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Molecular Connection between the Endocrine System and Body Regulation

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

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 49784

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Prof. Dr. Barbara Predieri

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Guest Editor

Pediatric Unit, Department of Medical and Surgical Sciences of the Mother, Children and Adults, University of Modena and Reggio Emilia, 41100 Modena, Italy
Interests: diabetes; obesity; cardiovascular disease; dyslipidemia; bone diseases; endocrine systems; endocrine disruptors; endocrine-related tumor and cancer

Special Issue Information

Dear Colleagues,

Communication within the human body involves the transmission of signals to control and coordinate actions in an effort to maintain homeostasis. One of the major organ systems responsible for providing these communication pathways is the endocrine system. In addition to the major endocrine glands, other organs of the body show endocrine function including the hypothalamus, heart, kidneys, gastrointestinal tract, and liver. Moreover, adipose tissue has long been known to produce hormones and pro-inflammatory cytokines while bone-derived hormones play an important role in metabolism. Disruption of the gut microbiota and both inflammatory and metabolic biomarkers affect neuroendocrine homeostasis and promote several peripheral endocrine system diseases.

In this Special Issue of IJMS, we wish to offer a platform for high-quality research and current review articles on the relationship between the endocrine system and body regulation. Moreover, we will highlight recent research and review the role of gut microbiota and metabolic and inflammatory biomarkers in the mechanisms underlying the development of endocrine diseases and their related complications.

Prof. Dr. Barbara Predieri
Guest Editor

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Keywords

appetite regulation
bone metabolism
cardiovascular disease
diabetes
endocrine system
endocrine-related diseases
growth and development
inflammatory cytokines
microbiota
obesity

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Published Papers (10 papers)

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Research

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20 pages, 4224 KiB

Open AccessArticle

Fecal Microbiota Transplant in a Pre-Clinical Model of Type 2 Diabetes Mellitus, Obesity and Diabetic Kidney Disease

by Rosana M. C. Bastos, Antônio Simplício-Filho, Christian Sávio-Silva, Luiz Felipe V. Oliveira, Giuliano N. F. Cruz, Eliza H. Sousa, Irene L. Noronha, Cristóvão L. P. Mangueira, Heloísa Quaglierini-Ribeiro, Gleice R. Josefi-Rocha and Érika B. Rangel

Int. J. Mol. Sci. 2022, 23(7), 3842; https://doi.org/10.3390/ijms23073842 - 31 Mar 2022

Cited by 30 | Viewed by 4328

Abstract

Diabetes mellitus (DM) burden encompasses diabetic kidney disease (DKD), the leading cause of end-stage renal disease worldwide. Despite compelling evidence indicating that pharmacological intervention curtails DKD progression, the search for non-pharmacological strategies can identify novel targets for drug development against metabolic diseases. One of those emergent strategies comprises the modulation of the intestinal microbiota through fecal transplant from healthy donors. This study sought to investigate the benefits of fecal microbiota transplant (FMT) on functional and morphological parameters in a preclinical model of type 2 DM, obesity, and DKD using BTBR^ob/ob mice. These animals develop hyperglycemia and albuminuria in a time-dependent manner, mimicking DKD in humans. Our main findings unveiled that FMT prevented body weight gain, reduced albuminuria and tumor necrosis factor-α (TNF-α) levels within the ileum and ascending colon, and potentially ameliorated insulin resistance in BTBR^ob/ob mice. Intestinal structural integrity was maintained. Notably, FMT was associated with the abundance of the succinate-consuming Odoribacteraceae bacteria family throughout the intestine. Collectively, our data pointed out the safety and efficacy of FMT in a preclinical model of type 2 DM, obesity, and DKD. These findings provide a basis for translational research on intestinal microbiota modulation and testing its therapeutic potential combined with current treatment for DM. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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13 pages, 1744 KiB

Open AccessArticle

Neurosecretory Protein GL Accelerates Liver Steatosis in Mice Fed Medium-Fat/Medium-Fructose Diet

by Yuki Narimatsu, Eiko Iwakoshi-Ukena, Mana Naito, Shogo Moriwaki, Megumi Furumitsu and Kazuyoshi Ukena

Int. J. Mol. Sci. 2022, 23(4), 2071; https://doi.org/10.3390/ijms23042071 - 13 Feb 2022

Cited by 5 | Viewed by 1981

Abstract

Sugar consumption can readily lead to obesity and metabolic diseases such as liver steatosis. We previously demonstrated that a novel hypothalamic neuropeptide, neurosecretory protein GL (NPGL), promotes fat accumulation due to the ingestion of sugar by rats. However, differences in lipogenic efficiency of sugar types by NPGL remain unclear. The present study aimed to elucidate the obesogenic effects of NPGL on mice fed different sugars (i.e., sucrose or fructose). We overexpressed the NPGL-precursor gene (Npgl) in the hypothalamus of mice fed a medium-fat/medium-sucrose diet (MFSD) or a medium-fat/medium-fructose diet (MFFD). Food intake and body mass were measured for 28 days. Body composition and mRNA expression of lipid metabolic factors were measured at the endpoint. Npgl overexpression potently increased body mass with fat accumulation in the white adipose tissue of mice fed MFFD, although it did not markedly affect food intake. In contrast, we observed profound fat deposition in the livers of mice fed MFFD but not MFSD. In the liver, the mRNA expression of glucose and lipid metabolic factors was affected in mice fed MFFD. Hence, NPGL induced liver steatosis in mice fed a fructose-rich diet. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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19 pages, 6499 KiB

Open AccessArticle

Architecture of the Pancreatic Islets and Endocrine Cell Arrangement in the Embryonic Pancreas of the Grass Snake (Natrix natrix L.). Immunocytochemical Studies and 3D Reconstructions

by Magdalena Kowalska and Weronika Rupik

Int. J. Mol. Sci. 2021, 22(14), 7601; https://doi.org/10.3390/ijms22147601 - 16 Jul 2021

Cited by 2 | Viewed by 4034

Abstract

During the early developmental stages of grass snakes, within the differentiating pancreas, cords of endocrine cells are formed. They differentiate into agglomerates of large islets flanked throughout subsequent developmental stages by small groups of endocrine cells forming islets. The islets are located within the cephalic part of the dorsal pancreas. At the end of the embryonic period, the pancreatic islet agglomerates branch off, and as a result of their remodeling, surround the splenic “bulb”. The stage of pancreatic endocrine ring formation is the first step in formation of intrasplenic islets characteristics for the adult specimens of the grass snake. The arrangement of endocrine cells within islets changes during pancreas differentiation. Initially, the core of islets formed from B and D cells is surrounded by a cluster of A cells. Subsequently, A, B, and D endocrine cells are mixed throughout the islets. Before grass snake hatching, A and B endocrine cells are intermingled within the islets, but D cells are arranged centrally. Moreover, the pancreatic polypeptide (PP) cells are not found within the embryonic pancreas of the grass snake. Variation in the proportions of different cell types, depending on the part of the pancreas, may affect the islet function—a higher proportion of glucagon cells is beneficial for insulin secretion. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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14 pages, 1269 KiB

Open AccessArticle

Placental Glucose Transporters and Response to Bisphenol A in Pregnancies from of Normal and Overweight Mothers

by Leonardo Ermini, Anna Maria Nuzzo, Francesca Ietta, Roberta Romagnoli, Laura Moretti, Bianca Masturzo, Luana Paulesu and Alessandro Rolfo

Int. J. Mol. Sci. 2021, 22(12), 6625; https://doi.org/10.3390/ijms22126625 - 21 Jun 2021

Cited by 7 | Viewed by 2952

Abstract

Bisphenol A (BPA) is a synthetic phenol extensively used in the manufacture of polycarbonate plastics and epoxy resins and a component of liquid and food storages. Among health disorders potentially attributed to BPA, the effects on metabolism have been especially studied. BPA represents a hazard in prenatal life because of its presence in tissues and fluids during pregnancy. Our recent study in rats fed with BPA showed a placental increase in glucose type 1 transporter (GLUT-1), suggesting a higher uptake of glucose. However, the role of BPA on GLUT transporters in pregnant women with metabolic dysfunction has not yet been investigated. In this study, placental tissue from 26 overweight (OW) women and 32 age-matched normal weight (NW) pregnant women were examined for expression of GLUT1 and GLUT4. Placental explants from OW and NW mothers were exposed to BPA 1 nM and 1 μM and tested for GLUTs expression. The data showed a different response of placental explants to BPA in GLUT1 expression with an increase in NW mothers and a decrease in OW ones. GLUT4 expression was lower in the explants from OW than NW mothers, while no difference was showed between OW and NW in placental biopsies for any of the transporters. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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15 pages, 2977 KiB

Open AccessArticle

Nuclear Magnetic Resonance Therapy Modulates the miRNA Profile in Human Primary OA Chondrocytes and Antagonizes Inflammation in Tc28/2a Cells

by Bibiane Steinecker-Frohnwieser, Birgit Lohberger, Nicole Eck, Anda Mann, Cornelia Kratschmann, Andreas Leithner, Werner Kullich and Lukas Weigl

Int. J. Mol. Sci. 2021, 22(11), 5959; https://doi.org/10.3390/ijms22115959 - 31 May 2021

Cited by 9 | Viewed by 3370

Abstract

Nuclear magnetic resonance therapy (NMRT) is discussed as a participant in repair processes regarding cartilage and as an influence in pain signaling. To substantiate the application of NMRT, the underlying mechanisms at the cellular level were studied. In this study microRNA (miR) was extracted from human primary healthy and osteoarthritis (OA) chondrocytes after NMR treatment and was sequenced by the Ion PI Hi-Q™ Sequencing 200 system. In addition, T/C-28a2 chondrocytes grown under hypoxic conditions were studied for IL-1β induced changes in expression on RNA and protein level. HDAC activity an NAD⁽⁺⁾/NADH was measured by luminescence detection. In OA chondrocytes miR-106a, miR-27a, miR-34b, miR-365a and miR-424 were downregulated. This downregulation was reversed by NMRT. miR-365a-5p is known to directly target HDAC and NF-ĸB, and a decrease in HDAC activity by NMRT was detected. NAD⁺/NADH was reduced by NMR treatment in OA chondrocytes. Under hypoxic conditions NMRT changed the expression profile of HIF1, HIF2, IGF2, MMP3, MMP13, and RUNX1. We conclude that NMRT changes the miR profile and modulates the HDAC and the NAD⁽⁺⁾/NADH signaling in human chondrocytes. These findings underline once more that NMRT counteracts IL-1β induced changes by reducing catabolic effects, thereby decreasing inflammatory mechanisms under OA by changing NF-ĸB signaling. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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15 pages, 1049 KiB

Open AccessArticle

Maternal Heat Stress Alters Expression of Genes Associated with Nutrient Transport Activity and Metabolism in Female Placentae from Mid-Gestating Pigs

by Weicheng Zhao, Fan Liu, Christina D. Marth, Mark P. Green, Hieu H. Le, Brian J. Leury, Alan W. Bell, Frank R. Dunshea and Jeremy J. Cottrell

Int. J. Mol. Sci. 2021, 22(8), 4147; https://doi.org/10.3390/ijms22084147 - 16 Apr 2021

Cited by 17 | Viewed by 3054

Abstract

Placental insufficiency is a known consequence of maternal heat stress during gestation in farm animals. The molecular regulation of placentae during the stress response is little known in pigs. This study aims to identify differential gene expression in pig placentae caused by maternal heat exposure during early to mid-gestation. RNA sequencing (RNA-seq) was performed on female placental samples from pregnant pigs exposed to thermoneutral control (CON; constant 20 °C; n = 5) or cyclic heat stress (HS; cyclic 28 to 33 °C; n = 5) conditions between d40 and d60 of gestation. On d60 of gestation, placental efficiency (fetal/placental weight) was decreased (p = 0.023) by maternal HS. A total of 169 genes were differentially expressed (FDR ≤ 0.1) between CON and HS placentae of female fetuses, of which 35 genes were upregulated and 134 genes were downregulated by maternal HS. The current data revealed transport activity (FDR = 0.027), glycoprotein biosynthetic process (FDR = 0.044), and carbohydrate metabolic process (FDR = 0.049) among the terms enriched by the downregulated genes (HS vs. CON). In addition, solute carrier (SLC)-mediated transmembrane transport (FDR = 0.008) and glycosaminoglycan biosynthesis (FDR = 0.027), which modulates placental stroma synthesis, were identified among the pathways enriched by the downregulated genes. These findings provide evidence that heat-stress induced placental inefficiency may be underpinned by altered expression of genes associated with placental nutrient transport capacity and metabolism. A further understanding of the molecular mechanism contributes to the identification of placental gene signatures of summer infertility in pigs. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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Review

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43 pages, 2425 KiB

Open AccessReview

Endocrine Disrupting Chemicals’ Effects in Children: What We Know and What We Need to Learn?

by Barbara Predieri, Lorenzo Iughetti, Sergio Bernasconi and Maria Elisabeth Street

Int. J. Mol. Sci. 2022, 23(19), 11899; https://doi.org/10.3390/ijms231911899 - 7 Oct 2022

Cited by 30 | Viewed by 7961

Abstract

Thousands of natural or manufactured chemicals were defined as endocrine-disrupting chemicals (EDCs) because they can interfere with hormone activity and the endocrine system. We summarize and discuss what we know and what we still need to learn about EDCs’ pathogenic mechanisms of action, as well as the effects of the most common EDCs on endocrine system health in childhood. The MEDLINE database (PubMed) was searched on 13 May 2022, filtering for EDCs, endocrine diseases, and children. EDCs are a group of compounds with high heterogeneity, but usually disrupt the endocrine system by mimicking or interfering with natural hormones or interfering with the body’s hormonal balance through other mechanisms. Individual EDCs were studied in detail, while humans’ “cocktail effect” is still unclear. In utero, early postnatal life, and/or pubertal development are highly susceptible periods to exposure. Human epidemiological studies suggest that EDCs affect prenatal growth, thyroid function, glucose metabolism, obesity, puberty, and fertility through several mechanisms. Further studies are needed to clarify which EDCs can mainly act on epigenetic processes. A better understanding of EDCs’ effects on human health is crucial to developing future regulatory strategies to prevent exposure and ensure the health of children today, in future generations, and in the environment. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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22 pages, 3679 KiB

Open AccessReview

The Role of Cannabinoids in Bone Metabolism: A New Perspective for Bone Disorders

by Federica Saponaro, Rebecca Ferrisi, Francesca Gado, Beatrice Polini, Alessandro Saba, Clementina Manera and Grazia Chiellini

Int. J. Mol. Sci. 2021, 22(22), 12374; https://doi.org/10.3390/ijms222212374 - 16 Nov 2021

Cited by 8 | Viewed by 5353

Abstract

Novel interest has arisen in recent years regarding bone, which is a very complex and dynamic tissue deputed to several functions ranging from mechanical and protective support to hematopoiesis and calcium homeostasis maintenance. In order to address these tasks, a very refined, continuous remodeling process needs to occur involving the coordinated action of different types of bone cells: osteoblasts (OBs), which have the capacity to produce newly formed bone, and osteoclasts (OCs), which can remove old bone. Bone remodeling is a highly regulated process that requires many hormones and messenger molecules, both at the systemic and the local level. The whole picture is still not fully understood, and the role of novel actors, such as the components of the endocannabinoids system (ECS), including endogenous cannabinoid ligands (ECs), cannabinoid receptors (CBRs), and the enzymes responsible for endogenous ligand synthesis and breakdown, is extremely intriguing. This article reviews the connection between the ECS and skeletal health, supporting the potential use of cannabinoid receptor ligands for the treatment of bone diseases associated with accelerated osteoclastic bone resorption, including osteoporosis and bone metastasis. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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21 pages, 579 KiB

Open AccessReview

The Role of the Noradrenergic System in Eating Disorders: A Systematic Review

by Jacopo Pruccoli, Antonia Parmeggiani, Duccio Maria Cordelli and Marcello Lanari

Int. J. Mol. Sci. 2021, 22(20), 11086; https://doi.org/10.3390/ijms222011086 - 14 Oct 2021

Cited by 13 | Viewed by 4160

Abstract

Noradrenaline (NE) is a catecholamine acting as both a neurotransmitter and a hormone, with relevant effects in modulating feeding behavior and satiety. Several studies have assessed the relationship between the noradrenergic system and Eating Disorders (EDs). This systematic review aims to report the existing literature on the role of the noradrenergic system in the development and treatment of EDs. A total of 35 studies were included. Preclinical studies demonstrated an involvement of the noradrenergic pathways in binge-like behaviors. Genetic studies on polymorphisms in genes coding for NE transporters and regulating enzymes have shown conflicting evidence. Clinical studies have reported non-unanimous evidence for the existence of absolute alterations in plasma NE values in patients with Anorexia Nervosa (AN) and Bulimia Nervosa (BN). Pharmacological studies have documented the efficacy of noradrenaline-modulating therapies in the treatment of BN and Binge Eating Disorder (BED). Insufficient evidence was found concerning the noradrenergic-mediated genetics of BED and BN, and psychopharmacological treatments targeting the noradrenergic system in AN. According to these data, further studies are required to expand the existing knowledge on the noradrenergic system as a potential target for treatments of EDs. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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17 pages, 883 KiB

Open AccessReview

Insulin Signal Transduction Perturbations in Insulin Resistance

by Mariyam Khalid, Juma Alkaabi, Moien A. B. Khan and Abdu Adem

Int. J. Mol. Sci. 2021, 22(16), 8590; https://doi.org/10.3390/ijms22168590 - 10 Aug 2021

Cited by 84 | Viewed by 10779

Abstract

Type 2 diabetes mellitus is a widespread medical condition, characterized by high blood glucose and inadequate insulin action, which leads to insulin resistance. Insulin resistance in insulin-responsive tissues precedes the onset of pancreatic β-cell dysfunction. Multiple molecular and pathophysiological mechanisms are involved in insulin resistance. Insulin resistance is a consequence of a complex combination of metabolic disorders, lipotoxicity, glucotoxicity, and inflammation. There is ample evidence linking different mechanistic approaches as the cause of insulin resistance, but no central mechanism is yet described as an underlying reason behind this condition. This review combines and interlinks the defects in the insulin signal transduction pathway of the insulin resistance state with special emphasis on the AGE-RAGE-NF-κB axis. Here, we describe important factors that play a crucial role in the pathogenesis of insulin resistance to provide directionality for the events. The interplay of inflammation and oxidative stress that leads to β-cell decline through the IAPP-RAGE induced β-cell toxicity is also addressed. Overall, by generating a comprehensive overview of the plethora of mechanisms involved in insulin resistance, we focus on the establishment of unifying mechanisms to provide new insights for the future interventions of type 2 diabetes mellitus. Full article

(This article belongs to the Special Issue Molecular Connection between the Endocrine System and Body Regulation)

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