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Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 12113

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Special Issue Editor

Prof. Dr. Don-Kyu Kim

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Guest Editor

Department of Integrative Food, Bioscience and Biotechnology, Chonnam National University, Gwangju, Republic of Korea
Interests: gene regulation; cell signaling; nuclear hormone receptor; transcription factor; transcriptional regulation; liver metabolism; metabolic disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Maintenance of endocrine and metabolic homeostasis is highly important for healthy life. Any turbulences in endocrine or metabolic regulation such as hormonal imbalance or metabolic dysregulation will lead to various pathological conditions ranging from very mild to life-threatening diseases. Gene regulation and cell-to-cell signaling are key factors in maintaining normal endocrine and metabolic regulation. Hostile conditions such as drug toxicity, stress, obesity, dyslipidemia, hypo/hyperglycemia and adrenal, thyroid or pituitary dysregulation alter gene expression which, in turn, activates or shuts down specific cell signaling pathways. Alteration in cell signaling status disturbs the endocrine, anabolic and/or catabolic pathways, which leads to acute or chronic metabolic diseases. Finding targetable genes or signaling pathways will enrich the treatment availability against endocrine or metabolic diseases.

This Special Issue entitled “Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation” will address the latest research investigating mechanisms of gene regulation and signaling pathways in response to endocrine and metabolic alterations/homeostasis. Authors are welcome to submit their original research or review papers dealing with this topic.

Prof. Dr. Don-Kyu Kim
Guest Editor

Guest Editor Assistant
Prof. Dr. Kamalakannan Radhakrishnan

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

transcriptional regulation
cell signaling
gene expression
epigenetic modifications
metabolic regulations
metabolomics
metabolic diseases
molecular mechanism
endocrinology
endocrine disruption

Published Papers (4 papers)

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Research

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13 pages, 2089 KiB

Open AccessArticle

Glucose Stimulates Glial Cell Line-Derived Neurotrophic Factor Gene Expression in Microglia through a GLUT5-Independent Mechanism

by Muhammad S. Aldhshan, Gursagar Jhanji, Nicole J. Poritsanos and Tooru M. Mizuno

Int. J. Mol. Sci. 2022, 23(13), 7073; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137073 - 25 Jun 2022

Cited by 2 | Viewed by 1865

Abstract

Feeding-regulating neurotrophic factors are expressed in both neurons and glial cells. However, nutritional regulation of anorexigenic glial cell line-derived neurotrophic factor (GDNF) and orexigenic mesencephalic astrocyte-derived neurotrophic factor (MANF) expression in specific cell types remains poorly understood. Hypothalamic glucose sensing plays a critical role in the regulation of food intake. It has been theorized that local glucose concentration modulates microglial activity partially via glucose transporter 5 (GLUT5). We hypothesized that an increased local glucose concentration stimulates GDNF expression while inhibiting MANF expression in the hypothalamus and microglia via GLUT5. The present study investigated the effect of glucose on Gdnf and Manf mRNA expression in the mouse hypothalamus and murine microglial cell line SIM-A9. Intracerebroventricular glucose treatment significantly increased Gdnf mRNA levels in the hypothalamus without altering Manf mRNA levels. Exposure to high glucose caused a significant increase in Gdnf mRNA expression and a time-dependent change in Manf mRNA expression in SIM-A9 cells. GLUT5 inhibitor treatment did not block glucose-induced Gdnf mRNA expression in these cells. These findings suggest that microglia are responsive to changes in the local glucose concentration and increased local glucose availability stimulates the expression of microglial GNDF through a GLUT5-independent mechanism, contributing to glucose-induced feeding suppression. Full article

(This article belongs to the Special Issue Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation)

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14 pages, 3660 KiB

Open AccessArticle

Impact of Environmentally Relevant Concentrations of Bisphenol A (BPA) on the Gene Expression Profile in an In Vitro Model of the Normal Human Ovary

by Aeman Zahra, Rachel Kerslake, Ioannis Kyrou, Harpal S. Randeva, Cristina Sisu and Emmanouil Karteris

Int. J. Mol. Sci. 2022, 23(10), 5334; https://doi.org/10.3390/ijms23105334 - 10 May 2022

Cited by 9 | Viewed by 2449

Abstract

Endocrine-disrupting chemicals (EDCs), including the xenoestrogen Bisphenol A (BPA), can interfere with hormonal signalling. Despite increasing reports of adverse health effects associated with exposure to EDCs, there are limited data on the effect of BPA in normal human ovaries. In this paper, we present a detailed analysis of the transcriptomic landscape in normal Human Epithelial Ovarian Cells (HOSEpiC) treated with BPA (10 and 100 nM). Gene expression profiles were determined using high-throughput RNA sequencing, followed by functional analyses using bioinformatics tools. In total, 272 and 454 differentially expressed genes (DEGs) were identified in 10 and 100 nM BPA-treated HOSEpiCs, respectively, compared to untreated controls. Biological pathways included mRNA surveillance pathways, oocyte meiosis, cellular senescence, and transcriptional misregulation in cancer. BPA exposure has a considerable impact on 10 genes: ANAPC2, AURKA, CDK1, CCNA2, CCNB1, PLK1, BUB1, KIF22, PDE3B, and CCNB3, which are also associated with progesterone-mediated oocyte maturation pathways. Future studies should further explore the effects of BPA and its metabolites in the ovaries in health and disease, making use of validated in vitro and in vivo models to generate data that will address existing knowledge gaps in basic biology, hazard characterisation, and risk assessment associated with the use of xenoestrogens such as BPA. Full article

(This article belongs to the Special Issue Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation)

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12 pages, 1800 KiB

Open AccessArticle

Melatonin Regulates Iron Homeostasis by Inducing Hepcidin Expression in Hepatocytes

by Woo-Ram Park, Byungyoon Choi, Yu-Ji Kim, Yong-Hoon Kim, Min-Jung Park, Dong-Il Kim, Hueng-Sik Choi and Don-Kyu Kim

Int. J. Mol. Sci. 2022, 23(7), 3593; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073593 - 25 Mar 2022

Cited by 7 | Viewed by 2735

Abstract

The pineal hormone, melatonin, plays important roles in circadian rhythms and energy metabolism. The hepatic peptide hormone, hepcidin, regulates iron homeostasis by triggering the degradation of ferroportin (FPN), the protein that transfers cellular iron to the blood. However, the role of melatonin in the transcriptional regulation of hepcidin is largely unknown. Here, we showed that melatonin upregulates hepcidin gene expression by enhancing the melatonin receptor 1 (MT1)-mediated c-Jun N-terminal kinase (JNK) activation in hepatocytes. Interestingly, hepcidin gene expression was increased during the dark cycle in the liver of mice, whereas serum iron levels decreased following hepcidin expression. In addition, melatonin significantly induced hepcidin gene expression and secretion, as well as the subsequent FPN degradation in hepatocytes, which resulted in cellular iron accumulation. Melatonin-induced hepcidin expression was significantly decreased by the melatonin receptor antagonist, luzindole, and by the knockdown of MT1. Moreover, melatonin activated JNK signaling and upregulated hepcidin expression, both of which were significantly decreased by SP600125, a specific JNK inhibitor. Chromatin immunoprecipitation analysis showed that luzindole significantly blocked melatonin-induced c-Jun binding to the hepcidin promoter. Finally, melatonin induced hepcidin expression and secretion by activating the JNK-c-Jun pathway in mice, which were reversed by the luzindole treatment. These findings reveal a previously unrecognized role of melatonin in the circadian regulation of hepcidin expression and iron homeostasis. Full article

(This article belongs to the Special Issue Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation)

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Review

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15 pages, 2357 KiB

Open AccessReview

Relationship between Brain Metabolic Disorders and Cognitive Impairment: LDL Receptor Defect

by Dong-Yong Hong, Dong-Hun Lee, Ji-Young Lee, Eun-Chae Lee, Sang-Won Park, Man-Ryul Lee and Jae-Sang Oh

Int. J. Mol. Sci. 2022, 23(15), 8384; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158384 - 29 Jul 2022

Cited by 12 | Viewed by 4315

Abstract

The low-density-lipoprotein receptor (LDLr) removes low-density lipoprotein (LDL), an endovascular transporter that carries cholesterol from the bloodstream to peripheral tissues. The maintenance of cholesterol content in the brain, which is important to protect brain function, is affected by LDLr. LDLr co-localizes with the insulin receptor and complements the internalization of LDL. In LDLr deficiency, LDL blood levels and insulin resistance increase, leading to abnormal cholesterol control and cognitive deficits in atherosclerosis. Defects in brain cholesterol metabolism lead to neuroinflammation and blood–brain-barrier (BBB) degradation. Moreover, interactions between endoplasmic reticulum stress (ER stress) and mitochondria are induced by ox-LDL accumulation, apolipoprotein E (ApoE) regulates the levels of amyloid beta (Aβ) in the brain, and hypoxia is induced by apoptosis induced by the LDLr defect. This review summarizes the association between neurodegenerative brain disease and typical cognitive deficits. Full article

(This article belongs to the Special Issue Gene Regulation and Cell Signaling in Endocrine and Metabolic Regulation)

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