Endocrine regulations最新文献

Objective. Post-traumatic stress disorder (PTSD) is a complex psychiatric disorder that can develop after exposure to a severe traumatic event and is connected with behavioral changes and adult neurogenesis impairment. Atypical antipsychotics including aripiprazole (ARI) or enriched environment can ameliorate disturbances connected to PTSD. This study was aimed to reveal whether ARI treatment supplemented by improved living conditions, i.e. toy rotation (TR), will ameliorate behavioral outcomes and reverse assumed changes in neurogenesis more effectively than sole ARI treatment in a single prolonged stress (SPS) animal model of PTSD. Methods. Adult male Sprague-Dawley rats weighing 176-200 g were randomly assigned to 5 experimental groups: (1) VEH - control non-stressed animals injected with vehicle (VEH, 2% Tween 20 in the saline); (2) SPS - animals exposed to SPS injected with VEH; (3) SPS+ARI - SPS animals injected with ARI (5 mg/kg in VEH); (4) SPS+TR - SPS animals exposed to TR and injected with VEH; (5) SPS+ARI+TR - SPS animals exposed to TR and injected with ARI. Animals in TR groups were housed in the standard cages with two toys per cage, which were replaced every other day. Elevated plus maze (EPM), open field (OF), and novel object recognition test (NOR) were used to assess the anxiety-like behavior and learning/memory. Changes in gene and protein expression of selected neurogenic markers (BDNF, GFAP, Sox2, DCX, NeuN) and transcription factors (ΔFosB, pCREB) in the subventricular zone (SVZ) and the gyrus dentatus (GD) of the hippocampus were determined by semi-quantitative real-time PCR and immunohistochemistry, respectively. Results. SPS animals showed increased anxiety-like behavior that was suppressed by TR and ARI+TR treatment combination. Although SPS did not affect the expression of studied neurogenic markers, ARI treatment increased the expression of doublecortin in the SVZ and TR increased expression of NeuN in the GD of PTSD-like animals. TR enhanced ARI effect on NeuN expression in the SVZ. SPS induced increase of ΔFosB positive cells, which was reduced by ARI+TR complementary treatment. Conclusions. Obtained results indicate that TR, in contrary to ARI, suppressed the anxiety-like behavior in PTSD-like animals. SPS does not affect the neurogenic markers expression in the SVZ or GD, but ARI and TR or their combination seems to increase the survival of the newborn cells.

Objective. The aim of the study was to evaluate the influence of GHRL (rs696217) and LEPR (rs1137101) gene polymorphisms on weight loss dynamics and endocrine marker changes following various bariatric procedures. Patients and Methods. A total of 76 patients undergoing laparoscopic sleeve gastrectomy (LSG), gastric plication (LGCP), and gastric artery embolization (GAE) were genotyped for GHRL (rs696217) and LEPR (rs1137101). Body mass index (BMI), total weight loss (TWL), excess weight loss (EWL), and hormonal markers (ghrelin, leptin, adiponectin, resistin, HbA1c) were assessed preoperatively and at 3, 6, and 12 months postoperatively. Results. Carriers of the T allele of GHRL (rs696217) experienced significantly greater reductions in BMI, TWL, and EWL, particularly following LSG and GAE (p<0.05). A notable reduction in total ghrelin levels was observed in T allele carriers (up to -46.75%, p<0.001) 6 months after surgery. Improvements in resistin (p=0.0002) and HbA1c (p=0.014) levels were also more pronounced in this group. LEPR (rs1137101) polymorphism showed limited impact on outcomes after LGCP, but it was associated with improved TWL and EWL in A allele carriers after LSG (p=0.006 and p=0.016, respectively). Conclusion. The T allele of GHRL (rs696217) appears to be a promising predictive marker for greater metabolic and hormonal improvement following bariatric procedures targeting the ghrelin-producing stomach zones. LEPR (rs1137101) may also influence postoperative outcomes in a procedure-specific manner. These findings support the potential role of genetic screening in optimizing patient selection and predicting surgical success.

Sarcopenia, initially described as a disease of the elderly and its coexistence with obesity, now termed as 'sarcopenic obesity' (SO), are now emerging to be important health problems worldwide. Their relatively recent recognition as distinct clinical entities with growing research has shown an increasing prevalence of both sarcopenia and SO. There is a strong independent association, which exists between sarcopenia/SO, type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD). Studies investigating prevalence of sarcopenia/SO indicate considerable heterogeneity, likely due to the lack of a universally accepted definition, differences in age groups, gender, ethnicity, and socio-demographic factors of the population studied, apart from use of distinct diagnostic criteria and methods of estimation based on either muscle mass or strength.

Diabetes mellitus has become a major global health concern with increasing prevalence worldwide. Recent studies have highlighted the critical role of the circadian rhythm, the body's internal biological clock, in the pathogenesis of diabetes. The circadian system regulates glucose metabolism, insulin secretion, and energy homeostasis. Modern lifestyle factors such as sleep disturbances shift work and irregular eating patterns disrupt circadian rhythms promoting insulin resistance and glucose intolerance. At the molecular level, mutations or altered expression of clock genes contribute to diabetes development. Clinical and experimental evidence suggests that maintaining the circadian integrity can reduce the diabetes risk and the chronotherapy time-based treatment approaches may enhance the therapeutic efficacy. The future advances including genetic profiling, AI-assisted monitoring and microbiota modulation hold promise for improved diabetes management. This review comprehensively examines the relationship between diabetes and circadian disruption emphasizing the importance of circadian biology in preventing and treating the metabolic diseases.

Objective. The purpose of this study was to investigate the role of the HLA-DQA1 and HLADQB1 alleles in Indonesian children who had autoimmune thyroiditis (AITD) and Down syndrome (DS). Methods. At Dr. Soetomo Hospital, 49 DS-AITD patients and 42 controls participated in a cross-sectional study. Alleles of HLA-DQA1*0103 and HLA-DQB1*0401 were genotyped by PCRRFLP assays. Allelic relationships were assessed by statistical studies. Results. In the DS-AITD group, the HLA-DQA1*0103 and HLA-DQB1*0401 alleles were more frequently found. The HLA-DQB1*0303, *0402, and *0501/0604 alleles, on the other hand, were significantly more common in the control group. While the HLA-DQB1 *0303 (odds ratio [OR]=0.169, 95% confidence interval [CI]: 0.065-0.435, p=0.000) alleles significantly reduced AITD risk, the HLA-DQA1*0103 (OR=3.9, 95% CI: 1.552-9.797, p=0.003), and HLA-DQB1*0401 (OR=4.5, 95% CI: 1.326-15.277, p=0.010) alleles considerably increased AITD risk. Conclusion. HLA-DQA1*0103 and HLA-DQB1*0401 are risk alleles, while HLA-DQB1 *0303 are protective alleles for AITD in children with DS. Further studies are required to obtain more data on Indonesians with DS.

Objective. The objective of the present study was to determine if there would be statistically significant differences among apolipoprotein E genotypes in the responsiveness of members of a cluster of seven measures in persons with type 2 diabetes consuming a flaxseed oil supplement (FOS). The cluster of seven are: abdominal obesity, hypertension, platelet hyperaggregability, hyperglycemia, dyslipidemia (decreased serum levels of high-density lipoprotein cholesterol (HDLc) and increased serum levels of triglycerides), increased serum low-density lipoprotein (LDL) oxidation (LDL conjugated dienes) and increased inflammation. All cluster members exacerbate type 2 diabetes. Methods. Thirty-two patients with well-controlled type 2 diabetes participated in this double-blind, placebo (safflower oil supplementation (SOS))-controlled study consisting of three visits. Apolipoprotein E genotyping was done at visit one. The cluster of seven was assessed at each visit. Results. Only platelet aggregability decreased as the result of the FOS relative to placebo while it appeared that there might be some potential for FOS to decrease LDL conjugated dienes. No apolipoprotein E genotype affected any of the cluster of seven responsiveness. Conclusions. Identified apolipoprotein E genotypes played no role in the responsiveness of any member of the cluster of seven to FOS in this study.

Objectives. The aim of the present study was 1) to describe the phenotypic spectrum of non-21-alfa-hydroxylase deficiency (non-21-OHD) congenital adrenal hyperplasia (CAH) encountered in a tertiary care endocrine center; 2) to identify the key biochemical, hormonal, and genetic markers that aid in differentiating non-21-OHD CAH subtypes; 3) to highlight the diagnostic challenges faced in distinguishing non-21-OHD CAH from classic 21OHD CAH and other adrenal disorders; and 4) to discuss the clinical implications and management challenges associated with non-21-OHD CAH. Methods. A retrospective analysis identified 13 cases of non-21-OHD CAH out of 87 CAH patients between 2008 to 2022. Clinical, biochemical, imaging and genetic data were analyzed. The diagnosis was confirmed by hormonal assays and next-generation sequencing (NGS)-based genetic analysis. Results. Of the 13 cases, six patients had 11β-hydroxylase deficiency (11β-OHD), primarily presenting with precocious puberty, hypertension, and hyperpigmentation, with elevated ACTH, 17-hydroxyprogesterone (17-OHP), and suppressed renin levels. Three patients with 3β-hydroxysteroid dehydrogenase type 2 (3β-HSD2) deficiency were diagnosed in early infancy following salt-wasting crises. 17α-hydroxylase deficiency (17α-OHD) was diagnosed in three adolescent females presenting with primary amenorrhea, tall stature, hypertension, and elevated gonadotropins. One case of StAR deficiency was diagnosed at 45 days of life, presenting with adrenal crisis and severe adrenal insufficiency. Conclusion. Non-21-OHD CAH presents diagnostic challenges due to its varied clinical spectrum. Hypertension and hypokalemia are key differentiators for 11β-OHD and 17α-OHD, while steroid profiling (LC-MS) aids in diagnosing 3β-HSD2 deficiency. However, the most crucial aspect is the early diagnosis, which is a significant factor in preventing complications like hypertensive cardiomyopathy and adrenal crises.

Objective. Metabolic disorders such as essential hypertension (EH) have increasingly contributed to the global health burden. The aim of this study was to assess differences in the hematological parameters among hypertensive adults with and without cardiovascular comorbidity and to explore the association between the complete blood count (CBC) indices and the effectiveness of hypertension control, defined by achieving target blood pressure levels (TBPLs) of <140/90 mmHg. Methods. The study involved 140 outpatients with EH of municipal non-profit enterprise "Hulsk outpatient clinic of general practice of family medicine" of the Stryiv village council (Hylsk village, Zviahel district, Zhytomyr region, Ukraine), which were divided into 3 groups: 1) hypertensive patients without cardiovascular comorbidity (with EH only), 2) hypertensive patients with coronary artery disease (CAD), and 3) hypertensive patients with CAD and chronic heart failure (CHF). The CBC was examined using an automatic hematological analyzer BC-6000 ("Mindray", China). Results. When comparing the CBC indices in patients with EH versus normotensive individuals, statistically significant differences were found in total white blood cells (WBC) count, relative neutrophil, eosinophil, lymphocyte, monocyte counts, mean platelet volume (MPV), and platelet distribution width (PDW). Moreover, relative lymphocyte count (RLC) was lower by 7.05% (p=0.003) in the EH+CAD+CHF group compared to patients with EH only; relative monocyte count (RMC) was higher by 26.09% (p=0.004) and 23.91% (р=0.010) in the EH+CAD+CHF and the EH+CAD groups, respectively, compared to patients with EH only. MPV and PDW were higher by 12.77 % (p=0.022) and 5.66 % (p=0.021) in the EH+CAD group, respectively, compared to patients with EH only. In addition, significant differences were found in the RMC, which was higher in individuals who achieved TBPLs compared to individuals who did not achieve TBPLs (by 25.00% in the EH group, by 26.53% in the EH+CAD group and by 20.00% in the EH+CAD+CHF group). Conclusions. We demonstrated that in patients with EH+CAD relative monocyte count and MPV and PDW were significantly higher vs. patients with EH only; in patients with EH+CAD+CHF relative lymphocyte count was significantly lower and relative monocyte count was significantly higher vs. patients with EH only. Furthermore, both in hypertensive patients with cardiovascular comorbidity and patients without cardiovascular comorbidity, relative monocyte counts in individuals who achieved TBPLs was significantly higher than in individuals who did not achieve TBPLs. Improved understanding of the cellular mechanisms connecting monocyte count to blood pressure regulation could enhance our insight into the pathogenesis of EH and contribute to the development of more effective strategies for the prevention of hypertension incidents.