Steroid Hormones Research Articles

Mini-Review on Vitamin D in Pediatric Population and its Role in Respiratory and Atopic Disorders.

In recent years, our comprehension of the function of vitamin D has significantly evolved. The ubiquitous presence of the vitamin D receptor (Vitamin D Receptor- VDR) in the body has led to its redefinition from a steroidal hormone primarily involved in skeletal functions to a hormone with pleiotropic effects, exerting its influence on the circulatory, nervous, and immune systems. This has prompted investigations into its potential use in preventing and treating chronic metabolic disorders, cardiovascular diseases, infections, and allergic and autoimmune diseases. This comprehensive review explores the various aspects of vitamin D, including its sources, synthesis, functions, and its impact on different physiological systems. It delves into the epidemiology of vitamin D deficiency, highlighting its occurrence among various age demographics and geographic regions. The impact of vitamin D on the immune system is also explored, elucidating its immunomodulatory and anti-inflammatory properties, particularly in the context of respiratory infections. The review discusses emerging evidence concerning the potential advantages of vitamin D in respiratory diseases, pediatric asthma and atopic dermatitis. It also addresses vitamin D supplementation recommendations for various pediatric populations, including term and preterm infants. The growing concern regarding the global health impacts of insufficient vitamin D levels necessitates further research to bridge gaps in knowledge, particularly in enhancing screening, prevention, and approaches to address vitamin D deficiency from birth onwards. In summary, this comprehensive overview underscores the vital role of vitamin D, highlighting the significance of understanding its multifaceted functions and the need for tailored supplementation strategies, especially in vulnerable populations.

CYP19A1 polymorphisms and bladder cancer risk in the Chinese Han population.

The expression of CYP19A1 has implications for the prognosis of female bladder cancer. However, this study aimed to explore the association between single nucleotide polymorphisms (SNPs) in CYP19A1 and bladder cancer risk, as no prior research has addressed this association. We selected and genotyped five CYP19A1 SNPs (rs4646, rs6493487, rs1062033, rs17601876, and rs3751599) in 217 patients and 550 controls using the Agena MassARRAY system. Logistic regression analysis was employed to calculate the odds ratio (OR) and 95% confidence intervals (CIs). Bioinformatics predicted SNP functions and CYP19A1 involving pathways. Our study revealed a significant association between bladder cancer risk and four SNPs (rs4646 (AC vs. CC: OR = 1.71, FDR-p = 0.005), rs6493487 (G vs. A: OR = 0.68, FDR-p = 0.011), rs1062033 (G vs. C: OR = 0.36, FDR-p < 0.001), and rs17601876 (GA vs. GG: OR = 1.66, FDR-p = 0.008)) in CYP19A1. The three SNPs (rs4646, rs1062033, and rs17601876) were significantly correlated with CYP19A1 expression levels in normal whole blood (p < 0.05). Moreover, CYP19A1 were found to primarily participate in the steroid hormone biosynthesis and metabolic pathways. Consequently, CYP19A1 gene polymorphisms may play a crucial role in the genetic susceptibility to bladder cancer.

GC–MS-based untargeted plasma metabolomics identifies a 2-biomarker panel for possible diagnosis of precancerous cervical intraepithelial neoplasia stages from cervical cancer

Cervical cancer (CC) remains a major health concern globally, much of the brunt of which is experienced by the low- and middle-income countries where screening in terms of cytology and DNA genotyping for the high-risk oncogenic subtypes of the human papilloma virus (hr-HPV) is either inadequate or performed rather late. In this study, we aimed to determine biomarkers or panels of biomarkers that are capable of diagnosing the precancerous cervical intraepithelial neoplasia (CIN) stages from healthy and CC patients via untargeted gas chromatography–mass spectrometry-based metabolomics. Various cross-comparisons were conducted from which differential metabolites were identified. The underlying metabolic pathways based on the differential metabolites identified from the various cross-comparisons mainly related to amino acids biosynthesis and metabolism and steroid hormone biosynthesis. From all cross-comparisons, two common metabolites namely, 2-methyl-1-propylamine (also known as isobutylamine) and estrone were found to possess excellent to good diagnostic abilities, especially in distinguishing the early stages of CIN (CIN I, CIN II) from healthy women and CC patients. These findings have clinical significance in the sense that, once validated the 2-biomarker panel could be adopted in clinical practice for early diagnosis of CIN and invasive carcinoma. This would therefore inform the choice of treatment to be initiated by the clinician.

Exposure to synthetic steroid hormones and precocious puberty in girls: A case-control study

Synthetic steroid hormones are an emerging class of environmental pollutants, but their influence on pubertal timing remains unclear. This case-control study explored the association between synthetic steroid hormone exposure and precocious puberty. Using ultrahigh performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), synthetic steroid hormones were detected in urine samples from 229 Chinese girls, aged 6–9 years. Puberty status was assessed using Tanner staging by professional pediatricians. We conducted the least absolute shrinkage and selection operator (LASSO) regression combined with logistic regression. Besides, we evaluated the joint effects of steroid hormone mixture and identified the main contributor using the Weighted quantile sum (WQS) model and Bayesian kernel machine regression (BKMR) model. The logistic regression model reflected an inverse individual association between precocious puberty and halcinonide [OR (95 %CI): 0.20 (0.07, 0.46)], and budesonide [OR (95 %CI): 0.77 (0.62, 0.95)]. In the joint effects utilizing the WQS model, precocious puberty showed a marginal association with steroid hormone mixture, but was not significant [OR (95 %CI): 0.88 (0.75, 1.04)]. Prednisolone (0.31), fluorometholone acetate (0.24), and dexamethasone acetate (0.12) had the highest weight. Consistently, mixture exposure was not associated with precocious puberty in the BKMR model. In conclusion, precocious puberty was associated with halcinonide and budesonide exposure, but not steroid hormone mixture among girls. It highlighted the management of the residual synthetic steroid hormones in the environment and provided a direction for the prevention of precocious puberty.

Estrogen receptor knockdown suggests its role in gonadal development regulation in Manila clam Ruditapes philippinarum.

The estrogen receptor (ER), a ligand-dependent transcription factor, is critical for vertebrate reproduction. However, its role in bivalves is not well understood, with ongoing debates regarding its function in regulating reproduction similarly to vertebrates. To investigate ER's function, we conducted a 21-day RNA interference experiment focusing on its role in gonadal development in bivalves. Histological analyses revealed that ER inhibition significantly suppressed ovarian development in females and, conversely, promoted gonadal development in males. Additionally, levels of 17β-estrogen (E2) were markedly reduced in the gonads of both sexes following ER suppression. Transcriptomic analysis from RNA-seq of testes and ovaries after ER interference showed changes in the expression of key genes such as Vtg, CYP17, 3β-HSD, and 17β-HSD. These genes are involved in the estrogen signaling pathway and steroid hormone biosynthesis. Furthermore, ER suppression significantly affected the expression of genes linked to gametogenesis and the reproductive cycle. Our findings highlight ER's crucial, yet complex and sex-specific roles in gonadal development in bivalves, emphasizing the need for further detailed studies.

Hepatoprotective effects of Xiaoyao San formula on hepatic steatosis and inflammation via regulating the sex hormones metabolism.

The modified Xiaoyao San (MXS) formula is an adjuvant drug recommended by the National Health Commission of China for the treatment of liver cancer, which has the effect of preventing postoperative recurrence and metastasis of hepatocellular carcinoma and prolonging patient survival. However, the molecular mechanisms underlying that remain unclear. To investigate the role and mechanisms of MXS in ameliorating hepatic injury, steatosis and inflammation. A choline-deficient/high-fat diet-induced rat nonalcoholic steatohepatitis (NASH) model was used to examine the effects of MXS on lipid accumulation in primary hepatocytes. Liver tissues were collected for western blotting and immunohistochemistry (IHC) assays. Lipid accumulation and hepatic fibrosis were detected using oil red staining and Sirius red staining. The serum samples were collected for biochemical assays and NMR-based metabonomics analysis. The inflammation/lipid metabolism-related signaling and regulators in liver tissues were also detected to reveal the molecular mechanisms of MXS against NASH. MXS showed a significant decrease in lipid accumulation and inflammatory response in hepatocytes under metabolic stress. The western blotting and IHC results indicated that MXS activated AMPK pathway but inhibited the expression of key regulators related to lipid accumulation, inflammation and hepatic fibrosis in the pathogenesis of NASH. The metabonomics analysis systemically indicated that the arachidonic acid metabolism and steroid hormone synthesis are the two main target metabolic pathways for MXS to ameliorate liver inflammation and hepatic steatosis. Mechanistically, we found that MXS protected against NASH by attenuating the sex hormone-related metabolism, especially the metabolism of male hormones. MXS ameliorates inflammation and hepatic steatosis of NASH by inhibiting the metabolism of male hormones. Targeting male hormone related metabolic pathways may be the potential therapeutic approach for NASH.

Molecular mechanism of geniposide against ANIT-induced intrahepatic cholestasis by integrative analysis of transcriptomics and metabolomics.

Geniposide (GE), a bioactive compound extracted from the fruit of Gardenia jasminoides Ellis, has attracted significant attention for its hepatoprotective therapeutic applications. Although GE displays a protective effect on treating intrahepatic cholestasis (IC), the underlying mechanism remains elusive. In this study, we aimed to elucidate the pharmacological mechanisms of GE in treating IC by an integrated analysis of transcriptomics and metabolomics. Firstly, we evaluated the hepatoprotective effect of GE in α-naphthylisothiocyanate (ANIT)-induced IC rats by examining biochemical indices, inflammatory factors, and oxidative stress levels. Secondly, by transcriptomics and serum metabolomics, we identified differentially expressed genes and metabolites, revealing phenotype-related metabolic pathways and gene functions. Lastly, we screened the core targets of GE in the treatment of IC by integrating transcriptomic and metabolomic data and validated these targets using western blotting. The results indicated that GE improved serum indexes and alleviated inflammation reactions and oxidative stress in the liver. The transcriptomics analysis revealed 739 differentially expressed genes after GE treatment, mainly enriched in retinol metabolism, steroid hormone synthesis, PPAR signal transduction, bile secretion metabolism, and other pathways. The metabolomics analysis identified 98 differential metabolites and 10 metabolic pathways. By constructing a "genes-targets-pathways-compounds" network, we identified two pathways: the bile secretion pathway and the glutathione pathway. Within these pathways, we discovered nine crucial targets that were subsequently validated through western blotting. The results revealed that the GE group significantly increased the expression of ABCG5, NCEH1, OAT3, and GST, compared with the ANIT group. We speculate that GE has a therapeutic effect on IC by modulating the bile secretion pathway and the glutathione pathway and regulating the expression of ABCG5, NCEH1, OAT3, and GST.

The Influence of Sex Steroid Hormone Fluctuations on Capsaicin-Induced Pain and TRPV1 Expression

Sexual dimorphism among mammals includes variations in the pain threshold. These differences are influenced by hormonal fluctuations in females during the estrous and menstrual cycles of rodents and humans, respectively. These physiological conditions display various phases, including proestrus and diestrus in rodents and follicular and luteal phases in humans, distinctly characterized by varying estrogen levels. In this study, we evaluated the capsaicin responses in male and female mice at different estrous cycle phases, using two murine acute pain models. Our findings indicate that the capsaicin-induced pain threshold was lower in the proestrus phase than in the other three phases in both pain assays. We also found that male mice exhibited a higher pain threshold than females in the proestrus phase, although it was similar to females in the other cycle phases. We also assessed the mRNA and protein levels of TRPV1 in the dorsal root and trigeminal ganglia of mice. Our results showed higher TRPV1 protein levels during proestrus compared to diestrus and male mice. Unexpectedly, we observed that the diestrus phase was associated with higher TRPV1 mRNA levels than those in both proestrus and male mice. These results underscore the hormonal influence on TRPV1 expression regulation and highlight the role of sex steroids in capsaicin-induced pain.

Role of blood metabolites in mediating the effect of gut microbiome on the mutated-RAS/BRAF metastatic colorectal cancer-specific survival

BackgroundRecent studies have linked alterations in the gut microbiome and metabolic disruptions to the invasive behavior and metastasis of colorectal cancer (CRC), thus affecting patient prognosis. However, the specific relationship among gut microbiome, metabolite profiles, and mutated-RAS/BRAF metastatic colorectal cancer (M-mCRC) remains unclear. Furthermore, the potential mechanisms and prognostic implications of metabolic changes induced by gut microbiome alterations in patients with M-mCRC still need to be better understood.MethodsWe conducted Mendelian randomization (MR) to evaluate the causal relationship of genetically predicted 196 gut microbiome features and 1400 plasma metabolites/metabolite ratios on M-mCRC-specific survival. Additionally, we identified significant gut microbiome-metabolites/metabolite ratio associations based on M-mCRC. Metabolite information was annotated, and functional annotation and pathway enrichment analyses were performed on shared proteins corresponding to significant metabolite ratios, aiming to reveal potential mechanisms by which gut microbiome influences M-mCRC prognosis via modulation of human metabolism.ResultsWe identified 11 gut microbiome features and 49 known metabolites/metabolite ratios correlated with M-mCRC-specific survival. Furthermore, we identified 17 gut microbiome-metabolite/metabolite ratio associations specific to M-mCRC, involving eight lipid metabolites and three bilirubin degradation products. The shared proteins corresponding to significant metabolite ratios were predominantly localized within the integral component of the membrane and exhibited enzymatic activities such as glucuronosyltransferase and UDP-glucuronosyltransferase, crucial in processes such as glucuronidation, bile secretion, and lipid metabolism. Moreover, these proteins were significantly enriched in pathways related to ascorbate and aldarate metabolism, pentose and glucuronate interconversions, steroid hormone biosynthesis, and bile secretion.ConclusionOur study offers novel insights into the potential mechanisms underlying the impact of the gut microbiome on the prognosis of M-mCRC. These findings serve as a meaningful reference for exploring potential therapeutic targets and strategies in the future.

Sex steroid hormones: an overlooked yet fundamental factor in oral homeostasis in humans

Sex steroid hormones (SSH) are extremely versatile molecules with a myriad of physiological functions. Next to their well-known role in sexual development and reproduction, SSH play active roles in practically every tissue in the human body, including the oral cavity. It has long been demonstrated that periodontal tissues express SSH receptors and therefore are responsive to the presence of SSH. Interestingly, SSH not only interact with the periodontal tissues but also with other tissues in the oral cavity such as dental enamel, pulp, cementum, oral mucosa, and salivary glands. Questions concerning the possible physiological functions of these receptors and their role in maintenance of oral health, remain unanswered. The purpose of this scoping review was to gather and summarize all the available evidence on the role of SSH in physiological processes in the oral cavity in humans. Two comprehensive literature searches were performed. References were screened and selected based on title, abstract and full text according to our inclusion criteria. Both searches yielded 18,992 results of which 73 were included. Results were divided into four categories: (1) Periodontium; (2) Dental structure; (3) Mucosa; and (4) Salivary glands. The interaction of these tissues with progestagens, androgens and estrogens are summarized. Sex steroid hormones are an overlooked yet fundamental factor in oral homeostasis. They play important roles in the development and function of the periodontium, dental structure, mucosa and salivary glands. Dentists and healthcare providers should consider these hormonal factors when assessing and treating oral health conditions.

Prostate cancers with distinct transcriptional programs in Black and White men

BackgroundBlack men are at a higher risk of prostate cancer (PC) diagnosis and present with more high-grade PC than White men in an equal access setting. This study aimed to identify differential transcriptional regulation between Black and White men with PC.MethodsWe performed microarray of radical prostatectomy tissue blocks from 305 Black and 238 White men treated at the Durham Veterans Affairs Medical Center. Differential expression, gene set enrichment analysis, master regulator analysis, and network modeling were conducted to compare gene expression by race. Findings were validated using external datasets that are available in the Gene Expression Omnibus (GEO) database. The first was a multi-institutional cohort of 1152 prostate cancer patients (596 Black, 556 White) with microarray data (GEO ID: GSE169038). The second was an Emory cohort of 106 patients (22 Black, 48 White, 36 men of unknown race) with RNA-seq data (GEO ID: GSE54460). Additionally, we analyzed androgen receptor (AR) chromatin binding profiles using paired AR ChIP-Seq datasets from Black and White men (GEO IDs: GSE18440 and GSE18441).ResultsWe identified 871 differentially expressed genes between Black and White men. White men had higher activity of MYC-related pathways, while Black men showed increased activity of inflammation, steroid hormone responses, and cancer progression-related pathways. We further identified the top 10 transcription factors (TFs) in Black patients, which formed a transcriptional regulatory network centered on the AR. The activities of this network and the pathways were significantly different in Black vs. White men across multiple cohorts and PC molecular subtypes.ConclusionsThese findings suggest PC in Black and White men have distinct tumor transcriptional profiles. Furthermore, a highly interactive TF network centered on AR drives differential gene expression in Black men. Additional study is needed to understand the degree to which these differences in transcriptional regulatory elements contribute to PC health disparities.

Endogenous glucocorticoids are required for normal macrophage activation and gastric Helicobacter pylori immunity.

Glucocorticoids are steroid hormones well-known for their potent anti-inflammatory effects. However, their immunomodulatory properties are multifaceted. Increasing evidence suggests that glucocorticoid signaling promotes effective immunity and that disruption of glucocorticoid signaling impairs immune function. In this study, we conditionally deleted the glucocorticoid receptor (GR) in the myeloid lineage using the LysM-Cre driver (myGRKO). We examined the impact on macrophage activation and gastric immune responses to Helicobacter pylori, the best-known risk factor of gastric cancer. Our results indicate that, compared to WT, GRKO macrophages exhibited higher expression of proinflammatory genes in steroid-free conditions. However, when challenged in vivo, GRKO macrophages exhibited aberrant chromatin landscapes and impaired proinflammatory gene expression profiles. Moreover, gastric colonization with Helicobacter pylori revealed impaired gastric immune responses and reduced T cell recruitment in myGRKO mice. As a result, myGRKO mice were protected from atrophic gastritis and pyloric metaplasia development. These results demonstrate a dual role for glucocorticoid signaling in preparing macrophages to respond to bacterial infection but limiting their pathogenic activation. In addition, our results support that macrophages are critical for gastric Helicobacter pylori immunity.

The Efficacy of β-Carotene in Cow Reproduction: A Review.

β-carotene supplementation improves the reproductive performance of cattle. However, the research results on this topic have been inconsistent, and no clear conclusion has been reached. In previous reviews of this topic, the functional mechanism of β-carotene in reproduction remained unclear, but subsequent studies have shown that the antioxidant effects of β-carotene protect enzymes involved in ovarian sex steroid hormone production from the effects of oxygen radicals. This role consequently affects normal ovarian follicle dynamics, maintenance of luteal function, and the estrous cycle, and indirectly improves reproductive performance by preventing perinatal diseases and facilitating recovery from these diseases. Several factors must be considered in feeding management to determine whether β-carotene supplementation is effective for improving reproductive performance in cows. The same is true when the animal consumes a large amount of the antioxidant β-carotene due to lactation, aging, or season. Therefore, it is important to consider the balance between the supply and consumption of β-carotene and evaluate whether β-carotene supplementation has an effect on reproductive performance in cows.

Modern view of the problem: the influence of obesity as a key component of metabolic syndrome on the development and progression of endometrial cancer

Unlike many other malignancies, the incidence and mortality of endometrial cancer continues to rise. This unfortunate trend is in no small part the result of the worldwide obesity epidemic, which is caused by reduced physical activity, poor diet and chronic stress. Currently, more than 50 % of endometrial cancer cases are associated with obesity, which is recognized as an independent risk factor for the development of this disease. Adipose tissue is not only the main place of storage of excess energy, but also a full-fledged endocrine organ that affects the metabolism, immune response and production of biologically active substances involved in cell growth and differentiation, angiogenesis, apoptosis and carcinogenesis. In this review, we assess the impact of obesity as a key component of metabolic syndrome on the development and progression of endometrial cancer. There are several mechanisms by which obesity enlarges the risk of endometrial cancer, including increased endogenous sex steroid hormones, hyperglycemia, insulin resistance, adipokine secretion, and chronic inflammation. The purpose of this review is to analyze publications, reflecting the already known aspects of the biological effect of obesity, as well as new data from recent years.

Potential role of mitochondria and endoplasmic reticulum in the response elicited by D-aspartate in TM4 Sertoli cells

D-Aspartic Acid (D-Asp) affects spermatogenesis by enhancing the biosynthesis of the sex steroid hormones acting either through the hypothalamus-pituitary–testis axis or directly on Leydig cells. Recently, in vitro studies have also demonstrated the direct effects of D-Asp on the proliferation and/or activity of germ cells. However, although D-Asp is present in Sertoli cells (SC), the specific role of the amino acid in these cells remains unknown. This study investigated the effects of D-Asp on the proliferation and activity of TM4 SC, focusing on the mitochondrial compartment and its association with the endoplasmic reticulum (ER). We found that D-Asp enhanced the proliferation and activity of TM4 cells as evidenced by the activation of ERK/Akt/PCNA pathway and the increase in the protein levels of the androgen receptor. Furthermore, D-Asp reduced both the oxidative stress and apoptotic process. An increase in mitochondrial functionality and dynamics, as well as a reduction in ER stress, were also found in D-Asp-treated TM4 cells. It is known that mitochondria are closely associated with ER to form the Mitochondrial-Associated Endoplasmic Reticulum Membranes (MAM), the site of calcium ions and lipid transfer from ER to the mitochondria, and vice versa. The data demonstrated that D-Asp induced stabilization of MAM in TM4 cells. In conclusion, this study is the first to demonstrate a direct effect of D-Asp on SC activity and to clarify the cellular/molecular mechanism underlying these effects, suggesting that D-Asp could stimulate spermatogenesis by improving the efficiency of SC.

Exposure to Synthetic Endocrine-Disrupting Chemicals in Relation to Maternal and Fetal Sex Steroid Hormones: A Scoping Review.

Many synthetic endocrine-disrupting chemicals (EDCs) are ubiquitous in the environment and highly detected among pregnant people. These chemicals may disrupt maternal and/or fetal sex steroid hormones, which are critical to pregnancy maintenance and fetal development. Here, we review the epidemiological literature examining prenatal exposure to common synthetic EDCs in relation to maternal and fetal sex steroid hormones. We performed a literature search using PubMed, SCOPUS, and Embase, ultimately identifying 29 articles for full review. Phenols, parabens, and persistent organic pollutants generally showed inverse associations with androgens, estrogens, and progesterone. Phthalates and per-and polyfluoroalkyl substances tended to be inversely associated with progesterone, while evidence regarding androgens and estrogens was mixed. Inconsistent, but noteworthy, differences by fetal sex and timing of exposure/outcome were observed. Overall, the literature suggests EDCs may disrupt maternal and fetal sex steroid activity, though findings are mixed. Given the pervasive, high-volume production of these synthetic chemicals and the critical functions sex steroid hormones play during gestation, additional research is warranted.

Effect of the gonadotropin surge on steroid receptor regulation in preovulatory follicles and newly formed corpora lutea in the cow

The objective of the study was to characterize the mRNA expression patterns of specific steroid hormone receptors namely, estrogen receptors (ESRRA—estrogen related receptor alpha and ESRRB—estrogen related receptor beta) and progesterone receptors (PGR) in superovulation-induced bovine follicles during the periovulation and subsequent corpus luteum (CL) formation. The bovine ovaries (n = 5 cow / group), containing preovulatory follicles or early CL, were collected relative to injection of the gonadotropin-releasing hormone (GnRH) at (I) 0 h, (II) 4 h, (III) 10 h, (IV) 20 h, (V) 25 h (preovulatory follicles) and (VI) 60 h (CL, 2–3 days after induced ovulation). In this experiment, we analyzed the steroid receptor mRNA expression and their localization in the follicle and CL tissue. The high mRNA expression of ESRRA, ESRRB, and PGR analyzed in the follicles before ovulation is significantly reduced in the group of follicles during ovulation (25 h after GnRH), rising again significantly after ovulation in newly formed CL, only for ESRRA and PGR (P < 0.05). Immunohistochemically, the nuclei of antral follicles' granulosa cells showed a positive staining for ESRRA, followed by higher activity in the large luteal cells just after ovulation (early CL). In contrast, the lower PGR immunopresence in preovulatory follicles increased in both small and large luteal cell nuclei after follicle ovulation. Our results of steroid receptor mRNA expression in this experimentally induced gonadotropin surge provide insight into the molecular mechanisms of the effects of steroid hormones on follicular–luteal tissue in the period close to the ovulation and subsequent CL formation in the cow.

The Improvement Effects of a Nutritional Fortifier on the Reproductive Performance, Sex Steroid Hormone Production, and Health of the Striped Bamboo Shark Chiloscyllium plagiosum.

To explore a method of improving the reproductive performance of the striped bamboo shark, three groups (D0, D1, and D2) of mature individuals were fed squid with (D1 and D2) or without (D0) a nutritional fortifier during the breeding seasons of 2022 and 2023. Compared with the D0 group, the D1 and D2 groups had an increase of 20.90% and 31.34% in total eggs, increases of 32.73% and 41.82% in the proportion of lecithal eggs, and a total 119.07% increase in hatching rate, respectively, in 2022. In 2023, the corresponding increase was 17.12% and 9.91% in total eggs, 19.63% and 12.15% in the proportion of lecithal eggs, 43.37% and 43.94% in fertilization rate, 23.94% and 22.22% in hatchability rate, and 66.70% and 8.70% in the survival rate of fry. Moreover, the levels of serum estradiol, testosterone, progesterone, albumin, and total antioxidant capacity and the levels of ARA, EPA, DHA, n-3 PUFA, and n-6 PUFA in both serum and lecithal eggs significantly increased, while the levels of serum triglyceride and total cholesterol were the opposite (p < 0.05). The results demonstrate that feeding the sharks with a nutritional fortifier can increase spawn production and the quality of eggs, regulate the production of sex steroids, and improve the nutrition of eggs and the health of broodstocks.

Bilirubin Levels in Infancy and Their Associations with Body Weight, Levels of Iron-Related Parameters and Steroid Hormone Levels.

It is assumed that bilirubin is hormonally regulated and influences weight development by preventing weight gain. However, studies in healthy infants are limited. The present study established reference values for bilirubin and investigated whether bilirubin levels are significantly associated with body weight, levels of ferritin and transferrin as well as steroid hormone levels in a study population of three- and six-month-old healthy infants. Data from a total of 411 study visits from the LIFE Child study (Leipzig, Germany) were analyzed. Associations were examined using linear regression analyses. Besides laboratory parameters, anthropometric data were gathered. We found statistically significant associations between body weight and bilirubin levels. In girls, we observed additional associations between bilirubin levels and both ferritin and transferrin concentrations at three months of age. At six months, steroid hormone levels were significantly associated with concentrations of total and indirect bilirubin, with effects differing by sex. Our study thus confirms associations already reported from animal studies and studies in adult populations. Furthermore, we showed that these associations already exist in the first year of life, are influenced by sex and age and, further, depend on the bilirubin type. Our results provide reference values for bilirubin and assist, therefore, in interpreting bilirubin levels in infancy.

Is there a relationship of cortisol and sex steroid hormones with mental health in middle-aged adults? the FIT-AGEING study

Mental health has emerged as a worldwide concern given the rising incidence of anxiety and depression disorders in the last years. Cortisol and sex steroid hormones have been demonstrated to be important regulators of mental health processes in older adults. However, the evidence considering these integrated variables in apparently healthy middle-aged individuals has not been thoroughly addressed. The present study was aimed at investigating the association of plasma cortisol, testosterone, free testosterone, Sex Hormone-Binding Globulin (SHBG) and Dehydroepiandrosterone-sulfate (DHEAS) levels with mental health in middle-aged adults. This cross-sectional study included a cohort of 73 middle-aged adults with 45-65 years of age (53% women). Plasma cortisol, testosterone, SHBG, and DHEAS were assessed using a competitive chemiluminescence immunoassay. Free testosterone was calculated from the total testosterone and SHBG. Self-reported depression severity, generic health-related quality of life, hope, satisfaction with life, and optimism-pessimism were evaluated using the Beck Depression Inventory-II (BDI-II), the 36-item Short-Form Health Survey, the Adult Hope Scale (AHS), the Satisfaction with Life Scale (SWLS), and the Life Orientation Test Revised, respectively - higher total scores of these scales indicating greater levels of these variables -. Testosterone and free testosterone levels were inversely associated with BDI-II values in men (all P≤0.042). Cortisol levels were positively related with SWLS scores, whereas testosterone, free testosterone, SHBG, and DHEAS levels were negatively correlated with BDI-II values in women (all P≤0.045). In summary, these results suggest that increased levels of steroid hormones - within the normal values - may be associated with better mental health in middle-aged adults.