Endokrynologia Polska最新文献

Radioactive iodine therapy (RIT) is an effective, safe, and cheap method in benign and malignant thyroid diseases. There is still an unresolved question of whether RIT treatment also plays a role in the treatment of, for example, breast cancer, lung cancer, or glioblastoma multiforme (GBM). These studies are currently being carried out in rats in combination with genes, but it may be an interesting challenge to assess "pure" RIT alone, thanks to the expression of sodium iodide symporter (NIS), is effective in other organ nodules, both benign and malignant. Cloning of the NIS in 1996 provided an opportunity to use NIS as a powerful theranostic transgene. In addition, NIS is a sensitive reporter gene that can be monitored by high-resolution PET imaging using the radiolabels [¹²⁴I]sodium iodide ([¹²⁴I]NaI) or [18F] tetrafluoroborate ([¹⁸F]TFB). Based on published positron emission tomography (PET) results, [¹²⁴I]sodium iodide and internally synthesized [18F]TFB were compared in an orthotopic animal model of NIS-expressing glioblastoma. The results showed improved image quality using [¹⁸F]TFB. Based on these results, we will be able to extend the NIS gene therapy approach using non-viral gene delivery vehicles to target orthotopic tumour models with low-volume disease such as GBM. Is it possible to treat RIT alone without using the NIS gene in GBM? After all, the NIS symporter was detected not only in the thyroid gland, but also in different tumours. The administration of RIT is completely harmless; the only complication is hypothyroidism. Indeed, recently it has been shown that, for example, in the case of thyroid cancer, the maximum RIT is 37000 MBq (1000 mCi). When beneficial effects of therapy in GBM are not possible (e.g. neurosurgery, modulated electro-hyperthermia, chemotherapy, immunotherapy, cancer vaccines, or oncolytic viruses), could RIT provide a "revolution" using NIS?

Introduction: The most common cause of death in nonalcoholic fatty liver disease (NAFLD) is cardiovascular disease. Choroidal microvascular structure in the eye may be a predictor of systemic vascular disease. We aimed to evaluate the effects of NAFLD on the choroidal microvascular structure using enhanced depth optical coherence tomography (EDI-OCT).

Material and methods: This prospective study was conducted by evaluating a total of 96 patients, 52 with steatosis and 44 without steatosis. After anthropometric measurements and ultrasonography were performed in the Gastroenterology Clinic, venous blood samples were taken for biochemical examinations. Then, all patients underwent an eye examination by an ophthalmologist. Subfoveolar choroidal thickness (SFCT) values of the cases were measured with EDI-OCT. Choroid vascular index (CVI) measurements were obtained by dividing the subfoveal choroidal area in the EDI-OCT images into luminal and stromal areas using the image binarization technique (ImageJ). In statistical analysis, the chi-square test was used to compare categorical data, and the independent t-test and Mann-Whitney U test were used to compare quantitative data.

Results: The mean age of those with fatty liver was 41±15.7 years, and of those without fatty liver it was 46 ± 10.7 years. There was nostatistically significant difference between the groups in terms of age (p = 0.064). Body mass index (BMI), waist circumference (WC), glucose, uric acid, alanine aminotransferase (ALT), gamma glutamyl transpeptidase (GGT), total cholesterol (TC), ferritin, insulin, and Homestatic Model Assesment - Insuline Restistance (HOMA-IR) were statistically significantly higher in the NAFLD group. On the other hand, there was no statistically significant difference between the groups in terms of low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, triglyceride, and aspartate aminotransferase (AST) values. The mean SFCT was measured as 280.26 ± 23.68 microns in the NAFLD group, and 308.96 ± 18.57 microns in the control group. There was no statistically significant difference in SFCT between the groups (p = 0.077). CVI measurements were 0.63 and 0.65, respectively, and they were significantly lower in the group with NAFLD (p = 0.045).

Conclusions: This is the first study in the literature to compare patients with and without ultrasonographic fatty liver in terms of choroidal vascular changes. We found that the choroidal vascular index decreased in NAFLD. This result proves that NAFLD causes changes at the microvascular level and is a multisystemic disease.

The health of post-menopausal women has become of paramount concern due to the aging of the world's population. Concurrently, the prevalence of obesity among postmenopausal women is expected to increase, presenting a significant public health challenge. Although weight gain during menopause is a well-observed phenomenon, its underlying causes and mechanisms remain incompletely understood. This manuscript reviews the literature to explore potential hormonal factors and pathomechanisms contributing to obesity during perimenopause, aiming to identify pathogenic factors that can guide treatment selection. Menopause-induced hormonal changes, including hypoestrogenaemia, hypergonadotropinaemia, relative hyperandrogenaemia, growth hormone deficiency, leptin resistance, and chronic stress affecting the hypothalamic-pituitary-adrenal axis, have been implicated in the onset of obesity in perimenopausal women. These hormonal fluctuations, alongside lowered daily energy expenditure, lead to metabolic alterations that elevate the risk of developing metabolic disorders and cardiovascular diseases. Weight gain in perimenopausal women is associated with higher total and abdominal adipose tissue and lower lean body mass. Addressing this issue requires individualized behavioural management, supported by effective pharmacological therapy, and, when warranted, complemented by bariatric surgery. Modern obesity treatment therapies have demonstrated safety and efficacy in clinical trials, offering the potential to reduce excess body fat, improve metabolic profiles, lower cardiovascular risk, and enhance the quality and longevity of women's lives. In addition to standard obesity therapies, the article examines different treatment strategies based on obesity's pathogenic factors, which may offer promising options for treating obesity with or without complications in perimenopausal women. One such potential approach is menopausal hormone therapy (MHT), which hypothetically targets visceral obesity by reducing visceral adipose tissue accumulation, preserving metabolically active lean body mass, and improving lipid profiles. However, despite these reported benefits, gynaecological and endocrinological societies currently do not recommend the use of MHT for obesity prevention or treatment, necessitating further research for validation. Emerging evidence suggests that visceral obesity could result from hypoestrogenaemia during perimenopause, potentially justifying the use of MHT as a causal treatment. This highlights the importance of advancing research efforts to unravel the intricate hormonal and metabolic changes that occur during perimenopause and their role in obesity development.

Introduction: The antifracture efficacy of vitamin D is still controversial. The aim of this systematic review was to examine if the vitamin D trials were designed adequately to reliably assess its antifracture activity.

Material and methods: The electronic databases PubMed, Medline, Embase, Web of Science, and Cochrane Library were searched to identify clinical trials evaluating the antifracture efficacy of vitamin D in adults. We compared the protocols of the trials against the opinions of the American Society for Bone and Mineral Research (ASBMR), International Society for Clinical Densitometry (ISCD), National Osteoporosis Foundation (NOF), European Medicines Agency (EMEA) experts, and the consensus statement from the 2nd International Conference on Controversies in Vitamin D, and against the protocols of the trials of the medications with proven antifracture efficacy (bisphosphonates, teriparatide, abaloparatide, raloxifene, denosumab, romosozumab). We assessed the prospective character, study design, group description, number of patients, study duration, and vitamin D (serum examination and dosage) supplementation. A description of the desired characteristics of the study protocol was presented.

Results: Thirteen eligible trials were identified. All but 2 were conducted in the elderly population only. Nine trials were included in the final analysis. Serum 25-hydroxy vitamin D (25OHD) was not measured in a representative number of subjects before (except in 2 studies), during, or after treatment in any study.

Conclusions: The analysed studies did not conclusively assess the vitamin D antifracture efficacy in patients with prestudy low serum vitamin levels, due to the lack of assessment of whether sufficient doses of vitamin D were used. They informed about the relevant doses and preparations of vitamin D in particular groups (specific fracture risk, age, place of residence) only.

Introduction: Recent studies have shown that a decline in isletβ cells quality is due to β-cell dedifferentiation, not only β-cell apoptosis. Angiotensin (1-7) [Ang(1-7)] could attenuate high glucose-induced apoptosis and dedifferentiation of pancreaticβ cells by combining with MAS receptors. However, the mechanism of such action has not been elucidated. Recent studies have revealed that Wnt/β-catenin and forkhead box transcription factor O1 (FoxO1) are associated with β-cell dedifferentiation. Our study aims to explore whether the effects of Ang(1-7)on islet b cell dedifferentiation are mediated through the Wnt/β-catenin/FoxO1 pathway.

Material and methods: Isletβ cells were divided into 6 groups: a control group, a high-glucose group, high glucose with Ang(1-7) group, high-glucose with Ang(1-7) and A779 group, high-glucose with angiotensin(1-7) and CHIR99021 group, and high-glucose with CHIR99021 group. A779 is a kind of MAS receptor antagonist that blocks the action of Ang(1-7), and CHIR99021 is a Wnt pathway activator. The morphology of pancreaticβ cells was observed in each group after 48 hours of intervention. β-cell insulin secretory function and expressions of relevant factors were measured.

Results: Compared with the control group, the cell morphology became degraded in the high-glucose group and the capability of insulin secretion was reduced. Meanwhile, the expressions of matureβ cells markers [pancreatic and duodenal homeobox 1 (Pdx1) and MAF BZIP transcription factor A (MafA)] were reduced, while the expressions of endocrine progenitor cells makers [octamer-binding transcription factor 4 (Oct4) and Nanog] were increased. The addition of CHIR99021 resulted in profound deep destruction ofβ cells compared with the high-glucose group. However, such changes were dramatically reversed following the treatment of Ang(1-7). The addition of A779 significantly inhibited the improvement caused by Ang(1-7).

Conclusion: Ang(1-7) can effectively reverseβ cell dedifferentiation through Wnt/β-catenin/FoxO1 pathway. It might be a new strategy for preventing and treating diabetes.

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Adipose tissue is a large hormonally active organ that secretes several substances (adipokines), and an important site for the synthesis and metabolism of steroid hormones. With energy balance, the secretory and metabolic activity of adipose tissue determines the normal function of many organs, including the endocrine glands. However, in the course of overweight and obesity, adverse changes occur in the structure and function of adipocytes. Obesity-related adipose tissue dysfunction translates into a change in the profile of secreted adipokines, and it impairs steroidogenesis. These phenomena contribute to the development of obesity-related complications, which also affect the major tropic axes regulating the endocrine glands. However, there is increasing evidence that weight reduction is an effective treatment for obesity-related adipose tissue dysfunction, thereby restoring endocrine function. This narrative review presents the impact of adipose tissue on endocrine gland activity both in the physiological state and in obesity-related dysfunction. It also discusses how functional (related to excess adiposity) changes in the endocrine system can be restored with effective treatment of obesity.

Secondary hyperparathyroidism (SHPT) is one of the most common metabolic complications resulting from chronic kidney disease (CKD). The complexity of calcium and phosphate disorders associated with CKD is defined by the Kidney Disease Improvement Global Outcomes (KDIGO) working group as CKD-related mineral and bone disorders (CKD-MBD). The last update of the KDIGO guidelines on the conduct in CKD-MBD was published in 2017. The treatment of SHPT is based on 2 strategies: counteracting hyperphosphataemia and suppressing parathyroid hormone (PTH) secretion. Therapy should be based on optimally selected drugs, taking into account additional effects to reduce the risk of chronic complications and side effects. The creation of new drugs with a better safety profile, significant reduction of side effects, and greater efficiency in achieving target serum phosphorus and PTH values forces the gradual replacement of existing treatment with new pharmacotherapies. The aim of this study is to discuss the latest issues (in connection with the latest KDIGO guidelines) regarding the pathomechanism of secondary hyperparathyroidism and the current directions of the therapy in these disorders.