Journal of Endocrinology and Reproduction

Histopathological and Immunohistochemical Analysis of Ruptured Tubal Ectopic Pregnancy

2023-05-02T06:43:08+0530

Ectopic Pregnancy (EP) is reported to be causative of high incidence of maternal death and morbidity. It must be diagnosed during the first trimester immediately after symptoms of severe bleeding, abdominal pain, and cramping. Ultrasonography is the only possible detection method to confirm EP. Patients are at greater risk of EP due to inefficient early detection methods. An early detection of the EP based on cellular markers would possibly improve the diagnosis and clinical management. Therefore, an attempt was made to study the histoarchitecture of, and to identify the biomarkers in, the fallopian tube during rupture of ectopic pregnancy. Histological analysis revealed the formation of hematosalpinx and hydrosalpinx in the fallopian tube. Further, immunohistochemical study of the fallopian tissue of EP patients showed remarkable evidence of protein markers such as Bcl₂ and desmin which may be considered as potential cellular markers for the detection of EP.

Impacts of Protein-, L-Tryptophan-, Carbohydrate-, Oil-Rich Diets on Growth Performance, Levels of Melatonin, Oxidative Stress, Antioxidative Agents, and Vital Digestive Enzymes in the Gut of Juvenile Carp (Catla catla)

2023-08-02T17:06:03+0530

The dietary protein, tryptophan, carbohydrate, and oil content of fish feed has many vital roles in the growth performances, stress management, and digestive physiology of fish. However, in this context, the functions of gut melatonin, which depends on the availability of food, timing of food supply, frequency of feeds/day, quality of food, and growth stages of carp, still need to be clarified. The present study aimed to investigate the impact of different experimental diets on growth performances, melatonin, oxidative stress and its essential antioxidants in the gut, and vital digestive enzymes of juvenile carp, Catla catla (mean body weight ~50g). The fish were fed any one of the seven diets viz. (i) a standard diet (SD/control) (with 34.99% protein, 14.56% carbohydrate, 9.84% oil, and 0.36% L-tryptophan) (ii) two protein (PRD1 with 41.02%, and PRD2 with 50.55% protein), (iii) two L-tryptophan (TrpRD1 with 0.96%, and TrpRD2 with 1.36% tryptophan), (iv) one carbohydrate (CRD with 24.62% carbohydrate), and (v) one oil (ORD with 14.68% oil) - rich diets for 30 days. Results indicated that the growth performance was better in PRDs, TrpRDs, and CRD compared to SD but not in ORD-fed carp. Further, PRDs and TrpRDs stimulated gut melatonin and suppressed oxidative stress by enhancing all the studied antioxidant levels. Upregulated digestive enzyme activities were also recorded after the PRDs and TrpRDs supply. However, CRD and ORD-fed groups exhibit less/no impact on most studied parameters, except digestive physiology. Nonetheless, the current study reports for the first time that PRDs and TrpRDs can modulate gut melatonin, oxidative stress, different antioxidants, and digestive efficacy.

Evaluating the Relative Efficacy of Synthetic and Natural Drugs in Endometriosis Adopting Molecular Modelling Approach

2023-05-24T07:07:05+0530

Background: Endometriosis is a chronic inflammatory condition of high incidence and with serious consequences. Several synthetic compounds proved to be useful in treating its symptoms by inhibiting aromatase, which is responsible for the pathogenesis of this painful illness. Nevertheless, synthetic drugs inflict several side effects, including headaches, osteoporosis, and so on. This scenario advocates the search for therapeutic formulations based on natural compounds. Thus, the present study was hypothesized to evaluate the comparative efficacy of the synthetic and natural drugs used in endometriosis, using the bioinformatics approach. Methods: CB-Dock was employed to perform molecular docking of the aromatase enzyme with two synthetic and three natural drugs for predicting their molecular interactions, and binding affinities. The curcumin-aromatase complex was further subjected to MD simulations to determine its stability, and to apply it to natural compound-based computer-aided drug discovery. Results: Curcumin was observed to dock with a greater binding interaction with aromatase. The RMSD profile, hydrogen bonds, and the RMSF and Rg values of the complex were stabilised after 50 ns, which was an indicator of the stable binding pose of the curcumin-aromatase complex. Conclusion: These in-silico findings are the basis for proposing that curcumin can be considered as a potential binding agent to inhibit the aromatase enzyme in the treatment of endometriosis. Molecular modelling and dynamics results suggest that curcumin and aromatase form a stable complex and that curcumin can be targeted as a drug in the treatment of endometriosis

Adipose Tissue Dysfunction in PCOS

2023-06-21T10:16:30+0530

Polycystic Ovary Syndrome (PCOS) is one of the most common endocrine diseases among women of reproductive age; however, its aetiology is unclear. PCOS is linked to many metabolic manifestations and alterations such as obesity, insulin resistance, and cardiovascular diseases (CVD). Women with PCOS have intra-ovarian and systemic changes in their metabolite levels. Adipose tissue dysfunction plays a significant role in the pathophysiology of PCOS. Adipose tissue growth is disrupted by metabolic stress, leading to hypertrophy of adipocytes, which begin to express stress signals. Adipose tissue secretes autocrine and paracrine factors, called adipokines or adipocytokines. Adiponectin is an adipocyte-derived protein abundant in the bloodstream. Plasma adiponectin concentration is low in women with PCOS, obesity, CVD, and hypertension. Other adipocytokines with altered secretion in PCOS include leptin, resistin, apelin, visfatin, IL-6, IL-8, and TNF-α. Hormonal imbalance, untimely action of high LH, and consequent hyperandrogenism in women with PCOS may cause metabolic defects associated with adipose tissue dysfunction; however, there are no reports on the role of higher LH levels in adipose dysfunction and altered adipokine secretion. New medications with therapeutic potential have been developed that target adipokines for the treatment of PCOS. This review discusses the association between PCOS and altered adipokine production as a consequence of adipose dysfunction.

An Update on the Genetics of Polycystic Ovary Syndrome

2023-09-25T18:50:11+0530

PCOS is a common endocrinopathy among women of reproductive age, with a worldwide prevalence of 8 to 13%, depending on the criteria used for diagnosis. It is characterized by a constellation of features, including oligo/anovulation, clinical and/or biochemical hyperandrogenism, and polycystic ovarian morphology. PCOS is one of the common causes of female infertility. It is also associated with metabolic derangements, including obesity, insulin resistance, and compensatory hyperinsulinemia, which increase the likelihood of developing type 2 diabetes mellitus. Despite extensive research, the etiology of PCOS remains largely unknown. It seems likely that the hypothalamic-pituitary-ovarian axis dysfunction, partial folliculogenesis arrest, insulin resistance, and ovarian and adrenal androgen secretion may play a role in the pathogenesis of PCOS. Familial clustering of the cases of PCOS points to a genetic component linked with it. The initial genetic studies suggest an autosomal dominant pattern of inheritance of the disorder in some families; however, most studies support multifactorial origin. Since PCOS is a complex trait, the typical form of inheritance of PCOS follows a non-Mendelian pattern and involves complex genetic mechanisms. Studies involving linkage and association have suggested a connection between genetic variations and the risk of developing PCOS in certain families or populations. Through genome-wide association studies and next-generation sequencing techniques, several candidate genes have been identified that play a role in the etiopathogenesis of the disorder. Pathogenic variants of various genes such as INSR, IRS1, GHRL, LDLR, MC4R, ADIPOQ, UCP1, UCP2, UCP3, FTO, PCSK9, FBN3, NEIL2, FDFT1, PCSK9, CYP11, CYP17, CYP21, HSD17, STAR, POR, AKR1C3, AMH, AMHR2, INHBA, AR, SHBG, LHR, FSHR, FSH β, SRD5A, GATA4, THADA, YAP1, ERBB2, DENND1A, FEM1B, FDFT1, NEIL2, TCF7L2, etc. in some PCOS cases are linked as underlying etiologic associations. This review aims to provide insight into the current genetic knowledge about PCOS. Discovering the genetic factors and pathways involved in the disorder will help us better comprehend the underlying mechanisms of the disorder.