Trends in Endocrinology and Metabolism最新文献

The past decades have witnessed the rise and fall of several, largely unsuccessful, therapeutic attempts to bring the escalating obesity pandemic to a halt. Looking back to look ahead, the field has now put its highest hopes in translating insights from how the gastrointestinal (GI) tract communicates with the brain to calibrate behavior, physiology, and metabolism. A major focus of this review is to summarize the latest advances in comprehending the neuroendocrine aspects of this so-called 'gut-brain axis' and to explore novel concepts, cutting-edge technologies, and recent paradigm-shifting experiments. These exciting insights continue to refine our understanding of gut-brain crosstalk and are poised to promote the development of additional therapeutic avenues at the dawn of a new era of antiobesity therapeutics.

Central ceramides regulate energy metabolism by impacting hypothalamic neurons. This allows ceramides to integrate endocrine signals - such as leptin, ghrelin, thyroid hormones, or estradiol - and to modulate the central control of puberty. In this forum article we discuss recent evidence suggesting that specific ceramide species and neuronal populations are involved in these effects.

Dietary fiber is degraded by commensal gut microbes to yield host-beneficial short-chain fatty acids (SCFAs), but personalized responses to fiber supplementation highlight a role for other microbial metabolites in shaping host health. In this review we summarize recent findings from dietary fiber intervention studies describing health impacts attributed to microbial metabolites other than SCFAs, particularly secondary bile acids (2°BAs), aromatic amino acid derivatives, neurotransmitters, and B vitamins. We also discuss shifts in microbial metabolism occurring through altered maternal dietary fiber intake and agricultural practices, which warrant further investigation. To optimize the health benefits of dietary fibers, it is essential to survey a range of metabolites and adapt recommendations on a personalized basis, according to the different functional aspects of the microbiome.

A recent study by Peterson et al. that characterized individuals with metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO) in depth provides insights into the potential pathogenesis of MUO that accounts for much of the cardiometabolic disease and excess mortality caused by the obesity epidemic.

Eating behaviour and circadian rhythms are closely related. The type, timing, and quantity of food consumed, and host circadian rhythms, directly influence the intestinal microbiota, which in turn impacts host circadian rhythms and regulates food intake beyond homeostatic eating. This Opinion discusses the impact of food intake and circadian disruptions induced by an obesogenic environment on gut-brain axis signalling. We also explore potential mechanisms underlying the effects of altered gut microbiota on food intake behaviour and circadian rhythmicity. Understanding the crosstalk between gut microbiota, circadian rhythms, and unhealthy eating behaviour is crucial to addressing the obesity epidemic, which remains one of the biggest societal challenges of our time.

Premenopausal women and endurance-trained individuals of either sex have reduced cardiovascular disease (CVD) risk. Endurance training shifts fuel selection towards fats to spare carbohydrates; interestingly, women prioritize fats as an energy resource more than men do during exercise. Relying on fats during exercise drives whole-body lipolysis and promotes lipid uptake and oxidation capacity in skeletal muscles. These metabolic adaptations during exercise result in protection against diet-induced obesity, a healthy body fat distribution, and reduced plasma triacylglycerol (TG) concentrations. Here, we analyze how sex differences and endurance training mediate changes in skeletal muscles, including exercise-induced lipolysis, lipid uptake and β-oxidation, intramuscular TG storage, and postexercise lipid metabolism, and discuss how regulating this processes affects CVD risk.

Lipids are metabolic messengers essential for energy production, membrane structure, and signal transduction. Beyond their recognized role, lipids have emerged as metabolic rheostats of T cell responses, with distinct species differentially modulating CD8+ T cell (CTL) fate and function. Indeed, lipids can influence T cell signaling by altering their membrane composition; in addition, they can affect the differentiation path of T cells through cellular metabolism. This Review discusses the ability of lipids to shape T cell phenotypes and functions. Based on this link between lipid metabolism, metabolic fitness and immunosurveillance, we suggest that lipid could be rationally integrated in the context of immunotherapies to fine-tune fitness and function of adoptive T cell therapy (ACT) products.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine and metabolic disorder, affecting approximately 11-13% of women of reproductive age. Women with PCOS experience a higher prevalence of infertility, pregnancy complications, and cardiometabolic disorders such as obesity, insulin resistance, and type 2 diabetes mellitus. Furthermore, psychiatric comorbidities, including depression and anxiety, significantly impact the quality of life in this population. Although obesity exacerbates these health risks, the exact etiology and pathophysiology of PCOS remain complex and only partially understood. Emerging research suggests potential transgenerational inheritance through genetic and epigenetic mechanisms, highlighting the possibility of PCOS-related risks affecting subsequent generations, including sons. This review synthesizes recent findings on PCOS inheritance patterns and underscores areas for future clinical and research exploration.

Ferroptosis has been implicated in several reproductive disorders, but the underlying mechanisms remain unknown; thus, interventions targeting this pathway are lacking. Here we summarize the emerging findings on ferroptosis in reproductive biology and corresponding disorders, and highlight perspectives and challenges on future ferroptosis research with potential clinical applications.

Circadian rhythms are highly conserved biorhythms of ~24 h that govern many fundamental biological processes, including cardiovascular (CV) homeostasis. Disrupting the timing of cellular oscillators promotes cellular stress, and induction of pathogenic pathways underpins the pathogenesis of many CV diseases (CVDs). Thus, shift work, late eating, sleep disturbances, and other disruptors can result in an elevated risk of heart disease and increased incidence of adverse CV events. Here, we discuss the importance of circadian rhythms for CV homeostasis, recent developments in understanding the impact of disrupted circadian rhythms on CV health and disease progression, and how understanding the interactions between circadian and CV physiology is crucial for improving interventions to mitigate CVD, especially in populations impacted by disrupted circadian rhythms.