Vitamins & Hormones (VITAM HORM )

Publisher: Elsevier

Journal description

Current impact factor: 1.78

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.784
2012 Impact Factor 2.296
2011 Impact Factor 2.19
2010 Impact Factor 2.89
2009 Impact Factor 2.439
2008 Impact Factor 3.196
2007 Impact Factor 3.889
2006 Impact Factor 2.24
2005 Impact Factor 4.394
2004 Impact Factor 3.889
2003 Impact Factor 3.439
2002 Impact Factor 3.733
2001 Impact Factor 5.178
2000 Impact Factor 5.407
1999 Impact Factor 3.857
1998 Impact Factor 2.077
1997 Impact Factor 6.118
1996 Impact Factor 5.875
1995 Impact Factor 7
1994 Impact Factor 10
1993 Impact Factor 3.8
1992 Impact Factor 1.6

Impact factor over time

Impact factor

Additional details

5-year impact 2.65
Cited half-life 6.00
Immediacy index 0.26
Eigenfactor 0.00
Article influence 0.85
Website Vitamins & Hormones website
Other titles Vitamins and hormones
ISSN 0083-6729
OCLC 1587931
Document type Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Pulmonary hypertension is a condition characterized by vasoconstriction, vascular cell proliferation, inflammation, microthrombosis, and vessel wall remodelation. Pulmonary endothelial cells produce vasoactive substances with vasoconstrictive as well as vasodilatative effects. The imbalance of these endothelium-derived vasoactive substances induced by endothelial dysfunction is very important in the pathogenesis of PH. One of most important substances with vasodilatative effect is nitric oxide. We provide a comprehensive insight into role of NO in the pathgenesis of PH and discuss perspectives and challenges in PH therapy based on NO administration.
    Vitamins & Hormones 09/2014;
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    ABSTRACT: Activated protein C (APC) is derived from its precursor, protein C (PC). Originally thought to be synthesized exclusively by the liver, recent reports have shown that PC is also produced by many other cells including pancreatic islet β cells. APC functions as a physiological anticoagulant with anti-inflammatory, anti-apoptotic, and barrier-stabilizing properties. APC exerts its protective effects via an intriguing mechanism requiring combinations of endothelial PC receptor, protease-activated receptors, epidermal growth factor receptor, Tie2 or CD11b, depending on cell types. Diabetes is a chronic condition resulted from the body's inability to produce and/or properly use insulin. The prevalence of diabetes has risen dramatically and has become one of the major causes of premature mortality and morbidity worldwide. Diabetes prevention is an ideal approach to reduce this burden. Type 1 and type 2 diabetes are the major forms of diabetes mellitus, and both are characterized by an autoimmune response, intraislet inflammation, β-cell apoptosis, and progressive β-cell loss. Protecting β-cell from damage is critical in both prevention and treatment of diabetes. Recent in vitro and animal studies show that APC's strong anti-inflammatory and anti-apoptotic properties are beneficial in preventing β-cell destruction and diabetes in the NOD mouse model of type 1 diabetes. Future preventive and therapeutic uses of APC in diabetes look very promising.
    Vitamins & Hormones 01/2014; 95:323-63.
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    ABSTRACT: The hormone insulin-like factor 3 (INSL3) is produced by testicular Leydig cells. Production of INSL3 is dependent on the state of Leydig cell differentiation and is stimulated by the long-term trophic effects of luteinizing hormone. INSL3 is, along with the other major Leydig cell hormone testosterone, essential for testicular descent, which in humans should be completed before birth. The incidence of cryptorchidism (incomplete descent of the testis) may have increased in some developed countries during recent decades. Experimental studies have shown that maternal exposure to endocrine-disrupting chemicals (EDCs), such as phthalates, can result in cryptorchidism among male offspring and that INSL3 production, like steroidogenesis, is susceptible to phthalate exposure. Inhibition of these hormones may occur via a general phthalate-induced impairment of Leydig cell development and maturation. Recent studies have also addressed the sensitivity of human Leydig cells to EDCs, though with varied conclusions.
    Vitamins & Hormones 01/2014; 94C:327-348.
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    ABSTRACT: The onset and course of puberty is under the control of the neuroendocrine system. Factors affecting the regulation of timing and order of this system's functions may alter the onset and course of puberty. Several environmental endocrine disruptors (EDs) with significant influences on the normal course of puberty have been identified. Despite the numerous animal and human studies on EDs that may extensively affect human health, there are still several issues that need to be clarified. This chapter discusses the effects of pesticides, which constitute a significant portion of disruptors and have been increasingly used in agriculture, on precocious puberty.
    Vitamins & Hormones 01/2014; 94C:27-40.
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    ABSTRACT: Beta-cell replacement represents the optimal therapy for type 1 diabetes. Efforts to manipulate β-cell proliferation and differentiation could be advanced by a better understanding of the normal pathways regulating β-cell development and renewal. NOTCH signaling is a highly conserved pathway which plays a central role in pancreas development. Cell-lineage tracing has revealed the reactivation of the NOTCH pathway in adult human β cells cultured under conditions which induce cell proliferation and dedifferentiation. Inhibition of NOTCH signaling in dedifferentiated cells following ex vivo expansion has been shown to promote restoration of the β-cell phenotype. This approach may increase the availability of functional β cells for transplantation.
    Vitamins & Hormones 01/2014; 95:391-405.
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    ABSTRACT: Heart mitochondria play a central role in cell energy provision and in signaling. Nitric oxide (NO) is a free radical which exerts an integral regulation of the cardiovascular system not only by adapting vascular smooth muscle tone but also by influencing ion channel function, myocyte contraction, energy metabolism, and hypertrophic myocardial remodeling. This chapter analyzes the available data about heart mitochondrial NOS (mtNOS) activity and identity. The regulation of heart mtNOS by the distinctive mitochondrial environment is described by showing the effects of Ca(2+), O2, l-arginine, NADPH, mitochondrial membrane potential (ΔΨ) and the metabolic states. Evidence about the regulation of heart mtNOS in chronic hypoxia and ischemia-reperfusion models is presented. Functional implications of heart mitochondrial NOS are delineated with emphasis on the chemical reactions through which NO interacts with mitochondrial targets and exerts some of its crucial roles.
    Vitamins & Hormones 01/2014; 96:29-58.
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    ABSTRACT: The potential involvement of nitric oxide (NO), a diffusible gaseous signaling messenger, in nociceptive transduction and transmission has been extensively investigated. However, there is no consistent and convincing evidence supporting the pronociceptive action of NO at the physiological concentration, and the discrepancies are possibly due to the nonspecificity of nitric oxide synthase inhibitors and different concentrations of NO donors used in various studies. At the spinal cord level, NO predominantly reduces synaptic transmission by inhibiting the activity of NMDA receptors and glutamate release from primary afferent terminals through S-nitrosylation of voltage-activated calcium channels. NO also promotes synaptic glycine release from inhibitory interneurons through the cyclic guanosine monophosphate/protein kinase G signaling pathway. Thus, NO probably functions as a negative feedback regulator to reduce nociceptive transmission in the spinal dorsal horn during painful conditions.
    Vitamins & Hormones 01/2014; 96:1-18.
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    ABSTRACT: The prevalence of obesity has increased remarkably in the past four decades. Because obesity can promote the development of type 2 diabetes and cardiovascular disease, understanding the mechanisms that engender weight gain and discovering safe antiobesity therapies are of critical importance. In particular, the gaseous signaling molecule, nitric oxide (NO), appears to be a central factor regulating adiposity and systemic metabolism. Obese and diabetic states are characterized by a deficit in bioavailable NO, with such decreases commonly attributed to downregulation of endothelial NO synthase (eNOS), loss of eNOS activity, or quenching of NO by its reaction with oxygen radicals. Gain-of-function studies, in which vascular-derived NO has been increased pharmacologically or genetically, reveal remarkable actions of NO on body composition and systemic metabolism. This review addresses the metabolic actions of eNOS and the potential therapeutic utility of harnessing its antiobesogenic effects.
    Vitamins & Hormones 01/2014; 96:323-46.
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    ABSTRACT: The peptide hormone somatostatin (SST) is produced in the brain, the gut, and in δ-cells in pancreatic islets of Langerhans. SST secretion from δ-cells is stimulated by glucose, amino acids, and glucagon-like peptide-1. Exogenous SST strongly inhibits the secretion of the blood glucose-regulating hormones insulin and glucagon from pancreatic β-cells and α-cells, respectively. Endogenous SST secreted from δ-cells is a paracrine regulator of insulin and glucagon secretion, although the exact physiological significance of this regulation is unclear. Secreted SST binds to specific receptors (SSTRs), which are coupled to Gi/o proteins. In both β- and α-cells, activation of SSTRs suppresses hormone secretion by reducing cAMP levels, inhibiting electrical activity, decreasing Ca(2+) influx through voltage-gated Ca(2+) channels and directly reducing exocytosis in a Ca(2+) and cAMP-independent manner. In rodents, β-cells express predominantly SSTR5, whereas α-cells express SSTR2. In human islets, SSTR2 is the dominant receptor in both β- and α-cells, but other isoforms also contribute to the SST effects. Evidence from rodent models suggests that SST secretion from δ-cells is dysregulated in diabetes mellitus, which may contribute to the metabolic disturbances in this disease. SST analogues are currently used for the treatment of hyperinsulinism and other endocrine disorders, including acromegaly and Cushing's syndrome.
    Vitamins & Hormones 01/2014; 95:165-93.
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    ABSTRACT: Pancreatic beta cells rely heavily on the endoplasmic reticulum (ER) to process folding and posttranslational modification of a large amount of insulin and many other proteins and are therefore vulnerable to ER stress. The role of the ER is thus crucial in the regulation of beta cell function and survival through the unfolded protein response (UPR) pathways. However, the UPR can either allow cells to survive by adapting to stress or kill cells through apoptosis in a context-dependent manner. How cell fate is determined following UPR activation remains enigmatic. In this review, we discuss the molecular mechanisms linking ER stress to beta cell survival or apoptosis. Specifically, we focus on the role of the cellular inhibitor of apoptosis protein-1 and propose a new model for understanding survival of beta cells undergoing ER stress.
    Vitamins & Hormones 01/2014; 95:269-98.
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    ABSTRACT: Autophagy plays a key role in maintaining pancreatic β-cell homeostasis. Deregulation of this process is associated with loss of β-cell mass and function, and it is likely to be involved in Type 2 diabetes development and progression. Evidence that modulation of autophagy may be beneficial to preserve β-cell mass and function is beginning to accumulate although the complexity of this process, the intricate link between autophagy and apoptosis, and the fine balance between the protective and the disruptive role of autophagy make it very difficult to develop interventional strategies. This chapter provides an overview of the role of constitutive and adaptive autophagy in pancreatic β-cell and in the context of Type 2 diabetes.
    Vitamins & Hormones 01/2014; 95:145-64.
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    ABSTRACT: Regulation of human inducible nitric oxide synthase (iNOS) expression involves both transcriptional and posttranscriptional mechanisms. Human iNOS gene transcription is controlled in a cell type-specific manner by extracellular cytokines. Transcriptional regulation of human iNOS gene involves transcription factors NF-κB, Stat-1, AP-1, C/EBPβ, KLF6, Oct 1, and NRF. Important posttranscriptional mechanisms also regulate human iNOS mRNA stability through RNA binding proteins HuR, TTP, KSRP, and PABP. Recently, there are several miRNAs that were validated to regulate human and rodent iNOS gene expression. Among them, miR-939 and miR-26a were identified to bind with the human iNOS 3'-UTR and exert a translational blockade of human iNOS protein synthesis.
    Vitamins & Hormones 01/2014; 96:19-27.
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    ABSTRACT: Mutations in the genes encoding hepatocyte nuclear factor (HNF)1α and HNF4α cause a monogenic form of diabetes mellitus known as maturity-onset diabetes of the young (MODY). The primary cause of MODY is an impairment of glucose-stimulated insulin secretion by pancreatic β-cells, indicating the important roles of HNF1α and HNF4α in β-cells. Large-scale genetic studies have clarified that the common variants of HNF1α and HNF4α genes are also associated with type 2 diabetes, suggesting that they are involved in the pathogenesis of both diseases. Recent experimental studies revealed that HNF1α controls both β-cell function and growth by regulating target genes such as glucose transporter 2, pyruvate kinase, collectrin, hepatocyte growth factor activator, and HNF4α. In contrast, HNF4α mainly regulates the function of β-cells. Although direct target genes of HNF4α in β-cells are largely unknown, we recently identified Anks4b as a novel target of HNF4α that regulates β-cell susceptibility to endoplasmic reticulum stress. Studies of MODY have led to a better understanding of the molecular mechanism of glucose-stimulated insulin secretion by pancreatic β-cells.
    Vitamins & Hormones 01/2014; 95:407-23.
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    ABSTRACT: Bisphenol-A (BPA) is one of the highest-volume chemicals produced worldwide and the widespread exposure of individuals to BPA is suspected to affect a variety of physiological functions, including reproduction, development, and metabolism. Its estrogenic activity has been well documented in the last 15 years. In addition to estrogen receptors, BPA has been also shown to bind to and activate the estrogen-related receptor γ and pregnane X receptor and inhibit the androgen receptor. Halogenated BPAs were also shown to activate the peroxisome proliferator-activated receptor γ and inhibit thyroid hormone receptors. In this chapter, we review recent studies shedding light on the structural and molecular mechanisms by which BPA and its halogenated derivatives interfere with nuclear hormone receptor signaling. These data provide guidelines for the development of safer substitutes devoid of hormonal activity and may help environmental risk assessment.
    Vitamins & Hormones 01/2014; 94C:229-251.
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    ABSTRACT: Imprinting is an epigenetic form of gene regulation that mediates a parent-of-origin-dependent expression of the alleles of a number of genes. Imprinting, which occurs at specific sites within or surrounding the gene, called differentially methylated domains, consists in a methylation of CpGs. The appropriate transmission of genomics imprints is essential for the control of embryonic development and fetal growth. A number of endocrine disruptors (EDs) affect male reproductive tract development and spermatogenesis. It was postulated that the genetic effects of EDs might be induced by alterations in gene imprinting. We tested two EDs: methoxychlor and vinclozolin. Their administration during gestation induced in the offspring a decrease in sperm counts and significant modifications in the methylation pattern of a selection of paternally and maternally expressed canonical imprinted genes. The observation that imprinting was largely untouched in somatic cells suggests that EDs exert their damaging effects via the process of reprogramming that is unique to gamete development. Interestingly, the effects were transgenerational, although disappearing gradually from F1 to F3. A systematic analysis showed a heterogeneity in the CpG sensitivity to EDs. We propose that the deleterious effects of EDs on the male reproductive system are mediated by imprinting defects in the sperm. The reported effects of EDs on human male spermatogenesis might be mediated by analogous imprinting alterations.
    Vitamins & Hormones 01/2014; 94C:211-227.