other interventions.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 4","pages":"295-310"},"PeriodicalIF":0.0,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40578385","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":"Mitochondria and mitochondrial disorders: an overview update.","authors":"Vibhuti Rambani,&nbsp;Dominika Hromnikova,&nbsp;Daniela Gasperikova,&nbsp;Martina Skopkova","doi":"10.2478/enr-2022-0025","DOIUrl":"https://doi.org/10.2478/enr-2022-0025","url":null,"abstract":"<p><p>Mitochondria, the cell powerhouse, are membrane-bound organelles present in the cytoplasm of almost all the eukaryotic cells. Their main function is to generate energy in the form of adenosine triphosphate (ATP). In addition, mitochondria store calcium for the cell signaling activities, generate heat, harbor pathways of intermediate metabolism and mediate cell growth and death. Primary mitochondrial diseases (MDs) form a clinically as well as genetically heterogeneous group of inherited disorders that result from the mitochondrial energetic metabolism malfunctions. The lifetime risk of the MDs development is estimated at 1:1470 of newborns, which makes them one of the most recurrent groups of inherited disorders with an important burden for society. MDs are progressive with wide range of symptoms of variable severity that can emerge congenitally or anytime during the life. MD can be caused by mutations in the mitochondrial DNA (mtDNA) or nuclear DNA genes. Mutations inducing impairment of mitochondrial function have been found in more than 400 genes. Furthermore, more than 1200 nuclear genes, which could play a role in the MDs' genetic etiology, are involved in the mitochondrial activities. However, the knowledge regarding the mechanism of the mitochondrial pathogenicity appears to be most essential for the development of effective patient's treatment suffering from the mitochondrial disease. This is an overview update focused on the mitochondrial biology and the mitochondrial diseases associated genes.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 3","pages":"232-248"},"PeriodicalIF":0.0,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40609576","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":"ACTH-secreting parotid acinic cell carcinoma unusually reported as a paraneoplastic syndrome.","authors":"Magdelene Doris Amoateng,&nbsp;Georges El Hasbani,&nbsp;Armando Vera,&nbsp;Jose Vargas,&nbsp;Abraham Rodriguez,&nbsp;Renu Cheriyan,&nbsp;Imran Siddiqui,&nbsp;Ilja Hulinsky","doi":"10.2478/enr-2022-0017","DOIUrl":"https://doi.org/10.2478/enr-2022-0017","url":null,"abstract":"<p><p>Paraneoplastic syndromes, induced by an immunological cross-reaction or hormone/peptide secretion, are an atypical presentation of tumors. Some tumors, such as small cell lung cancer and bronchial carcinoid, can be adrenocorticotropic hormone (ACTH) secreting tumors. Less commonly, parotid acinic cell carcinoma can be ACTH-secreting tumor leading to Cushing's syndrome. Few literature cases have described ACTH related paraneoplastic syndrome of parotid adenocarcinoma. Because of the rarity of the condition, little is known about the management and prognosis of this phenomenon. In this report, we highlighted the case of a 59-year-old male with a past medical history of parotid adenocarcinoma treated with surgery, chemotherapy, and radiation therapy presented with clinical and biochemical signs of hyperaldosteronism. Abdominal ultra-sound, computed tomography, and magnetic resonance imaging showed hepatic mass. Liver biopsy with immunohistochemistry confirmed the presence of parotid adenocarcinoma secreting ACTH. He is on paclitaxel and carboplatin medication with good clinical response.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 3","pages":"163-167"},"PeriodicalIF":0.0,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40609575","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":"Exposure to nanographene oxide induces gene expression dysregulation in normal human astrocytes.","authors":"Olha V Rudnytska,&nbsp;Yuliia V Kulish,&nbsp;Olena O Khita,&nbsp;Dmytro O Minchenko,&nbsp;Dariia O Tsymbal,&nbsp;Yuliia M Viletska,&nbsp;Myroslava Y Sliusar,&nbsp;Dariia D Trufanova,&nbsp;Oleksandr H Minchenko","doi":"10.2478/enr-2022-0023","DOIUrl":"https://doi.org/10.2478/enr-2022-0023","url":null,"abstract":"<p><p><b>Objective.</b> Nanographene oxide, an oxidation derivative of graphene, is considered to be one of the nanomaterials attractive for biomedical applications, although this nanomaterial is toxic. The increasing exploitation of graphene-based materials necessitates a comprehensive evaluation of the potential impact of these materials on the human health. Moreover, it is necessary to investigate in detail the mechanisms of its toxic effect on living cells particularly at the genome level. The present study aimed to evaluate the impact of low doses of nanographene oxide on the expression of key regulatory genes in normal human astrocytes. <b>Methods.</b> Normal human astrocytes, line NHA/TS, were exposed to low doses of nanographene oxide (1 and 4 ng/ml) for 24 h. RNA was extracted from the cells and used for cDNA synthesis. The expression levels of NAMPT, TSPAN13, BCAR3, BRCA1, PTGS2, P4HA1, and P4HA2 mRNAs as well as microRNAs were measured by quantitative polymerase chain reaction. <b>Results.</b> It was found that the low doses of nanographene oxide induced a dysregulation in the expression of the key regulatory genes in normal human astrocytes in dose-dependent (1 and 4 ng/ml) and gene-specific manner. Nanographene oxide also strongly suppressed the expression of <i>NAMPT</i>, <i>BCAR3</i>, and <i>TSPAN13</i> genes and significantly up-regulated <i>BRCA1</i>, <i>PTGS2</i>, <i>P4HA1</i>, and <i>P4HA2</i> ones with a more significant effect in P4HA1 and P4HA2 genes. The expression of miR-96-5p and miR-145-5p was also down-regulated in astrocytes treated with nanographene oxide in a dose-dependent manner. <b>Conclusion.</b> The data obtained demonstrate that the low doses of nanographene oxide disturbed the genome functions by changing the expression levels of key regulatory genes in gene-specific and dose-dependent manner. Moreover, a higher dose of nanographene oxide induced more pronounced changes in expression of genes indicating for both genotoxic and neurotoxic possible effects in the normal human astrocytes.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 3","pages":"216-226"},"PeriodicalIF":0.0,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40609577","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":"Prediction of the cognitive impairment development in patients with autoimmune thyroiditis and hypothyroidism.","authors":"Iryna I Kamyshna,&nbsp;Larysa B Pavlovych,&nbsp;Aleksandr M Kamyshnyi","doi":"10.2478/enr-2022-0019","DOIUrl":"https://doi.org/10.2478/enr-2022-0019","url":null,"abstract":"<p><p><b>Objective.</b> The aim of the present work is to define the risk factors that can affect the presence of a cognitive impairment and analyze the associations of the brain-derived neurotrophic factor (BDNF) gene polymorphism (rs6265), vitamin D receptor (VDR) gene polymorphism (rs2228570), and N-methyl-D-aspartate (NMDA) receptor gene polymorphism (rs4880213) with the cognitive impairment in patients with autoimmune thyroiditis and hypothyroidism in the Western Ukraine population and predict the development of cognitive disorders in these patients. <b>Methods.</b> The study involved 153 patients with various forms of thyroid pathology (hypothyroidism, autoimmune thyroiditis, elevated serum antibodies anti-thyroglobulin and anti-thyroid peroxidase). Cognitive impairment in the examined patients was evaluated based on the results of the Mini-Mental State Examination (MMSE) test. BDNF, GRIN2B, and 25-OH Vitamin D levels in the serum of the patients and healthy individuals were quantified using highly sensitive commercial enzyme-linked immunosorbent assay kits. Genotyping of the VDR (rs2228570), BDNF (rs6265), and NMDA receptor (rs4880213) gene polymorphism was performed using TaqMan probes and Taq-Man Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions. <b>Results.</b> Strong direct relationship between the \"Level GRIN2B\" and cognitive impairments (p=0.006) was established after evaluating the complex model based on the values of the regression coefficient. An increase in the likelihood of cognitive impairment by 24.898-fold (p=0.012) was seen after assessing the effect of the CT rs6265 genotype. In addition, direct relationship between the influence of the TT rs6265 genotype and an increase in the likelihood of cognitive impairment by a factor of 21.734 (p=0.024) was also established. <b>Conclusion.</b> The present data indicate that the BDNF, TSH, fT4, and vitamin D levels prognostically belong to the significant indicators of the cognitive impairment development.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 3","pages":"178-189"},"PeriodicalIF":0.0,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40609580","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":"Comorbid overweight/obesity and chronic pancreatitis exacerbate the dyslipidemia progression in type 2 diabetic patients.","authors":"Mariya Marushchak,&nbsp;Kateryna Kozak,&nbsp;Inna Krynytska","doi":"10.2478/enr-2022-0018","DOIUrl":"https://doi.org/10.2478/enr-2022-0018","url":null,"abstract":"<p><p><b>Objective.</b> The aim of present study was to analyze the serum lipid profile parameters in patients with type 2 diabetes mellitus (T2DM) and comorbidities [overweight/obesity and/or chronic pancreatitis (CP)] to determine the contribution of these pathologic factors to lipid metabolism disorders in T2DM. <b>Methods.</b> The study involved 579 type 2 diabetic (T2D) patients with comorbid overweight/ obesity and/or CP. The serum lipid panel parameters [total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C)] were determined by commercially available kits on a Cobas 6000 analyzer (Roche Hitachi, Germany). Low-density lipoprotein cholesterol (LDL-C), non-HDL-C, and remnant cholesterol (RC) levels were calculated using formulas. The data were statistically analyzed using STATISTICA 7.0. <b>Results.</b> It was shown that dyslipidemia in T2D patients is characterized by unidirectional changes regardless the presence/absence of comorbid overweight/obesity or CP. At the same time, the most severe dyslipidemia was detected in T2D patients with a combination of comorbid over-weight/obesity and CP. Both the elevated body mass index (BMI) and CP can aggravate lipid metabolism disorders in T2DM. In our study, however, the BMI increase positively correlated with the number of dyslipidemia patients characterized by exceeding all target lipid levels for diabetic patients. This is in contrast to T2D patients with normal body weight and comorbid CP, in whom only LDL-C and TG exceeded the target lipid levels. <b>Conclusions.</b> A combination of comorbidities, such as obesity and CP in T2D patients, produced a mutually aggravating course defined particularly by common pathogenic links, insulin resistance, chronic generalized low-intensity inflammation, endothelial dysfunction, and dyslipidemia caused primarily by triglyceridemia.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"56 3","pages":"168-177"},"PeriodicalIF":0.0,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40597388","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}