International Journal of Endocrinology最新文献

Objective: To evaluate the association between sleep duration with serum estradiol concentrations and its variation by sex and age in American adults. Methods: Data were analyzed for 5406 men and women (≥ 20 years old) who participated in the cycles of the National Health and Nutrition Examination Survey 2013-2016, a cross-sectional study. Total estradiol (pg/mL) was measured and categorized (low, normal, and high) based on the NHANES protocol. Sleep duration was classified as ≤ 6, 6-9, and ≥ 9 h. Weighted multivariable adjusted and multinomial logistic regression models were conducted to assess these associations. Results: Our multivariable multinomial logistic regression analysis revealed no significant associations between sleep duration and serum estradiol concentrations among both American men and women. Specifically, comparisons of sleep durations (≤ 6 and ≥ 9 h) to the reference group (6-9 h) across various age categories showed odds ratios for low and high estradiol concentrations that remained statistically nonsignificant in fully adjusted models. These findings suggest that, unlike previous studies linking sleep duration with variations in other hormones, estradiol concentrations do not appear to be significantly affected by differences in sleep duration in either sex across all age groups studied. Conclusion: The lack of significant associations between sleep duration and serum estradiol concentrations indicates that sleep duration may not influence estradiol levels in the general population of American men and women. These results underscore the importance of continued research into how sleep influences hormonal balance. However, it is important to note that the NHANES data we used are from a cross-sectional study, which cannot establish a causal relationship between sleep duration and serum estradiol. Future studies should investigate additional factors, such as genetic predispositions, lifestyle habits, and environmental influences, that may modulate the relationship between sleep and hormone levels.

Prolactinomas (PRLs) are benign tumors with malignant characteristics that can invade the surrounding tissue structures and are challenging to treat. It has been reported that miR-21-5p expression in pituitary adenomas is correlated with tumor invasion and size. However, the mechanism of action of miR-21-5p in PRL remains unclear. Dysregulation of the phosphoinositide-3-kinase (PI3K) regulatory Subunit 1 pathway occurs frequently in cancer and plays an important role in tumor progression as an important component of the PI3K pathway. However, the role of PIK3R1 in PRL and its regulatory mechanism are unknown. In this study, we first explored the effect of miR-21-5p in PRL and then confirmed that PIK3R1 is a direct target of miR-21-5p using bioinformatics and cellular experiments. Subsequent in vitro experiments demonstrated that overexpression of PIK3R1 significantly attenuated the biological effects of miR-21-5p in PRL cells, such as promoting proliferation and invasion. Finally, we explored the mechanism by which PIK3R1 affects PRL progression and found that the inhibition of IκBa degradation by PIK3R1 impacts PRL progression via the miR-21-5p/PIK3R1/MMP pathway.

Introduction: Endogenous estrogen has a protective cardiovascular effect. Estrogen loss, such as during menopause and amenorrhea, results in stiffer vessels and endothelial dysfunction. It is unknown if reversing amenorrhea and regaining a regular menstrual cycle leads to the restoration of cardiovascular function. Methods: Sixteen women were divided into groups: eumenorrheic (n = 10; 23 ± 3 years) women who had a consistent menstrual cycle and amenorrheic (n = 6; 22 ± 1 year) women who previously were without their menstrual cycle for at least 6 consecutive months. Endothelial function, arterial stiffness, and brachial and aortic blood pressure were assessed. Results: There were no differences between groups in endothelial function or arterial stiffness measures. The previously amenorrheic group displayed lower brachial systolic and mean pressures and aortic systolic, diastolic, and mean pressures. When controlling for physical activity, only central pressure remained significantly lower in the amenorrheic group. Conclusions: Previous amenorrhea in young women does not result in long-term cardiovascular consequences in arterial and endothelial function measures assuming regular menstruation resumes. Physical activity shows a blood pressure-lowering effect in the peripheral arteries, while the previously amenorrheic group demonstrated lower central pressures, independent of physical activity.

The purpose of this review is to investigate the impacts of blood glucose fluctuations on diabetic osteoporosis, a complication of Type 2 diabetes mellitus (T2DM) that remains poorly understood. We reviewed the current evidence of the relationship between blood glucose fluctuations and diabetic osteoporosis in patients with T2DM. The findings indicate that blood glucose fluctuations may contribute to inhibiting the processes of bone formation and resorption, promoting diabetic osteoporosis and fractures in T2DM. Mechanistic studies, both in vitro and in vivo, reveal that these effects are largely mediated by oxidative stress, advanced glycation end products, inflammatory mediators, and multiple pathways inducing cell apoptosis or autophagy. Thus, maintaining the long-term stability of blood glucose levels emerges as a target to be pursued in clinical practice in order to safely reduce mean blood glucose and for its direct effects on osteoporosis and fractures in T2DM.

Background: This study aimed to investigate the potential mechanisms of puerarin in alleviating diabetic nephropathy (DKD) in mice. Method: The DKD model was induced by multiple low-dose injections of streptozotocin (STZ) and a high-sugar and high-fat diet in male C57BL/6J mice. After confirming the onset of DKD, mice were given irbesartan, distilled water, or different concentrations of puerarin (40 and 80 mg/kg/d) by gavage for 8 weeks. HE staining and PAS staining were adopted to assess the pathological changes in the kidney tissues. Meanwhile, the levels of superoxide dismutase, catalase, creatinine, and cystatin C in the serum and the urine albumin and creatinine were measured, and the renal indices as well as the urinary albumin-to-creatinine ratio (UACR) were calculated. The changes of podocin and protein expression levels associated with AMPK/Nrf2 signaling pathway were evaluated by western blot. Results: Puerarin significantly reduced the level of fasting blood glucose, renal index, glomerular mesangial expansion index, renal function, and oxidative stress induced by STZ (p < 0.05). The pathological injuries in kidney tissues were also alleviated. Furthermore, we demonstrated that the expression level of podocin and protein related to the AMPK/Nrf2 signaling pathway was also decreased significantly by the treatment of puerarin. At the same time, the efficacy of puerarin in the treatment of DKD was better than that of irbesartan, and the treatment effect of the high-dose group (80 mg/kg/d) was also significantly better than that of the low-dose group (40 mg/kg/d). Conclusion: Puerarin could attenuate the severity of DKD and protect the podocyte in mice in a dose-dependent way. Also, it might be performed by regulating the AMPK/Nrf2 pathway. These findings may provide a theoretical basis for updating the clinical management of DKD.

Type 2 diabetes mellitus (T2DM), a metabolic disorder, has the hallmarks of persistent hyperglycemia, insulin resistance, and dyslipidemia. Protein-tyrosine phosphatase 1B (PTP1B) was found to be overexpressed in many tissues in the case of T2DM and involved in the negative regulation of insulin signaling. So, PTP1B inhibition can act as a therapeutic target for T2DM. Numerous studies claimed the anti-inflammatory, hypoglycemic, hepatoprotective, and hypolipidemic activities of Dodonaea viscosa. Previously, we generated the high-fat diet (HFD)-low dose streptozotocin (STZ)-induced diabetic male mice model and treated it with a PTP1B inhibitor (5, 7-dihydroxy-3, 6-dimethoxy-2- (4-methoxy-3- (3-methyl-2-enyl) phenyl)-4H-chromen-4-one), isolated from Dodonaea viscosa. In the current study, we aimed to investigate the De novo lipogenesis, adipocyte differentiation, augmentation of lipoproteins clearance, fatty acid uptake, antilipolysis activity, and hepatic steatosis of PTP1B inhibition in adipose and liver tissues of the HFD-STZ-induced diabetic mice model. We found the retrieval of normal morphology of adipocytes and hepatocytes in the compound-treated group. The biochemical parameters showed the gradual reduction of LDL, VLDL, TC, and TG in the serum of the compound-treated group. To further test our hypothesis, real-time PCR was performed, and data revealed the reduction of PTP1B and other inflammatory markers in both tissues, showing enhanced expression of insulin signaling markers (INSR, IRS1, IRS2, and PI3K). Our compound upregulated the adipogenic (PPARγ), lipogenic (SREBP1c, FAS, ACC, and DGAT2), lipoprotein clearance (LPL, LDLR, and VLDLR), fatty acid uptake (CD36 and FATP1), and lipid droplet forming (FSP27 and perilipin-1) markers expressions in adipocytes and downregulated in hepatocytes. Furthermore, we found elevated cholesterol efflux (in adipose and liver) and decreased lipolysis in adipocytes and elevated in hepatocytes. Hence, we can conclude that our compound protects the adipocytes from abrupt lipolysis and stimulates adipocyte differentiation. In addition, it plays a hepatic protective role by shifting clearance and uptake of lipoproteins and fatty acids to the peripheral tissues and retrieving the fatty liver condition.

Purpose: This study aimed to verify the effect of angiotensin (1-7) on improving islet function and further explore the signaling pathway that may be involved in this improvement. It also aimed to explore the effects of angiotensin (1-7) on blood glucose levels, islet function, and morphological changes in db/db mice and its potential signal pathway. Methods: Forty-five db/db mice were divided randomly into a model control group and different doses of angiotensin (1-7) intervention groups (0, 150, 300, and 600 μg/kg/d), while seven db/m mice were assigned as the normal control group. The angiotensin (1-7) intervention groups received daily intraperitoneal administration for 8 weeks, whereas the normal control group was injected intraperitoneally with an equal volume of normal saline every day for 8 weeks. Changes in weight and food intake of mice were detected. Effect of angiotensin (1-7) on lipid metabolism, islet function, the morphology of pancreatic islets, and β-cell mass on mice were evaluated. The expression of PDX-1 and GCK in pancreatic tissue was verified. Results: The group receiving angiotensin (1-7) at a dosage of 600 μg/kg/d showed a significant decrease in body weight, triglyceride levels, and fasting blood glucose, along with an improvement in glucose tolerance. In the 300 μg/kg/d group, angiotensin (1-7) tended to increase the total volume of islets. Moreover, the intervention groups exhibited a significant increase in the ratio of β cells, small islets (30-80 μm in diameter), as well as the expression levels of PDX-1 and GCK in pancreatic tissue. Conclusion: Angiotensin (1-7) could improve glucose and lipid metabolism and islet function by promoting the expression of PDX-1 and GCK genes in the pancreas of db/db mice.

Patients with atrial fibrillation (AF) are linked to an increased risk of cognitive dysfunction, and serum uric acid levels play an important factor in cognitive dysfunction. However, the optimal serum uric acid level in patients with AF remains unclear. Therefore, we aimed to explore the relationship between serum uric acid and cognitive dysfunction. 583 patients were conducted in the Affiliated Hospital of Jining Medical University. Cognitive dysfunction was assessed by the Montreal Cognitive Assessment (MoCA). The relationship between serum uric acid levels and the risk of cognitive dysfunction in patients with AF was analyzed using the smoothing spline fitting model and threshold analysis. The average serum uric acid level was (383.26 ± 110.11) μmol/L, and the incidence of cognitive dysfunction was 79.76%. There was a non-linear relationship between serum uric acid levels and the risk of cognitive dysfunction in patients with AF, and the inflection point was 352 μmol/L. At the left of the inflection point, the relationship was significant (OR = 1.02, 95% CI = 1.00-1.04). At the right of the inflection point, there was no statistical difference (p=0.101). When serum uric acid levels are less than 352 μmol/L, the risk of cognitive dysfunction increases by 2% for each unit increase in serum uric acid levels in patients with AF. The study provides evidence for the treatment of serum uric acid levels in patients with AF.

In this study, we evaluated the effects of intrabursal administration of cabergoline and N-acetylcysteine on ovarian hyperstimulation syndrome (OHSS) in an immature rat model. The study assessed body, ovarian, and uterine weights, as well as the concentrations of vascular endothelial growth factor A (VEGF-A). Moreover, levels of MDA, 4-HDA, and nitrites were assessed in ovarian homogenates, and vascular permeability was quantified in the peritoneal cavity. Ovarian morphology was characterized using histology and hematoxylin-eosin staining, determining the count of ovarian follicles and corpus luteum. Our results demonstrated a significant increase in lipoperoxidation, nitrite levels, and VEGF-A concentrations in the OHSS group compared to the control group. These biochemical alterations corroborate the successful induction of OHSS in the experimental model. Direct injection into the ovarian bursa resulted in reduced vascular permeability and VEGF-A levels, suggesting that the effects of cabergoline are predominantly ovarian. Particularly, cabergoline did not significantly alter other parameters such as ovarian weight, lipoperoxidation, nitrite levels, or morphology. Conversely, low concentrations of N-acetylcysteine (25-50 µg/kg) significantly reduced ovarian and uterine weights, VEGF-A levels, and vascular permeability. Interestingly, this dose-response relationship was not observed at higher NAC concentrations (100-200 μg/kg), suggesting a potential threshold beyond which NAC loses efficacy in these specific parameters. Our results suggest that the localized administration of N-acetylcysteine shows promise as a therapeutic strategy for OHSS by modulating key parameters associated with the syndrome. These promising results warrant further investigation into its mechanisms and efficacy, potentially expanding therapeutic options for OHSS management.

Endocrine-disrupting chemicals (EDCs), found in various cosmetic products, interfere with the normal functioning of the endocrine system, impacting hormone regulation and posing risks to human health. Common cosmetic EDCs, such as ultraviolet (UV) filters, parabens, and triclosan, can enter the human body through different routes, including skin absorption. Their presence has been linked to adverse effects on reproduction, immune function, and development. High-throughput in vitro assays, using various human cell lines, were employed to assess the effects of common cosmetic EDCs such as ethylhexyl methoxycinnamate (EHMC), benzophenone-3 (BP-3), homosalate, and parabens. Despite ongoing regulatory efforts, gaps persist in understanding their long-term impacts, particularly when they are present as mixtures or degradation products in the environment. This study focuses on recent in vitro research to investigate the mechanisms through which cosmetic-related EDCs disrupt the endocrine system and other physiological systems. The in vitro findings highlight the broader systemic impact of these chemicals, extending beyond the endocrine system to include immune, reproductive, and cardiovascular effects. This research underscores the importance of developing safer cosmetic formulations and enhancing public health protection, emphasizing the need for stricter regulations.