Vitamins and Hormones最新文献_第7页

Self-assembly of the insulin-responsive vesicles creates a signaling platform for the insulin action on glucose uptake. 胰岛素反应囊泡的自组装为胰岛素对葡萄糖摄取的作用创造了一个信号平台。

4区医学

Vitamins and Hormones Pub Date : 2025-01-01 Epub Date: 2024-07-25 DOI: 10.1016/bs.vh.2024.07.001

Konstantin V Kandror

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About the Editor. 关于编辑。

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Vitamins and Hormones Pub Date : 2025-01-01 DOI: 10.1016/S0083-6729(25)00011-1

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Hepcidin: A multifaceted hormone in iron homeostasis and tumor biology. Hepcidin：一种涉及铁稳态和肿瘤生物学的多层面激素。

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Vitamins and Hormones Pub Date : 2025-01-01 Epub Date: 2024-10-24 DOI: 10.1016/bs.vh.2024.10.003

Xiaoyu Liu, Xinyu Zhang, Yumei Fan, Ke Tan

{"title":"Hepcidin: A multifaceted hormone in iron homeostasis and tumor biology.","authors":"Xiaoyu Liu, Xinyu Zhang, Yumei Fan, Ke Tan","doi":"10.1016/bs.vh.2024.10.003","DOIUrl":"10.1016/bs.vh.2024.10.003","url":null,"abstract":"Iron is an essential trace element that plays a crucial role in various biological processes, including oxygen transport, DNA synthesis and cell proliferation. Iron homeostasis is a critical biological equilibrium that involves the balance of iron absorption, utilization, storage and excretion. Iron is intricately linked to the pathophysiology of cancer. Its dual role as a vital nutrient and a potential carcinogen highlights the complexity of iron's influence on tumorigenesis. Iron balance is finely tuned through a complex interplay of molecular components and regulatory mechanisms. Hepcidin, a liver-derived peptide hormone, is the principal regulator of systemic iron availability. Hepcidin exerts its effects by binding to the iron export protein ferroportin (FPN1), leading to its internalization and degradation, which in turn reduces the release of iron from macrophages and the intestinal absorption of dietary iron. In human cancers, the expression of hepcidin is significantly altered, leading to increased iron absorption and retention. Hepcidin has emerged as a significant player in cancer biology due to its potential as both a tumor suppressor and a promoter. Understanding the context-dependent role of hepcidin in cancer opens avenues for novel therapeutic strategies. Modulating hepcidin levels or its activity could be a potential approach to treat cancer, either by starving tumors of iron or by normalizing the iron-rich microenvironment to enhance the efficacy of existing cancer treatments. In this review, we provide a comprehensive overview of the critical functions of hepcidin in iron metabolism, summarize the upstream regulatory factors that control the expression of hepcidin, and delve deeply into the downstream signaling pathways and molecular mechanisms by which hepcidin regulates the tumorigenesis, as well as elucidate the promising potential of hepcidin as a novel therapeutic target in the treatment of cancer, underscoring the significance of understanding and harnessing the complex interplay between hepcidin, iron metabolism and cancer biology.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"129 ","pages":"317-360"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144857001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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The growing complexity of the control of the hypothalamic pituitary thyroid axis and brown adipose tissue by leptin. 瘦素对下丘脑-垂体-甲状腺轴和棕色脂肪组织的控制日益复杂。

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Vitamins and Hormones Pub Date : 2025-01-01 Epub Date: 2024-08-21 DOI: 10.1016/bs.vh.2024.07.005

Ricardo H Costa-E-Sousa, Virginia L Brooks

{"title":"The growing complexity of the control of the hypothalamic pituitary thyroid axis and brown adipose tissue by leptin.","authors":"Ricardo H Costa-E-Sousa, Virginia L Brooks","doi":"10.1016/bs.vh.2024.07.005","DOIUrl":"10.1016/bs.vh.2024.07.005","url":null,"abstract":"The balance between food intake and energy expenditure is precisely regulated to maintain adipose stores. Leptin, which is produced in and released from adipose in direct proportion to its size, is a major contributor to this control and initiates its homeostatic responses largely via binding to leptin receptors (LepR) in the hypothalamus. Decreases in hypothalamic LepR binding signals starvation, leading to hunger and reduced energy expenditure, whereas increases in hypothalamic LepR binding can suppress food intake and increase energy expenditure. However, large gaps persist in the specific hypothalamic sites and detailed mechanisms by which leptin increases energy expenditure, via the parallel activation of the hypothalamic pituitary thyroid (HPT) axis and brown adipose tissue (BAT). The purpose of this review is to develop a framework for the complex mechanisms and neurocircuitry. The core circuitry begins with leptin binding to receptors in the arcuate nucleus, which then sends projections to the paraventricular nucleus (to regulate the HPT axis) and the dorsomedial hypothalamus (to regulate BAT). We build on this core by layering complexities, including the intricate and unsettled regulation of arcuate proopiomelanocortin neurons by leptin and the changes that occur as the regulation of the HPT axis and BAT is engaged or modified by challenges such as starvation, hypothermia, obesity, and pregnancy.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"127 ","pages":"305-362"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nanoparticles in prevention of protein glycation. 纳米粒子在防止蛋白质糖化方面的作用。

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Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-05-10 DOI: 10.1016/bs.vh.2024.04.001

Aruna Sivaram, Nayana Patil

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Vitamin B6 and diabetes and its role in counteracting advanced glycation end products. 维生素 B6 与糖尿病及其在抵消高级糖化终产物方面的作用。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-05-07 DOI: 10.1016/bs.vh.2024.02.005

F Vernì

{"title":"Vitamin B6 and diabetes and its role in counteracting advanced glycation end products.","authors":"F Vernì","doi":"10.1016/bs.vh.2024.02.005","DOIUrl":"10.1016/bs.vh.2024.02.005","url":null,"abstract":"Naturally occurring forms of vitamin B6 include six interconvertible water-soluble compounds: pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM), and their respective monophosphorylated derivatives (PNP, PLP, and PMP). PLP is the catalytically active form which works as a cofactor in approximately 200 reactions that regulate the metabolism of glucose, lipids, amino acids, DNA, and neurotransmitters. Most of vitamers can counteract the formation of reactive oxygen species and the advanced glycation end-products (AGEs) which are toxic compounds that accumulate in diabetic patients due to prolonged hyperglycemia. Vitamin B6 levels have been inversely associate with diabetes, while vitamin B6 supplementation reduces diabetes onset and its vascular complications. The mechanisms at the basis of the relation between vitamin B6 and diabetes onset are still not completely clarified. In contrast more evidence indicates that vitamin B6 can protect from diabetes complications through its role as scavenger of AGEs. It has been demonstrated that in diabetes AGEs can destroy the functionality of macromolecules such as protein, lipids, and DNA, thus producing tissue damage that result in vascular diseases. AGEs can be in part also responsible for the increased cancer risk associated with diabetes. In this chapter the relationship between vitamin B6, diabetes and AGEs will be discussed by showing the acquired knowledge and questions that are still open.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"401-438"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Aging of the adrenal gland and its impact on the stress response. 肾上腺的老化及其对压力反应的影响。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-02-01 DOI: 10.1016/bs.vh.2023.12.004

Andreas Yiallouris, Charalampos Filippou, Sophia C Themistocleous, Katerina Menelaou, Vasiliki Kalodimou, Charalambos Michaeloudes, Elizabeth O Johnson

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Angiotensin II-dependent aldosterone production in the adrenal cortex. 肾上腺皮质中血管紧张素 II 依赖性醛固酮的产生。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2023-06-01 DOI: 10.1016/bs.vh.2023.05.001

Anastasios Lymperopoulos, Jordana I Borges, Malka S Suster

{"title":"Angiotensin II-dependent aldosterone production in the adrenal cortex.","authors":"Anastasios Lymperopoulos, Jordana I Borges, Malka S Suster","doi":"10.1016/bs.vh.2023.05.001","DOIUrl":"10.1016/bs.vh.2023.05.001","url":null,"abstract":"The adrenal cortex is responsible for production of adrenal steroid hormones and is anatomically divided into three distinct zones: zona glomerulosa secreting mineralocorticoids (mainly aldosterone), zona fasciculata secreting glucocorticoids (cortisol), and zona reticularis producing androgens. Importantly, due to their high lipophilicity, no adrenal steroid hormone (including aldosterone) is stored in vesicles but rather gets synthesized and secreted instantly upon cell stimulation with specific stimuli. Aldosterone is the most potent mineralocorticoid hormone produced from the adrenal cortex in response to either angiotensin II (AngII) or elevated K+ levels in the blood (hyperkalemia). AngII, being a peptide, cannot cross cell membranes and thus, uses two distinct G protein-coupled receptor (GPCR) types, AngII type 1 receptor (AT1R) and AT2R to exert its effects inside cells. In zona glomerulosa cells, AT1R activation by AngII results in aldosterone synthesis and secretion via two main pathways: (a) Gq/11 proteins that activate phospholipase C ultimately raising intracellular free calcium concentration; and (b) βarrestin1 and -2 (also known as Arrestin-2 and -3, respectively) that elicit sustained extracellular signal-regulated kinase (ERK) activation. Both pathways induce upregulation and acute activation of StAR (steroidogenic acute regulatory) protein, the enzyme that catalyzes the rate-limiting step in aldosterone biosynthesis. This chapter describes these two salient pathways underlying AT1R-induced aldosterone production in zona glomerulosa cells. We also highlight some pharmacologically important notions pertaining to the efficacy of the currently available AT1R antagonists, also known as angiotensin receptor blockers (ARBs) or sartans at suppressing both pathways, i.e., their inverse agonism efficacy at G proteins and βarrestins.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"124 ","pages":"393-404"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139974438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic variants in the renin-angiotensin-aldosterone system: Impact on cancer risk, prognosis, and therapeutic directions. 肾素-血管紧张素-醛固酮系统的基因变异：对癌症风险、预后和治疗方向的影响。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-01-08 DOI: 10.1016/bs.vh.2023.12.002

Muhammad T Abdel Ghafar, Aya A Helmy

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Sleep loss impairs blood-brain barrier function: Cellular and molecular mechanisms. 睡眠不足会损害血脑屏障功能：细胞和分子机制

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-04-08 DOI: 10.1016/bs.vh.2024.02.003

Jessica Janeth Avilez-Avilez, María Fernanda Medina-Flores, Beatriz Gómez-Gonzalez

{"title":"Sleep loss impairs blood-brain barrier function: Cellular and molecular mechanisms.","authors":"Jessica Janeth Avilez-Avilez, María Fernanda Medina-Flores, Beatriz Gómez-Gonzalez","doi":"10.1016/bs.vh.2024.02.003","DOIUrl":"10.1016/bs.vh.2024.02.003","url":null,"abstract":"Sleep is a physiological process that preserves the integrity of the neuro-immune-endocrine network to maintain homeostasis. Sleep regulates the production and secretion of hormones, neurotransmitters, cytokines and other inflammatory mediators, both at the central nervous system (CNS) and at the periphery. Sleep promotes the removal of potentially toxic metabolites out of the brain through specialized systems such as the glymphatic system, as well as the expression of specific transporters in the blood-brain barrier. The blood-brain barrier maintains CNS homeostasis by selectively transporting metabolic substrates and nutrients into the brain, by regulating the efflux of metabolic waste products, and maintaining bidirectional communication between the periphery and the CNS. All those processes are disrupted during sleep loss. Brain endothelial cells express the blood-brain barrier phenotype, which arises after cell-to-cell interactions with mural cells, like pericytes, and after the release of soluble factors by astroglial endfeet. Astroglia, pericytes and brain endothelial cells respond differently to sleep loss; evidence has shown that sleep loss induces a chronic low-grade inflammatory state at the CNS, which is associated with blood-brain barrier dysfunction. In animal models, blood-brain barrier dysfunction is characterized by increased blood-brain barrier permeability, decreased tight junction protein expression and pericyte detachment from the capillary wall. Blood-brain barrier dysfunction may promote defects in brain clearance of potentially neurotoxic metabolites and byproducts of neural physiology, which may eventually contribute to neurodegenerative diseases. This chapter aims to describe the cellular and molecular mechanisms by which sleep loss modifies the function of the blood-brain barrier.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"126 ","pages":"77-96"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141728227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0