Reviews in Endocrine and Metabolic Disorders

Galectin-3 is a member of the galectin family, widely expressed in immune cells and plays a role mainly in inflammation, autoimmunity, apoptosis, and chemotaxis. We summarized the roles of Galectin-3 in diabetes and its complications, as well as the underlying mechanisms. Clinical research has determined that the circulating level of Galectin-3 is closely related to diabetes and its complications, thus it is promising to use Galectin-3 as a predictor and biomarker for those diseases. Galectin-3 also may be considered as an ideal therapeutic target, which has broad prospects in the prevention and treatment of diabetes and its complications, especially macrovascular and microvascular complications.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) là hormone kiểm soát chính của sự hấp thu canxi ở ruột. Khi nhu cầu canxi của cơ thể tăng lên do chế độ ăn thiếu canxi, do sự tăng trưởng, mang thai hoặc cho con bú, quá trình tổng hợp 1,25(OH)2D3 được tăng cường, dẫn đến sự kích thích hấp thu canxi ở ruột. Tuy nhiên, mô tả đầy đủ về các cơ chế phân tử tham gia vào quá trình hấp thu canxi được điều chỉnh bởi 1,25(OH)2D3 vẫn chưa hoàn chỉnh. Sự hấp thu canxi ở ruột diễn ra qua cả một con đường tế bào chủ động có thể bão hòa và một con đường kẽ tế bào thụ động không bão hòa. Mỗi bước trong quá trình vận chuyển canxi tế bào chủ động (sự xâm nhập của canxi vào bề mặt trên của tế bào, quá trình vận chuyển canxi qua bên trong tế bào nhu mô và sự thải canxi ra bên ngoài tế bào qua bơm màng tế bào) đã được báo cáo là liên quan đến một thành phần phụ thuộc vào vitamin D. Bài viết này sẽ xem xét các nghiên cứu gần đây, bao gồm những nghiên cứu sử dụng chuột knockout, đã gợi ý rằng sự hấp thụ canxi do 1,25(OH)2D3 trung gian phức tạp hơn mô hình ba bước truyền thống của vận chuyển canxi tế bào chủ động. Các khái niệm hiện tại sẽ được xem xét lại và những câu hỏi còn tồn tại sẽ được thảo luận. Bằng chứng về vai trò của 1,25(OH)2D3 trong việc điều chỉnh con đường kẽ tế bào cũng sẽ được đề cập.

Sarcopenia, cachexia, and atrophy due to inactivity and disease states are characterized by a loss of skeletal muscle mass, often accompanied by reduced levels of anabolic hormones (e.g. testosterone). These conditions are associated with an increase in mortality, hospitalization and worsening in quality of life. Both physical exercise (EX) and anabolic–androgenic steroid (AAS) administration can improve the prognosis of patients as they increase physical functionality. However, there is a gap in the literature as to the impact of these therapies on the gains in strength and muscle mass and their implications for patient safety. Accordingly, we performed a random-effects meta-analysis to elucidate the effects of AAS and/or EX interventions on lean body mass (LBM) and muscle strength in conditions involving muscle loss. A systematic search for relevant clinical trials was conducted in MEDLINE, EMBASE, SCOPUS, Web of Science, and SPORTDiscus. Comparisons included AAS vs. Control, EX vs. Control, AAS vs. EX, AAS + EX vs. AAS and AAS + EX vs. EX. A total of 1114 individuals were analyzed. AAS increased LBM (effect size [ES]: 0.46; 95% CI: 0.25, 0.68, P = 0.00) and muscle strength (ES: 0.31; 95% CI: 0.08, 0.53, P = 0.01) when compared to a control group. EX promoted an increase in muscular strength (ES: 0.89; 95% CI: 0.53, 1.25, P = 0.00), with no effect on LBM when compared to the control group (ES: 0.15; 95% CI: -0.07, 0.38, P = 0.17). AAS did not demonstrate statistically significant differences when compared to EX for LBM and muscle strength. The combination of EX + AAS promoted a greater increase in LBM and muscular strength when compared to AAS or EX in isolation. Qualitatively, AAS administration had relatively few side effects. Significant heterogeneity was found in some analyses, which may be explained by the use of different AAS types and EX protocols. Our findings suggest that AAS administration in cachectic and sarcopenic conditions may be a viable interventional strategy to enhance muscle function when exercise is not a possible approach. Moreover, combining AAS with exercise may enhance positive outcomes in this population.

The hypothalamic pituitary adrenal (HPA) axis is the most common of the endocrine lines/axis’ to be affected by HIV infection. There are multiple factors that contribute to this HPA axis dysregulation. Direct invasion of the various organs in the axis can be either by opportunistic infections or infiltrative diseases. The soluble factors or cytokines released during viral infection and the chronic inflammatory state that follows, also contribute to these alterations. The actions of these cytokines released by the immune response can both activate the HPA axis and cause a glucocorticoid resistant state. Further, many of the anti-retroviral and other medications used to treat HIV infection can contribute to HPA axis dysfunction. While the diagnosis and treatment of endocrine dysfunction is the same as in any other patient, management pathways may be quite different. While some may be adaptive responses, life threatening adrenal insufficiency can also be present. It is important the latter be picked up expeditiously and treated promptly to avoid mortality.

The mammary gland (MG) is an exocrine gland present in female mammals responsible for the production and secretion of milk during the process of lactation. It is mainly composed by epithelial cells and adipocytes. Among the features that make the MG unique there are 1) its highly plastic properties displayed during pregnancy, lactation and involution (all steps belonging to the lactation cycle) and 2) its requirement to grow in close association with adipocytes which are absolutely necessary to ensure MG’s proper development at puberty and remodeling during the lactation cycle. Although MG adipocytes play such a critical role for the gland development, most of the studies have focused on its epithelial component only, leaving the role of the neighboring adipocytes largely unexplored. In this review we aim to describe evidences regarding MG’s adipocytes role and properties in physiologic conditions (gland development and lactation cycle), obesity and breast cancer, emphasizing the existing gaps in the literature which deserve further investigation.

Although the incidence of some malignancy has decreased over the recent years, this is not the case of papillary thyroid microcarcinoma (PTMC), whose incidence has increased worldwide. Most PTMC are found incidentally after histological examination of specimens from surgery for benign thyroid disease. Hashimoto’s thyroiditis, whose incidence has also increased, coexists in about one in three PTMC patients. Three different mechanisms have been proposed to clarify the association between chronic lymphocytic thyroiditis and PTMC, namely tumor development/growth by: (i) TSH stimulation, (ii) expression of certain proto-oncogenes, (iii) chemokines and other molecules produced by the lymphocytic infiltrate. Whether Hashimoto’s thyroiditis protects against lymph node metastasis is debated. Overall, autommune thyroiditis seems to contribute to the favorable prognosis of PTMC. Major limitations of the studies so far performed include: (i) retrospective design, (ii) limited statistical power, (iii) high risk of selection bias, (iv) and predominant Asian ethnicity of patients. Full genetic profiling of both diseases and identification of environmental factors capable to trigger them, as well as well-powered prospective studies on different ethnical groups, may help understand their causal association and why their frequencies are continuing raising.