Current Opinion in Endocrine and Metabolic Research最新文献

Obesity is a significant global burden for individuals and healthcare systems with its array of associated chronic cardiometabolic diseases. While lifestyle modifications such as dietary interventions and increased physical activity are effective in weight management, recent investigations highlight the critical role of timing these interventions in accordance with our body's circadian clock. Over the past decade, multiple studies and meta analyses have investigated how the timing of exercise training influences white adipose tissue (WAT) biology, fat mass loss, and obesity, but physical activity guidelines have not yet adopted a recommendation for exercise timing due to conflicting conclusions. This review aims to summarize the latest findings in this field and touches upon contributing factors such as sex disparities and nutrition timing.

The adaptation to changing environmental cues represents a key prerequisite for the survival of an organism. Mammals, including humans, have evolved intricate endocrine signals to convey information about the nutritional status to individual organs, cells, and eventually the cell nucleus, to trigger appropriate molecular-metabolic responses. To this end, mounting a proper fasting response is determined by not only intra-organ adaptations but also inter-tissue crosstalk mechanisms that orchestrate whole-body energy homeostasis under nutrient-deprived conditions. Here, we shortly summarize recent advances in our current understanding of the key processes driving the adaptive response to fasting with a focus on the crosstalk between the adipose tissue and liver ketogenesis.

Adipose tissue inflammation drives systemic pathophysiology, for instance, obesity-related cardiometabolic disease. Specialized pro-resolving lipid mediators are a superfamily of endogenously produced lipids that promote the resolution of inflammation, an actively regulated process. New evidence suggests that such lipids (e.g. lipoxins) could resolve adipose tissue inflammation and, thus, subvert obesity-related diseases. A key feature of pro-resolving lipids is their ability to promote an M2-like macrophage phenotype and enhance efferocytosis while avoiding adverse side-effects typically associated with anti-inflammatory drugs, such as increased sensitivity to infections. This brief review discusses the therapeutic potential of pro-resolving lipid mediators in mitigating systemic disease fueled by adipose tissue inflammation in both experimental and human disease models.

Bilateral adrenal cortex hyperplasias can present in various forms and are divided as either macronodular or micronodular. This review presents the recent identifications of the genetic alterations responsible for the various forms of cortisol-secreting adrenal hyperplasias. These include the tumor suppressor genes ARMC5 in bilateral primary macronodular adrenal hyperplasia (PBMAH) and KDM1A in GIP-dependent PBMAH with Cushing’s syndrome. Other genetic alterations are found in PBMAH associated with rare syndromic forms and various cAMP/PKA pathway gene mutations are involved in both macronodular and micronodular adrenal hyperplasias. We present as well certain clinical recommendations for each genetic etiology, including that ARMC5 or KDM1A genetic testing should be offered to all patients with PBMAH, depending on the Cushing syndrome’s GIP-dependence or not.

Human organism is tightly interconnected with its microbiota on physiological and signaling levels. Microbial endocrinology as an interdisciplinary area of studying host–microbiota interactions can focus on either player: how the microbiota affects the host via synthesis of host-targeted humoral factors and how the host-derived molecules regulate the microbial community homeostasis. The present mini-review presents the authors' perspective on the impact of human hormones on the microbiota. It discusses known effects, but especially outlines existing complications in this research area, and proposes directions for future investigation.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease which is characterized by the destruction of insulin-producing pancreatic β-cells. Current evidence supports the contribution of T-cells, macrophages, B-cells, and dendritic cells to the pathogenesis of T1DM as well. T1DM-associated risk factors, including defects in host immune response, socioeconomic conditions, and environmental factors create a dysbiotic environment in the oral cavity, which support the growth of pathogenic microbial biofilms. Changes in microbial composition, together with the diminished immune response, lead to the development of two most common oral diseases, caries and periodontal diseases. In the present review, we summarized the current evidence on oral manifestations of T1DM and described the shifts in oral microbial composition and oral immune response.

Pheochromocytomas and paragangliomas (PPGL) are neuroendocrine tumors which secrete catecholamines, causing cardiovascular compromise. While isolated tumors and locoregional disease can be treated surgically, treatment options for metastatic disease are limited, and no targeted therapies exist. Approximately 25% of PPGL are causatively associated with germline pathogenic variants, which are known risk factors for multifocal and metastatic PPGL. Knowledge of somatic driver mutations continues to evolve. Molecular classification of PPGL has identified three genomic subtypes: Cluster 1 (pseudohypoxia), Cluster 2 (kinase signaling) and Cluster 3 (Wnt-altered). This review summaries recent studies characterizing the tumor microenvironment, genomic drivers of tumorigenesis and progression, and current research on molecular targets for novel diagnostic and therapeutic strategies in PPGL.