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Start Over Creator Včelák, Josef

2. Endocrine disruptors, obesity, and cytokines: how relevant are they to PCOS?

Creator:
Šimková, Markéta, Vítků, Jana, Kolátorová Sosvorová, Lucie, Vrbíková, Jana, Vosátková, Michala, Včelák, Josef, and Dušková, Michaela
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
obezita, cytokiny, obesity, cytokines, bisphenols, parabens, liquid chromatography-mass spectrometry, 14, and 612
Language:
English
Description:
As environmental and genetic components contribute to the PCOS expression, we compared levels of endocrine disruptors, steroid hormones, cytokines, and metabolic parameters in twenty healthy, nine normal-weight PCOS women, and ten obese PCOS women. Steroid hormones, bisphenols (BPA, BPS, BPF, BPAF) and parabens (methyl-, ethyl-, propyl-, butyl-, benzyl-parabens) were measured by liquid chromatography-tandem mass spectrometry. Differences between the groups were assessed using the Mann-Whitney U test. Spearman correlation coefficients were calculated for the individual parameters relationship. Significantly higher levels of BPA, anti-Müllerain hormone, lutropine, lutropine/folitropine ratio, testosterone, androstenedione, 7β-OH-epiandrosterone, and cytokines (IL-6, VEGF, PDGF-bb), were found in normal-weight PCOS women compared to controls. Between normal-weight and obese PCOS women, there were no differences in hormonal, but in metabolic parameters. Obese PCOS women had significantly higher insulin resistance, fattyliver index, triglycerides, cytokines (IL-2, IL-13, IFN-γ). In healthy, but not in PCOS, women, there was a positive correlation of BPA with testosterone, SHBG with lutropine, and folitropine, while testosterone negatively correlated with SHBG. In obese women with PCOS, insulin resistance negatively correlated with SHBG and estradiol. No differences were observed in the paraben exposure. Levels of BPA were higher in PCOS women, indicating its role in the etiology. Obesity significantly worsens the symptoms., Markéta Šimková, Jana Vítků, Lucie Kolátorová, Jana Vrbíková, Michala Vosátková, Josef Včelák, Michaela Dušková., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

3. Familial hypocalciuric hypercalcemia in an index male: grey zones of the differential diagnosis from primary hyperparathyroidism in a 13-year clinical follow up

Creator:
Zajíčková, Kateřina, Dvořáková, Marcela, Moravcová, Jitka, Včelák, Josef, and Goltzman, David
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
fyziologie, physiology, bone mineral density, familial hypocalciuric hypercalcemia, calcium-sensing receptor, primary hyperparathyroidism, calcium-to-creatinine clearance ratio, 14, and 612
Language:
English
Description:
Familial hypocalciuric hypercalcemia (FHH) type 1, caused by a heterozygous inactivating mutation of the gene encoding the calcium-sensing receptor (CaSR), is characterized by mild to moderate hypercalcemia, hypocalciuria and inappropriately normal or elevated parathyroid hormone (PTH). FHH must be differentiated from primary hyperparathyroidism (PHPT) because parathyroidectomy is ineffective in the former. Herein, we report a 39-year-old male patient with a 13-year history of asymptomatic PTH-dependent hypercalcemia (mean calcium of 2.88 mmol/l; reference range 2.15-2.55 mmol/l) and calcium-tocreatinine clearance ratio (Ca/Cr) ranging from 0.007 to 0.0198, which is consistent with either FHH or PHPT. Although a family history of hypercalcemia was negative, and PET-CT with fluorocholine was suggestive of a parathyroid adenoma, genetic analysis of the CaSR gene identified a heterozygous inactivating mutation NM_000388.4:c.1670G>A p. (Gly557Glu) in exon 6 and a polymorphism NM_000388.4:c.1192G>A p. (Asp398Asn) in exon 4. The G557E mutation has been previously reported in a Japanese family in which all family members with the mutation had Ca/Cr below 0.01 consistent with FHH. The biochemical profile of FHH and PHPT may overlap. Our FHH patient with a G557E CaSR mutation illustrates that the differential diagnosis can be difficult in an index case with no family history, (false) positive parathyroid imaging and higher calciuria than expected for FHH. Calcium intake, vitamin D status and bone resorption might have contributed to the Ca/Cr variations over a 13-year clinical follow up. This case thus emphasizes the irreplaceable role of genetic testing of the CaSR gene when clinical evaluation is inconclusive., Kateřina Zajíčková, Marcela Dvořáková, Jitka Moravcová, Josef Včelák, David Goltzman., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

5. Insights into the physiology of C-peptide

Creator:
Vejražková, Daniela, Vaňková, Markéta, Lukášová, Petra, Včelák, Josef, and Bendlová, Běla
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
inzulin, diabetes mellitus, terapie, insulin, therapy, C-peptide, diabetes complications, 14, and 612
Language:
English
Description:
Current knowledge suggests a complex role of C-peptide in human physiology, but its mechanism of action is only partially understood. The effects of C-peptide appear to be variable depending on the target tissue, physiological environment, its combination with other bioactive molecules such as insulin, or depending on its concentration. It is apparent that C-peptide has therapeutic potential for the treatment of vascular and nervous damage caused by type 1 or late type 2 diabetes mellitus. The question remains whether the effect is mediated by the receptor, the existence of which is still uncertain, or whether an alternative non-receptor-mediated mechanism is responsible. The Institute of Endocrinology in Prague has been paying much attention to the issue of C-peptide and its metabolic effect since the 1980s. The RIA methodology of human C-peptide determination was introduced here and transferred to commercial production. By long-term monitoring of C-peptide oGTT-derived indices, the Institute has contributed to elucidating the pathophysiology of glucose tolerance disorders. This review summarizes the current knowledge of C-peptide physiology and highlights the contributions of the Institute of Endocrinology to this issue., Daniela Vejrazkova, Marketa Vankova, Petra Lukasova, Josef Vcelak, Bela Bendlova., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

6. Multiglandular parathyroid disease in primary hyperparathyroidism with inconclusive conventional imaging

Creator:
Zajíčková, Kateřina, Včelák, Josef, Lešková, Zuzana, Grega, Marek, Goltzman, David, and Zogala, David
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
multiglandular parathyroid disease, primary hyperparathyroidism, 18F-fluorocholine PET/CT, and persistent primary hyperparathyroidism
Language:
English
Description:
Inconclusive preoperative imaging is a strong predictor of multiglandular parathyroid disease (MGD) in patients with primary hyperparathyroidism (PHPT). MGD was investigated in a cohort of 17 patients with PHPT (mean age 64.9 years, total calcium 2.75 mmol/l and parathyroid hormone (PTH) 113.3 ng/l) who underwent 18F-fluorocholine PET/CT (FCH) imaging before surgery. The initial MIBI SPECT scintigraphy (MIBI) and/or neck ultrasound were not conclusive or did not localize all pathological parathyroid glands, and PHPT persisted after surgery. Sporadic MGD was present in 4 of 17 patients with PHPT (24 %). In 3 of 4 patients with MGD, FCH correctly localized 6 pathological parathyroid glands and surgery was successful. Excised parathyroid glands were smaller (p <0.02) and often hyperplastic in MGD than in single gland disease. In two individuals with MGD, excision of a hyperplastic parathyroid gland led to a false positive decline in intraoperative PTH and/or postoperative serum calcium. Although in one patient it was associated with partial false negativity, parathyroid imaging with FCH seemed to be superior to neck ultrasound and/or MIBI scintigraphy in MGD.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

8. Plasma levels of adipokines in patients with Alzheimer’s disease: Where is the "breaking point" in Alzheimer’s disease pathogenesis?

Creator:
Vaňková, Markéta, Vacínová, Gabriela, Včelák, Josef, Vejražková, Daniela, Lukášová, Petra, Rusina, Robert, Holmerová, Iva, Jarolímová, Eva, Vaňková, Hana, and Bendlová, Běla
Format:
počítač and online zdroj
Type:
model:article and TEXT
Subject:
Alzheimerova choroba, leptin, Alzheimer's disease, adiponectin, adipsin, bloodbased biomarker, 14, and 612
Language:
English
Description:
Peripheral insulin resistance is associated with decreasing adiponectin and increasing leptin plasma levels, and also with cognitive decline. The effects of adipokines on brain function have been published from both animal and human studies. In particular, the influence of leptin and adiponectin on the development of Alzheimer’s disease (AD) has been extensively investigated. However, the association between adipsin and AD is as yet unknown. In 37 patients with AD and 65 controls that followed the same study protocol, we tested whether adiponectin, leptin, and adipsin could be used as biomarkers in the early stages of AD. In contrast with conclusions of cognition studies in insulin resistant states, our study found a correlation of impaired neuropsychological performance with increasing adiponectin and decreasing leptin in AD patients. Nevertheless, no significant differences between patients and controls were found. AD women had significantly increased adipsin compared to controls, and there was a positive correlation of adipsin with age and disease duration. Although adipokines do not appear to be suitable biomarkers for early AD diagnosis, they certainly play a role in the pathogenesis of AD. Further studies will be needed to explain the cause of the adipokine “breaking point” that leads to the pathogenesis of overt AD., Markéta Vaňková, Gabriela Vacínová, Josef Včelák, Daniela Vejražková, Petra Lukášová, Robert Rusina, Iva Holmerová, Eva Jarolímová, Hana Vaňková, Běla Bendlová., and Obsahuje bibliografii
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public