Vitamins and Hormones最新文献_第9页

The changes in adrenal developmental programming and homeostasis in offspring induced by glucocorticoids exposure during pregnancy. 孕期糖皮质激素暴露对后代肾上腺发育程序和稳态的影响

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-02-09 DOI: 10.1016/bs.vh.2023.09.001

Yawen Chen, Hui Wang

{"title":"The changes in adrenal developmental programming and homeostasis in offspring induced by glucocorticoids exposure during pregnancy.","authors":"Yawen Chen, Hui Wang","doi":"10.1016/bs.vh.2023.09.001","DOIUrl":"10.1016/bs.vh.2023.09.001","url":null,"abstract":"Clinically, synthetic glucocorticoids are often used to treat maternal and fetal related diseases, such as preterm birth and autoimmune diseases. Although its clinical efficacy is positive, it will expose the fetus to exogenous glucocorticoids. Adverse environments during pregnancy (e.g., exogenous glucocorticoids exposure, malnutrition, infection, hypoxia, and stress) can lead to fetal overexposure to endogenous maternal glucocorticoids. Basal glucocorticoids levels in utero are crucial in determining fetal tissue maturation and its postnatal fate. As the synthesis and secretion organ of glucocorticoids, the adrenal development is crucial for the growth and development of the body. Studies have found that glucocorticoids exposure during pregnancy could cause abnormal fetal adrenal development, which could last after birth or even adulthood. As the key organ of fetal-originated adult disease, the adrenal developmental programming has a profound impact on the health of offspring, which can lead to many chronic diseases in adulthood. However, the aberrant adrenal development in offspring caused by glucocorticoids exposure during pregnancy and its intrauterine programming mechanism have not been systematically clarified. Therefore, this review summarizes recent research progress on the short and long-term hazards of aberrant adrenal development induced by glucocorticoids exposure during pregnancy, which is of great significance for the analysis of aberrant adrenal development and clarify the intrauterine origin mechanism of fetal-originated adult disease.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"124 ","pages":"463-490"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139974446","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

Antioxidant and antibrowning properties of Maillard reaction products in food and biological systems. 食品和生物系统中 Maillard 反应产物的抗氧化和抗褐变特性。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-03-19 DOI: 10.1016/bs.vh.2024.01.001

Majid Nooshkam, Mehdi Varidi

{"title":"Antioxidant and antibrowning properties of Maillard reaction products in food and biological systems.","authors":"Majid Nooshkam, Mehdi Varidi","doi":"10.1016/bs.vh.2024.01.001","DOIUrl":"10.1016/bs.vh.2024.01.001","url":null,"abstract":"Oxidative damage refers to the harm caused to biological systems by reactive oxygen species such as free radicals. This damage can contribute to a range of diseases and aging processes in organisms. Moreover, oxidative deterioration of lipids is a serious problem because it reduces the shelf life of food products, degrades their nutritional value, and produces reaction products that could be toxic. Antioxidants are effective compounds for preventing lipid oxidation, and synthetic antioxidants are frequently added to foods due to their high effectiveness and low cost. However, the safety of these antioxidants is a subject that is being discussed in the public more and more. Synthetic antioxidants have been found to have potential negative effects on health due to their ability to accumulate in tissues and disrupt natural antioxidant systems. During thermal processing and storage, foods containing reducing sugars and amino compounds frequently produce Maillard reaction products (MRPs). Through the chelation of metal ions, scavenging of reactive oxygen species, destruction of hydrogen peroxide, and suppression of radical chain reaction, MRPs exhibit excellent antioxidant properties in a variety of food products and biological systems. Also, the capacity of MRPs to chelate metals makes them as a potential inhibitor of the enzymatic browning in fruits and vegetables. In this book chapter, the methods used for the evaluation of antioxidant activity of MRPs are provided. Moreover, the antioxidant and antibrowning activities of MRPs in food and biological systems is discussed. MRPs can generally be isolated and used as commercial preparations of natural antioxidants.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"367-399"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602137","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

Functional interaction of Clock genes and bone morphogenetic proteins in the adrenal cortex. 肾上腺皮质中时钟基因和骨形态发生蛋白的功能相互作用

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2023-06-01 DOI: 10.1016/bs.vh.2023.05.002

Yoshiaki Soejima, Koichiro Yamamoto, Yasuhiro Nakano, Atsuhito Suyama, Nahoko Iwata, Fumio Otsuka

{"title":"Functional interaction of Clock genes and bone morphogenetic proteins in the adrenal cortex.","authors":"Yoshiaki Soejima, Koichiro Yamamoto, Yasuhiro Nakano, Atsuhito Suyama, Nahoko Iwata, Fumio Otsuka","doi":"10.1016/bs.vh.2023.05.002","DOIUrl":"10.1016/bs.vh.2023.05.002","url":null,"abstract":"The bone morphogenetic protein (BMP) system in the adrenal cortex plays modulatory roles in the control of adrenocortical steroidogenesis. BMP-6 enhances aldosterone production by modulating angiotensin (Ang) II-mitogen-activated protein kinase (MAPK) signaling, whereas activin regulates the adrenocorticotropin (ACTH)-cAMP cascade in adrenocortical cells. A peripheral clock system in the adrenal cortex was discovered and it has been shown to have functional roles in the adjustment of adrenocortical steroidogenesis by interacting with the BMP system. It was found that follistatin, a binding protein of activin, increased Clock mRNA levels, indicating an endogenous function of activin in the regulation of Clock mRNA expression. Elucidation of the interrelationships among the circadian clock system, the BMP system and adrenocortical steroidogenesis regulated by the hypothalamic-pituitary-adrenal (HPA) axis would lead to an understanding of the pathophysiology of adrenal disorders and metabolic disorders and the establishment of better medical treatment from the viewpoint of pharmacokinetics.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"124 ","pages":"429-447"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139974440","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

The dynamic roles of advanced glycation end products. 高级糖化终产物的动态作用。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-05-28 DOI: 10.1016/bs.vh.2024.02.008

Mariyam Khalid, Abdu Adem

{"title":"The dynamic roles of advanced glycation end products.","authors":"Mariyam Khalid, Abdu Adem","doi":"10.1016/bs.vh.2024.02.008","DOIUrl":"10.1016/bs.vh.2024.02.008","url":null,"abstract":"Advanced glycation end products (AGEs) are a heterogeneous group of potentially harmful molecules that can form as a result of a non-enzymatic reaction between reducing sugars and proteins, lipids, or nucleic acids. The total body pool of AGEs reflects endogenously produced AGEs as well as exogeneous AGEs that come from sources such as diet and the environment. Engagement of AGEs with their cellular receptor, the receptor for advanced glycation end products (RAGE), which is expressed on the surface of various cell types, converts a brief pulse of cellular activation to sustained cellular dysfunction and tissue destruction. The AGEs/RAGE interaction triggers a cascade of intracellular signaling pathways such as mitogen-activated protein kinase/extracellular signal-regulated kinase, phosphoinositide 3-kinases, transforming growth factor beta, c-Jun N-terminal kinases (JNK), and nuclear factor kappa B, which leads to the production of pro-inflammatory cytokines, chemokines, adhesion molecules, and oxidative stress. All these events contribute to the progression of several chronic diseases. This chapter will provide a comprehensive understanding of the dynamic roles of AGEs in health and disease which is crucial to develop interventions that prevent and mitigate the deleterious effects of AGEs accumulation.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"1-29"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602089","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

Advanced glycation end products and insulin resistance in diabetic nephropathy. 糖尿病肾病中的高级糖化终末产物和胰岛素抵抗。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-04-10 DOI: 10.1016/bs.vh.2024.02.007

Kirti Parwani, Palash Mandal

{"title":"Advanced glycation end products and insulin resistance in diabetic nephropathy.","authors":"Kirti Parwani, Palash Mandal","doi":"10.1016/bs.vh.2024.02.007","DOIUrl":"10.1016/bs.vh.2024.02.007","url":null,"abstract":"Insulin resistance is a central hallmark that connects the metabolic syndrome and diabetes to the resultant formation of advanced glycation end products (AGEs), which further results in the complications of diabetes, including diabetic nephropathy. Several factors play an important role as an inducer to diabetic nephropathy, and AGEs elicit their harmful effects via interacting with the receptor for AGEs Receptor for AGEs, by induction of pro-inflammatory cytokines, oxidative stress, endoplasmic reticulum stress and fibrosis in the kidney tissues leading to the loss of renal function. Insulin resistance results in the activation of other alternate pathways governed by insulin, which results in the hypertrophy of the renal cells and tissue remodeling. Apart from the glucose uptake and disposal, insulin dependent PI3K and Akt also upregulate the expression of endothelial nitric oxide synthase, that results in increasing the bioavailability of nitric oxide in the vascular endothelium, which further results in tissue fibrosis. Considering the global prevalence of diabetic nephropathy, and the impact of protein glycation, various inhibitors and treatment avenues are being developed, to prevent the progression of diabetic complications. In this chapter, we discuss the role of glycation in insulin resistance and further its impact on the kidney.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"117-148"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602136","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

Gene therapy targeting the blood-brain barrier. 针对血脑屏障的基因疗法。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-04-12 DOI: 10.1016/bs.vh.2024.03.001

Jakob Körbelin, Adriana Arrulo, Markus Schwaninger

{"title":"Gene therapy targeting the blood-brain barrier.","authors":"Jakob Körbelin, Adriana Arrulo, Markus Schwaninger","doi":"10.1016/bs.vh.2024.03.001","DOIUrl":"10.1016/bs.vh.2024.03.001","url":null,"abstract":"Endothelial cells are the building blocks of vessels in the central nervous system (CNS) and form the blood-brain barrier (BBB). An intact BBB limits permeation of large hydrophilic molecules into the CNS. Thus, the healthy BBB is a major obstacle for the treatment of CNS disorders with antibodies, recombinant proteins or viral vectors. Several strategies have been devised to overcome the barrier. A key principle often consists in attaching the therapeutic compound to a ligand of receptors expressed on the BBB, for example, the transferrin receptor (TfR). The fusion molecule will bind to TfR on the luminal side of brain endothelial cells, pass the endothelial layer by transcytosis and be delivered to the brain parenchyma. However, attempts to endow therapeutic compounds with the ability to cross the BBB can be difficult to implement. An alternative and possibly more straight-forward approach is to produce therapeutic proteins in the endothelial cells that form the barrier. These cells are accessible from blood circulation and have a large interface with the brain parenchyma. They may be an ideal production site for therapeutic protein and afford direct supply to the CNS.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"126 ","pages":"191-217"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141728221","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

Insulin and the blood-brain barrier. 胰岛素与血脑屏障

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-02-22 DOI: 10.1016/bs.vh.2024.02.002

Elizabeth M Rhea, William A Banks

引用次数: 0

Neurotoxic effects of metals on blood brain barrier impairment and possible therapeutic approaches. 金属对脑血屏障损伤的神经毒性效应及可能的治疗方法。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-05-21 DOI: 10.1016/bs.vh.2024.04.003

Saba Mehak Zahoor, Sara Ishaq, Touqeer Ahmed

{"title":"Neurotoxic effects of metals on blood brain barrier impairment and possible therapeutic approaches.","authors":"Saba Mehak Zahoor, Sara Ishaq, Touqeer Ahmed","doi":"10.1016/bs.vh.2024.04.003","DOIUrl":"10.1016/bs.vh.2024.04.003","url":null,"abstract":"Exposure to neurotoxic and heavy metals (Pb2+, As3+, Mn2+, Cd2+, etc) has increased over time and has shown to negatively affect brain health. Heavy metals can cross the blood brain barrier (BBB) in various ways including receptor or carrier-mediated transport, passive diffusion, or transport via gaps in the endothelial cells of the brain. In high concentrations, these metals have been shown to cause structural and functional impairment to the BBB, by inducing oxidative stress, ion dyshomeostasis, tight junction (TJ) loss, astrocyte/pericyte damage and interference of gap junctions. The structural and functional impairment of the BBB results in increased BBB permeability, which ultimately leads to accumulation of these heavy metals in the brain and their subsequent toxicity. As a result of these effects, heavy metals are correlated with various neurological disorders. The pathological effects of these heavy metals can be effectively mitigated via chelation. In addition, it is possible to treat the associated disorders by counteracting the molecular mechanisms associated with the brain and BBB impairment.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"126 ","pages":"1-24"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141728224","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

Glycation in the cardiomyocyte. 心肌细胞中的糖化。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-05-24 DOI: 10.1016/bs.vh.2024.04.005

Christine E Delligatti, Jonathan A Kirk

{"title":"Glycation in the cardiomyocyte.","authors":"Christine E Delligatti, Jonathan A Kirk","doi":"10.1016/bs.vh.2024.04.005","DOIUrl":"10.1016/bs.vh.2024.04.005","url":null,"abstract":"Glycation is a protein post-translational modification that can occur on lysine and arginine residues as a result of a non-enzymatic process known as the Maillard reaction. This modification is irreversible, so the only way it can be removed is by protein degradation and replacement. Small reactive carbonyl species, glyoxal and methylglyoxal, are the primary glycating agents and are elevated in several conditions associated with an increased risk of cardiovascular disease, including diabetes, rheumatoid arthritis, smoking, and aging. Thus, how protein glycation impacts the cardiomyocyte is of particular interest, to both understand how these conditions increase the risk of cardiovascular disease and how glycation might be targeted therapeutically. Glycation can affect the cardiomyocyte through extracellular mechanisms, including RAGE-based signaling, glycation of the extracellular matrix that modifies the mechanical environment, and signaling from the vasculature. Intracellular glycation of the cardiomyocyte can impact calcium handling, protein quality control and cell death pathways, as well as the cytoskeleton, resulting in a blunted contractility. While reducing protein glycation and its impact on the heart has been an active area of drug development, multiple clinical trials have had mixed results and these compounds have not been translated to the clinic-highlighting the challenges of modulating myocyte glycation. Here we will review protein glycation and its effects on the cardiomyocyte, therapeutic attempts to reverse these, and offer insight as to the future of glycation studies and patient treatment.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"47-88"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11578284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-enzymatic glycation and diabetic kidney disease. 非酶糖化与糖尿病肾病。

4区医学

Vitamins and Hormones Pub Date : 2024-01-01 Epub Date: 2024-02-06 DOI: 10.1016/bs.vh.2024.01.002

Anil K Pasupulati, Veerababu Nagati, Atreya S V Paturi, G Bhanuprakash Reddy

{"title":"Non-enzymatic glycation and diabetic kidney disease.","authors":"Anil K Pasupulati, Veerababu Nagati, Atreya S V Paturi, G Bhanuprakash Reddy","doi":"10.1016/bs.vh.2024.01.002","DOIUrl":"10.1016/bs.vh.2024.01.002","url":null,"abstract":"Chronic diabetes leads to various complications including diabetic kidney disease (DKD). DKD is a major microvascular complication and the leading cause of morbidity and mortality in diabetic patients. Varying degrees of proteinuria and reduced glomerular filtration rate are the cardinal clinical manifestations of DKD that eventually progress into end-stage renal disease. Histopathologically, DKD is characterized by renal hypertrophy, mesangial expansion, podocyte injury, glomerulosclerosis, and tubulointerstitial fibrosis, ultimately leading to renal replacement therapy. Amongst the many mechanisms, hyperglycemia contributes to the pathogenesis of DKD via a mechanism known as non-enzymatic glycation (NEG). NEG is the irreversible conjugation of reducing sugars onto a free amino group of proteins by a series of events, resulting in the formation of initial Schiff's base and an Amadori product and to a variety of advanced glycation end products (AGEs). AGEs interact with cognate receptors and evoke aberrant signaling cascades that execute adverse events such as oxidative stress, inflammation, phenotypic switch, complement activation, and cell death in different kidney cells. Elevated levels of AGEs and their receptors were associated with clinical and morphological manifestations of DKD. In this chapter, we discussed the mechanism of AGEs accumulation, AGEs-induced cellular and molecular events in the kidney and their impact on the pathogenesis of DKD. We have also reflected upon the possible options to curtail the AGEs accumulation and approaches to prevent AGEs mediated adverse renal outcomes.","PeriodicalId":51209,"journal":{"name":"Vitamins and Hormones","volume":"125 ","pages":"251-285"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141602144","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