Reviews in Endocrine and Metabolic Disorders最新文献

Obesity is a complex, multifactorial, chronic disease that acts as a gateway to a range of other diseases. Evidence from recent studies suggests that changes in oxygen availability in the microenvironment of metabolic organs may exert an important role in the development of obesity-related cardiometabolic complications. In this review, we will first discuss results from observational and controlled laboratory studies that examined the relationship between reduced oxygen availability and obesity-related metabolic derangements. Next, the effects of alterations in oxygen partial pressure (pO₂) in the adipose tissue, skeletal muscle and the liver microenvironment on physiological processes in these key metabolic organs will be addressed, and how this might relate to cardiometabolic complications. Since many obesity-related chronic diseases, including type 2 diabetes mellitus, cardiovascular diseases, chronic kidney disease, chronic obstructive pulmonary disease and obstructive sleep apnea, are characterized by changes in pO₂ in the tissue microenvironment, a better understanding of the metabolic impact of altered tissue oxygenation can provide valuable insights into the complex interplay between environmental and biological factors involved in the pathophysiology of metabolic impairments. This may ultimately contribute to the development of novel strategies to prevent and treat obesity-related cardiometabolic diseases.

Diabetes has arisen as a noteworthy global health issue, marked by escalating incidence and mortality rates. Insulin, crucial for preserving euglycemia, acts as a vital energy provider for various tissues. Iron metabolism notably plays a significant role in the development of insulin resistance, a key factor in the onset of various metabolic disorders. The intricate interaction between iron and insulin signaling encompasses complex regulatory mechanisms at the molecular level, thereby impacting cellular reactions to insulin. The intricate interplay between insulin and glucagon, essential for precise regulation of hepatic glucose production and systemic glucose levels, may be influenced by certain microelements for instance zinc, copper, iron, boron, calcium, cobalt, chromium, iodine, magnesium and selenium. While significant progress has been achieved in elucidating the pathophysiological connections between iron overload and glucose metabolism, our understanding of the involvement of the Fenton reaction and oxidative stress in insulin resistance influencing many chronical conditions remains limited. Furthermore, the exploration of the multifaceted roles of insulin in the human body continues to be a subject of active investigation by numerous scientific researchers. This review comprehensively outlines the potential adverse impact of iron overload on insulin function and glucose metabolism. Additionally, we provide a synthesis of findings derived from various research domains, encompassing population studies, animal models, and clinical investigations, to scrutinize the multifaceted relationship between iron and insulin sensitivity. Moreover, we delineate instances of correlations between serum iron levels and various medical conditions, including the diabetes also gestational diabetes and obesity.

Children born small for gestational age (SGA) are defined as those having birth weight and/or length below -2 SD for gestational age. In approximately 90% of cases, SGA children experience catch-up growth in the first two years of life and a subsequent regular growth rate, reaching normal adult height. However, in the remaining 10% of cases, SGA children fail to have catch-up growth, showing persistent short stature and a constantly impaired growth rate, leading to decreased adult height compared with both general population and their mid-parental height. Therefore, in these children GH treatment may be indicated to improve growth outcome. As it can be started in most countries from the age of 4 years and is usually recommended until the completion of puberty, long-term GH treatment in SGA children (namely, longer than three years) showed a persistent improvement in height and an initial improvement in growth rate in the first year of treatment, followed by a stable, regular growth rate over time. In the present article, we systematically reviewed the currently available reports about efficacy of long-term GH treatment in SGA children, with a particular focus on growth rate over time and adult height.

Isolated hypoprolactinemia (IHP) can be defined as the presence of consistently low serum levels of prolactin in the absence of other anterior pituitary hormone abnormalities. It is an extremely rare condition, and consequently incompletely understood and unrecognized. A recent study has reported the first cases of IHP caused by mutation in the PRL gene. There are also cases where the pathogenesis of IHP is likely secondary to an autoimmune response against the PRL-secreting cells. But most published cases are acquired and idiopathic. The best characterized function of PRL is to facilitate milk production in the puerperium. Analysis of the GTEX data repository, however, shows that PRL is the most abundantly expressed gene in the human pituitary, independently of gender and age, suggesting the presence of additional roles for PRL. Newer studies have indeed revealed a much larger spectrum of PRL functions and will likely uncover novel clinical phenotypes associated with severe PRL deficiency.

The physiological role of prolactin (PRL) in men is still not well defined. The pathological increase is characterized by sexual function impairment along with possible negative consequences in body composition and metabolic profile. Conversely, the clinical significance of reduced PRL levels was only partially investigated or mainly neglected. The present paper aims to summarize and critically discuss possible phenotypes characterizing male subjects with reduced PRL levels. When possible, meta-analytic results were provided. Available data derived from patients seeking medical care for sexual dysfunction as well as from cross-sectional and longitudinal studies showed that low PRL in males is associated with a worse metabolic phenotype (including diabetes mellitus), mood disturbances (including anxiety and depression), and sexual dysfunctions (including psychogenic erectile and ejaculatory dysfunctions). Whether or not these features are direct consequences of reduced PRL levels or whether the latter reflect other pathway impairments such as serotoninergic failure cannot be clarified. The present data, however, emphasize that a deficiency of PRL should be taken into account and need further investigations.

The diagnostic approach to hypopituitarism involves many disciplines. Clinical symptoms rarely are specific. Imaging techniques are helpful but cannot prove the specific functional defects. Therefore, the definitive diagnosis of pituitary insufficiency is largely based on laboratory tests. However, also laboratory methods come with inherent limitations, and it is essential for the clinician to know and recognize typical pitfalls. Most factors potentially impairing the quality of hormone measurements are introduced in the preanalytical phase, i.e. before the hormones are measured by the laboratory. For example, the timing of blood drawing with respect to circadian rhythm, stress, and medication can have an influence on hormone concentrations. During the actual analysis of the hormones, cross-reactions with molecules present in the sample presenting the same or similar epitopes than the intended analyte may affect immunoassays. Interference can also come from heterophilic or human anti-animal antibodies. Unexpected problems can also be due to popular nutritional supplements which interfere with the measurement procedures. An important example in this respect is the interference from biotin. It became only clinically visible when the use of this vitamin became popular among patients. The extreme serum concentrations reached when patients take it as a supplement can lead to incorrect measurements in immunoassays employing the biotin-streptavidin system. To some extent, hormone analyses using liquid chromatography mass spectrometry (LCMS) can overcome problems, although availability and cost-effectiveness of this method still imposes restrictions. In the post-analytical phase, appropriateness of reference intervals and cut-offs with respect to the specific analytical method used is of outmost importance. Furthermore, for interpretation, additional biological and pharmacological factors like BMI, age and concomitant diseases must be considered to avoid misinterpretation of the measured concentrations. It is important for the clinician and the laboratory to recognize when one or more laboratory values do not match the clinical picture. In an interdisciplinary approach, the search for the underlying cause should be initiated.

This review aimed to systematically quantify the differences in Metabolic Syndrome (MetS) prevalence across various ethnic groups in high-income countries by sex, and to evaluate the overall prevalence trends from 1996 to 2022. We conducted a systematic literature review using MEDLINE, Web of Science Core Collection, CINAHL, and the Cochrane Library, focusing on studies about MetS prevalence among ethnic groups in high-income countries. We pooled 23 studies that used NCEP-ATP III criteria and included 147,756 healthy participants aged 18 and above. We calculated pooled prevalence estimates and 95% confidence intervals (CI) using both fixed-effect and random-effect intercept logistic regression models. Data were analysed for 3 periods: 1996–2005, 2006–2009, and 2010–2021. The pooled prevalence of MetS in high-income countries, based on the NCEP-ATP III criteria, was 27.4% over the studied period, showing an increase from 24.2% in 1996–2005 to 31.9% in 2010–2021, with men and women having similar rates. When stratified by ethnicity and sex, ethnic minority women experienced the highest prevalence at 31.7%, while ethnic majority women had the lowest at 22.7%. Notably, MetS was more prevalent in ethnic minority women than men. Among ethnic minorities, women had a higher prevalence of MetS than men, and the difference was highest in Asians (about 15 percentage points). Among women, the prevalence of MetS was highest in Asians (41.2%) and lowest in Blacks/Africans (26.7%). Among men, it was highest in indigenous minority groups (34.3%) and lowest among in Blacks/Africans (19.8%). MetS is increasing at an alarming rate in high-income countries, particularly among ethnic minority women. The burden of MetS could be effectively reduced by tailoring interventions according to ethnic variations and risk profiles.

The results of many studies in recent years indicate a significant impact of pituitary function on bone health. The proper function of the pituitary gland has a significant impact on the growth of the skeleton and the appearance of sexual dimorphism. It is also responsible for achieving peak bone mass, which protects against the development of osteoporosis and fractures later in life. It is also liable for the proper remodeling of the skeleton, which is a physiological mechanism managing the proper mechanical resistance of bones and the possibility of its regeneration after injuries. Pituitary diseases causing hypofunction and deficiency of tropic hormones, and thus deficiency of key hormones of effector organs, have a negative impact on the skeleton, resulting in reduced bone mass and susceptibility to pathological fractures. The early appearance of pituitary dysfunction, i.e. in the pre-pubertal period, is responsible for failure to achieve peak bone mass, and thus the risk of developing osteoporosis in later years. This argues for the need for a thorough assessment of patients with hypopituitarism, not only in terms of metabolic disorders, but also in terms of bone disorders. Early and properly performed treatment may prevent patients from developing the bone complications that are so common in this pathology. The aim of this review is to discuss the physiological, pathophysiological, and clinical insights of bone involvement in pituitary disease.

Objectives

To propose the grounds for “diabetic sarcopenia” as a new comorbidity of diabetes, and to establish a muscle screening algorithm proposal to facilitate its diagnosis and staging in clinical practice. Method: A qualitative expert opinion study was carried out using the nominal technique. A literature search was performed with the terms “screening” or “diagnostic criteria” and “muscle loss” or “sarcopenia” and “diabetes” that was sent to a multidisciplinary group of 7 experts who, in a face-to-face meeting, discussed various aspects of the screening algorithm. Results: The hallmark of diabetic sarcopenia (DS) is muscle mass atrophy characteristic of people with diabetes mellitus (DM) in contrast to the histological and physiological normality of muscle mass. The target population to be screened was defined as patients with DM with a SARC-F questionnaire > 4, glycosylated haemoglobin (HbA1C) ≥ 8.0%, more than 5 years since onset of DM, taking sulfonylureas, glinides and sodium/glucose cotransporter inhibitors (SGLT2), as well as presence of chronic complications of diabetes or clinical suspicion of sarcopenia. Diagnosis was based on the presence of criteria of low muscle strength (probable sarcopenia) and low muscle mass (confirmed sarcopenia) using methods available in any clinical consultation room, such as dynamometry, the chair stand test, and Body Mass Index (BMI)-adjusted calf circumference. DS was classified into 4 stages: Stage I corresponds to sarcopenic patients with no other diabetes complication, and Stage II corresponds to patients with some type of involvement. Within Stage II are three sublevels (a, b and c). Stage IIa refers to individuals with sarcopenic diabetes and some diabetes-specific impairment, IIb to sarcopenia with functional impairment, and IIc to sarcopenia with diabetes complications and changes in function measured using standard tests Conclusion: Diabetic sarcopenia has a significant impact on function and quality of life in people with type 2 diabetes mellitus (T2DM), and it is important to give it the same attention as all other traditionally described complications of T2DM. This document aims to establish the foundation for protocolising the screening and diagnosis of diabetic sarcopenia in a manner that is simple and accessible for all levels of healthcare.

Relative adrenal insufficiency (RAI) is common in critically ill patients with cirrhosis, but it has been also documented in non-critically ill patients. Its pathophysiology is complex and not well understood yet. In this review, we aimed to present potential mechanisms and causal pathways implicated in the pathogenesis of RAI in cirrhosis. There is accumulating evidence supporting a suboptimal baseline adrenal function in cirrhosis mainly due to decreased cortisol synthesis and metabolism rates from the adrenal gland. Apart from this peripheral impairment, more recent studies suggest that there is a greater defect in the central stimulation of the hypothalamic-pituitary-adrenal (HPA) axis (hypothalamus/pituitary gland). Pro-inflammatory mediators, which are elevated in cirrhosis, have been also implicated through suppression of the HPA axis, decrease in cortisol synthesis and tissue glucocorticoid resistance. All abovementioned support the hepatoadrenal syndrome hypothesis that during episodes of acute decompensation there is suboptimal adrenocortical response that leads to worse outcomes. In conclusion, the complex pathophysiology of adrenal dysfunction in cirrhosis has not been fully elucidated yet and further research is needed in order to better understand this rather common entity in cirrhosis.