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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 (15 February 2021) | Viewed by 51670

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Prof. Dr. Víctor Sánchez-Margalet

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Department of Biochemistry and Molecular Biology, Hospital Universitario Virgen Macarena, Sevilla, Spain
Interests: leptin structure; leptin expression regulation; leptin receptor; leptin signaling; leptin action at central level; leptin as adipokine; leptin as a cornerstone of immunometabolism; leptin as link between obesity and associated pathophysiology, such as diabetes, cancer, rheumatologic diseases, or cardiovascular diseases
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Special Issue Information

Dear Colleagues,

Twenty five years ago, an important element in the regulation of weight was discovered: leptin. It was recognized as the adipocyte signal that informs the brain about fat stores, and it had been searched for for a long time. Thus, leptin could explain obesity as a failure of communication between fat and brain, either by leptin or leptin receptor mutation. However, soon after, leptin was found to be the first described adipokine that mediates the inflammatory state of obesity. In fact, leptin receptors and signalling share many features of of inflammatory cytokines. Thus, leptin has been found to be the cornerstone of immunometabolism, and there is a link between obesity and many associated pathophysiological conditions, such as diabetes, cardiovascular diseases, autoimmune diseases, pathology of reproduction and pregnancy, and cancer.

The aim of this Special Issue is to summarize the knowledge of leptin function and its role in the pathophysiology of obesity-associated diseases at the molecular level.

Topics of the Special Issue include but are not limited to the following:

Leptin structure and its importance for brain functioning;
Leptin expression regulation;
Leptin receptor structure and isoforms;
Leptin receptor expression regulation;
Leptin and leptin receptor mutations and polymorphisms;
Leptin and immunometabolism;
Leptin and diabetes;
Leptin and cardiovascular disease;
Leptin and autoimmune diseases;
Leptin and reproduction;
Leptin and cancer.

Prof. Dr. Víctor Sánchez-Margalet
Guest Editor

Manuscript Submission Information

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Keywords

Leptin
Leptin expression
Leptin receptor
Leptin action
Obesity
Immunometabolism
Obesity associated pathology

Published Papers (12 papers)

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Research

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18 pages, 2906 KiB

Open AccessArticle

Activation of Peripheral Blood Mononuclear Cells and Leptin Secretion: New Potential Role of Interleukin-2 and High Mobility Group Box (HMGB)1

by Andrea Coppola, Barbara Capuani, Francesca Pacifici, Donatella Pastore, Roberto Arriga, Alfonso Bellia, Aikaterini Andreadi, Nicola Di Daniele, Renato Lauro, David Della-Morte, Giuseppe Sconocchia and Davide Lauro

Int. J. Mol. Sci. 2021, 22(15), 7988; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22157988 - 26 Jul 2021

Cited by 6 | Viewed by 2407

Abstract

Activation of innate immunity and low-grade inflammation contributes to hyperglycemia and an onset of Type 2 Diabetes Mellitus (T2DM). Interleukin-2 (IL-2), leptin, High Mobility Group Box-1 (HMGB-1), and increased glucose concentrations are mediators of these processes also by modulating peripheral blood mononuclear cells (PBMCs) response. The aim of this study was to investigate if HMGB-1 and IL-2 turn on PBMCs and their leptin secretion. In isolated human PBMCs and their subpopulations from healthy individuals and naïve T2DM patients, leptin release, pro-inflammatory response and Toll-like Receptors (TLRs) activation was measured. After treatment with IL-2 and HMGB1, NK (Natural Killer) have the highest amount of leptin secretion, whilst NK-T have the maximal release in basal conditions. TLR4 (TAK242) and/or TLR2 (TLR2-IgA) inhibitors decreased leptin secretion after IL-2 and HMGB1 treatment. A further non-significant increase in leptin secretion was reported in PBMCs of naive T2DM patients in response to IL-2 and HMGB-1 stimulation. Finally, hyperglycemia or hyperinsulinemia might stimulate leptin secretion from PBMCs. The amount of leptin released from PBMCs after the different treatments was enough to stimulate the secretion of IL-1β from monocytes. Targeting leptin sera levels and secretion from PBMCs could represent a new therapeutic strategy to counteract metabolic diseases such as T2DM. Full article

(This article belongs to the Special Issue Leptin)

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14 pages, 1947 KiB

Open AccessArticle

Evaluation of the Influence of Adalimumab on the Expression Profile of Leptin-Related Genes and Proteins in Keratinocytes Treated with Lipopolysaccharide A

by Beniamin Oskar Grabarek, Tomasz Kasela, Iwona Adwent, Barbara Zawidlak-Węgrzyńska and Ryszard Brus

Int. J. Mol. Sci. 2021, 22(4), 1595; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041595 - 05 Feb 2021

Cited by 7 | Viewed by 2676

Abstract

Psoriasis is a disease with a proinflammatory base, in which an increased expression of leptin, tumor necrosis factor alpha (TNF-α), interleukin (IL) IL-12/23, IL-6, is observed. A drug used in the treatment of psoriasis of moderate and acute strength is the monoclonal antibody anti-TNF–adalimumab. The goal of this study was to evaluate the influence of adalimumab on changes in the expression profile of leptin-related genes in human keratinocyte cells exposed to lipopolysaccharide A and analyze if adalimumab acts via leptin pathways. The evaluation of changes of the pattern of genes connected with leptin and proteins coded by them was marked in a culture of human keratinocytes (HaCaT) exposed to 1 µg/mL lipopolysaccharide A (LPS) for 8 h in order to induce the inflammatory process, then to 8 µg/mL of adalimumab for 2.8 and 24 h in comparison with the control (cells not treated with the substances). The techniques used were mRNA microarray, Real-Time Quantitative Reverse Transcription Reaction (RTqPCR), Enzyme-Linked Immunosorbent Assay (ELISA), as well as transfections of HaCaT culture with leptin small interfering RNA (siRNA) in order to see whether adalimumab works through pathways dependent on leptin. A statistically lower expression of leptin and its receptors was observed under the influence of the drug, independent of the exposition time of keratinocytes to adalimumab. In the cells transfected with leptin siRNA, a lower concentration of JAK2 and STAT3 proteins was observed, which confirms that adalimumab works through pathways dependent on leptin. Adalimumab has a modulatory effect on the gene expression pattern and the proteins coded by them connected with leptin in keratinocytes treated with LPS in vitro. Full article

(This article belongs to the Special Issue Leptin)

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16 pages, 1208 KiB

Open AccessArticle

Increased Growth Differentiation Factor 15 in Patients with Hypoleptinemia-Associated Lipodystrophy

by Susan Kralisch, Annett Hoffmann, Juliane Estrada-Kunz, Michael Stumvoll, Mathias Fasshauer, Anke Tönjes and Konstanze Miehle

Int. J. Mol. Sci. 2020, 21(19), 7214; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197214 - 29 Sep 2020

Cited by 9 | Viewed by 2158

Abstract

Objective. Similar to obesity, lipodystrophy (LD) causes adipose tissue dysfunction and severe metabolic complications. Growth differentiation factor 15 (GDF15) belongs to the transforming growth factor β superfamily and is dysregulated in metabolic disease including obesity and diabetes mellitus. Circulating levels in LD and the impact of leptin treatment have not been investigated so far. Material and Methods. GDF15 serum levels were quantified in 60 LD patients without human immunodeficiency virus infection and 60 controls matched for age, gender, and body mass index. The impact of metreleptin treatment on circulating GDF15 was assessed in a subgroup of patients. GDF15 mRNA expression was determined in metabolic tissues of leptin-deficient lipodystrophic aP2-nSREBP1c-Tg mice, obese ob/ob mice, and control C57Bl6 mice. Results. Median GDF15 serum concentrations were significantly higher in LD patients (819 ng/L) as compared to the control group (415 ng/L) (p < 0.001). In multiple linear regression analysis, an independent and positive association remained between GDF15 on one hand and age, patient group, hemoglobin A1c, triglycerides, and C-reactive protein on the other hand. Moreover, there was an independent negative association between GFD15 and estimated glomerular filtration rate. Circulating GDF15 was not significantly affected by metreleptin treatment in LD patients. Gdf15 was upregulated in leptin-deficient lipodystrophic mice as compared to controls. Moreover, Gdf15 mRNA expression was downregulated by leptin treatment in lipodystrophic and obese animals. Conclusions. Serum concentrations of GDF15 are elevated in LD patients and independently associated with markers of metabolic dysfunction. Gdf15 expression is higher in lipodystrophic mice and downregulated by leptin treatment. Full article

(This article belongs to the Special Issue Leptin)

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15 pages, 728 KiB

Open AccessArticle

Changes in Expression of the Genes for the Leptin Signaling in Hypothalamic-Pituitary Selected Areas and Endocrine Responses to Long-Term Manipulation in Body Weight and Resistin in Ewes

by Dorota Anna Zieba, Weronika Biernat, Malgorzata Szczesna, Katarzyna Kirsz, Justyna Barć and Tomasz Misztal

Int. J. Mol. Sci. 2020, 21(12), 4238; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124238 - 14 Jun 2020

Cited by 8 | Viewed by 2024

Abstract

Both long-term undernutrition and overnutrition disturb metabolic balance, which is mediated partially by the action of two adipokines, leptin and resistin (RSTN). In this study, we manipulated the diet of ewes to produce either a thin (lean) or fat (fat) body condition and investigated how RSTN affects endocrine and metabolic status under different leptin concentrations. Twenty ewes were distributed into four groups (n = 5): the lean and fat groups were administered with saline (Lean and Fat), while the Lean-R (Lean-Resistin treated) and Fat-R (Fat-Resistin treated) groups received recombinant bovine resistin. Plasma was assayed for LH, FSH, PRL, RSTN, leptin, GH, glucose, insulin, total cholesterol, nonesterified fatty acid (NEFA), high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol and triglycerides. Expression levels of a suppressor of cytokine signaling (SOCS-3) and the long form of the leptin receptor (LRb) were determined in selected brain regions, such as the anterior pituitary, hypothalamic arcuate nucleus, preoptic area and ventro- and dorsomedial nuclei. The results indicate long-term alterations in body weight affect RSTN-mediated effects on metabolic and reproductive hormones concentrations and the expression of leptin signaling components: LRb and SOCS-3. This may be an adaptive mechanism to long-term changes in adiposity during the state of long-day leptin resistance. Full article

(This article belongs to the Special Issue Leptin)

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22 pages, 2926 KiB

Open AccessArticle

The Impact of Photoperiod on the Leptin Sensitivity and Course of Inflammation in the Anterior Pituitary

by Maciej Wójcik, Andrzej Przemysław Herman, Dorota Anna Zieba and Agata Krawczyńska

Int. J. Mol. Sci. 2020, 21(11), 4153; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114153 - 10 Jun 2020

Cited by 7 | Viewed by 2545

Abstract

Leptin has a modulatory impact on the course of inflammation, affecting the expression of proinflammatory cytokines and their receptors. Pathophysiological leptin resistance identified in humans occurs typically in sheep during the long-day photoperiod. This study aimed to determine the effect of the photoperiod with relation to the leptin-modulating action on the expression of the proinflammatory cytokines and their receptors in the anterior pituitary under physiological or acute inflammation. Two in vivo experiments were conducted on 24 blackface sheep per experiment in different photoperiods. The real-time PCR analysis for the expression of the genes IL1B, IL1R1, IL1R2, IL6, IL6R, IL6ST, TNF, TNFR1, and TNFR2 was performed. Expression of all examined genes, except IL1β and IL1R2, was higher during short days. The leptin injection increased the expression of all examined genes during short days. In short days the synergistic effect of lipopolysaccharide and leptin increased the expression of IL1B, IL1R1, IL1R2, IL6, TNF, and TNFR2, and decreased expression of IL6ST. This mechanism was inhibited during long days for the expression of IL1R1, IL6, IL6ST, and TNFR1. The obtained results suggest the occurrence of leptin resistance during long days and suggest that leptin modulates the course of inflammation in a photoperiod-dependent manner in the anterior pituitary. Full article

(This article belongs to the Special Issue Leptin)

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16 pages, 2639 KiB

Open AccessArticle

Evaluation of the Impact of Cisplatin on Variances in the Expression Pattern of Leptin-Related Genes in Endometrial Cancer Cells

by Dariusz Dąbruś, Robert Kiełbasiński, Beniamin Oskar Grabarek and Dariusz Boroń

Int. J. Mol. Sci. 2020, 21(11), 4135; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21114135 - 10 Jun 2020

Cited by 5 | Viewed by 2111

Abstract

This research aimed to assess the impact of cisplatin, depending on the concentration and exposure time, on the expression pattern of leptin in an endometrial cancer cell line. Ishikawa endometrial cancer cell cultures were incubated with cisplatin, at concentrations of 2.5–10 µM, or leptin in the concentration range 10–40 ng/mL, and for durations of 12, 24 and 48 h compared with the control. The microarray techniques: RTqPCR; ELISA; and RNAi assay were used. Statistical analysis was performed at p < 0.05. Already with the lowest concentration and incubation time, statistically substantial silencing of leptin expression on the mRNA level under the influence of cisplatin after its addition to the culture was observed. On the protein level, the expression for cisplatin at a concentration of 2.5 µM was only noticeable after 48 h of exposure and maintained themselves with consecutively larger concentrations. It was observed that cisplatin at a concentration of 5 µM is IC₅₀ and the drug activated apoptosis via caspases -3 and -9. Cisplatin at a concentration of 5 µM and higher has a significant effect on the concentration of leptin. The effect of cisplatin on the expression profile of genes associated with leptin-dependent signaling pathways and changes in the expression of leptin itself and its receptors was confirmed. It was also confirmed that cisplatin exerted its effect via the leptin pathway. Full article

(This article belongs to the Special Issue Leptin)

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21 pages, 3565 KiB

Open AccessArticle

Leptin Signaling Affects Survival and Chemoresistance of Estrogen Receptor Negative Breast Cancer

by Crystal C. Lipsey, Adriana Harbuzariu, Robert W. Robey, Lyn M. Huff, Michael M. Gottesman and Ruben R. Gonzalez-Perez

Int. J. Mol. Sci. 2020, 21(11), 3794; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21113794 - 27 May 2020

Cited by 14 | Viewed by 3396

Abstract

Estrogen-receptor-negative breast cancer (BCER−) is mainly treated with chemotherapeutics. Leptin signaling can influence BCER− progression, but its effects on patient survival and chemoresistance are not well understood. We hypothesize that leptin signaling decreases the survival of BCER− patients by, in part, inducing the expression of chemoresistance-related genes. The correlation of expression of leptin receptor (OBR), leptin-targeted genes (CDK8, NANOG, and RBP-Jk), and breast cancer (BC) patient survival was determined from The Cancer Genome Atlas (TCGA) mRNA data. Leptin-induced expression of proliferation and chemoresistance-related molecules was investigated in triple-negative BC (TNBC) cells that respond differently to chemotherapeutics. Leptin-induced gene expression in TNBC was analyzed by RNA-Seq. The specificity of leptin effects was assessed using OBR inhibitors (shRNA and peptides). The results show that OBR and leptin-targeted gene expression are associated with lower survival of BCER− patients. Importantly, the co-expression of these genes was also associated with chemotherapy failure. Leptin signaling increased the expression of tumorigenesis and chemoresistance-related genes (ABCB1, WNT4, ADHFE1, TBC1D3, LL22NC03, RDH5, and ITGB3) and impaired chemotherapeutic effects in TNBC cells. OBR inhibition re-sensitized TNBC to chemotherapeutics. In conclusion, the co-expression of OBR and leptin-targeted genes may be used as a predictor of survival and drug resistance of BCER− patients. Targeting OBR signaling could improve chemotherapeutic efficacy. Full article

(This article belongs to the Special Issue Leptin)

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Review

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26 pages, 2619 KiB

Open AccessReview

Revisiting the Impact of Local Leptin Signaling in Folliculogenesis and Oocyte Maturation in Obese Mothers

by Karolina Wołodko, Juan Castillo-Fernandez, Gavin Kelsey and António Galvão

Int. J. Mol. Sci. 2021, 22(8), 4270; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084270 - 20 Apr 2021

Cited by 11 | Viewed by 3210

Abstract

The complex nature of folliculogenesis regulation accounts for its susceptibility to maternal physiological fitness. In obese mothers, progressive expansion of adipose tissue culminates with severe hyperestrogenism and hyperleptinemia with detrimental effects for ovarian performance. Indeed, maternal obesity is associated with the establishment of ovarian leptin resistance. This review summarizes current knowledge on potential effects of impaired leptin signaling throughout folliculogenesis and oocyte developmental competence in mice and women. Full article

(This article belongs to the Special Issue Leptin)

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18 pages, 3923 KiB

Open AccessReview

Leptin and Cancer: Updated Functional Roles in Carcinogenesis, Therapeutic Niches, and Developments

by Tsung-Chieh Lin and Michael Hsiao

Int. J. Mol. Sci. 2021, 22(6), 2870; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22062870 - 11 Mar 2021

Cited by 44 | Viewed by 3131

Abstract

Leptin is an obesity-associated adipokine that is known to regulate energy metabolism and reproduction and to control appetite via the leptin receptor. Recent work has identified specific cell types other than adipocytes that harbor leptin and leptin receptor expression, particularly in cancers and tumor microenvironments, and characterized the role of this signaling axis in cancer progression. Furthermore, the prognostic significance of leptin in various types of cancer and the ability to noninvasively detect leptin levels in serum samples have attracted attention for potential clinical applications. Emerging findings have demonstrated the direct and indirect biological effects of leptin in regulating cancer proliferation, metastasis, angiogenesis and chemoresistance, warranting the exploration of the underlying molecular mechanisms to develop a novel therapeutic strategy. In this review article, we summarize and integrate transcriptome and clinical data from cancer patients together with the recent findings related to the leptin signaling axis in the aforementioned malignant phenotypes. In addition, a comprehensive analysis of leptin and leptin receptor distribution in a pancancer panel and in individual cell types of specific organs at the single-cell level is presented, identifying those sites that are prone to leptin-mediated tumorigenesis. Our results shed light on the role of leptin in cancer and provide guidance and potential directions for further research for scientists in this field. Full article

(This article belongs to the Special Issue Leptin)

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33 pages, 1426 KiB

Open AccessReview

Unraveling the Role of Leptin in Liver Function and Its Relationship with Liver Diseases

by Maite Martínez-Uña, Yaiza López-Mancheño, Carlos Diéguez, Manuel A. Fernández-Rojo and Marta G. Novelle

Int. J. Mol. Sci. 2020, 21(24), 9368; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249368 - 09 Dec 2020

Cited by 51 | Viewed by 4805

Abstract

Since its discovery twenty-five years ago, the fat-derived hormone leptin has provided a revolutionary framework for studying the physiological role of adipose tissue as an endocrine organ. Leptin exerts pleiotropic effects on many metabolic pathways and is tightly connected with the liver, the major player in systemic metabolism. As a consequence, understanding the metabolic and hormonal interplay between the liver and adipose tissue could provide us with new therapeutic targets for some chronic liver diseases, an increasing problem worldwide. In this review, we assess relevant literature regarding the main metabolic effects of leptin on the liver, by direct regulation or through the central nervous system (CNS). We draw special attention to the contribution of leptin to the non-alcoholic fatty liver disease (NAFLD) pathogenesis and its progression to more advanced stages of the disease as non-alcoholic steatohepatitis (NASH). Likewise, we describe the contribution of leptin to the liver regeneration process after partial hepatectomy, the mainstay of treatment for certain hepatic malignant tumors. Full article

(This article belongs to the Special Issue Leptin)

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26 pages, 1134 KiB

Open AccessReview

There and Back Again: Leptin Actions in White Adipose Tissue

by Noelia Martínez-Sánchez

Int. J. Mol. Sci. 2020, 21(17), 6039; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176039 - 21 Aug 2020

Cited by 64 | Viewed by 9969

Abstract

Leptin is a hormone discovered almost 30 years ago with important implications in metabolism. It is primarily produced by white adipose tissue (WAT) in proportion to the amount of fat. The discovery of leptin was a turning point for two principle reasons: on one hand, it generated promising expectations for the treatment of the obesity, and on the other, it changed the classical concept that white adipose tissue was simply an inert storage organ. Thus, adipocytes in WAT produce the majority of leptin and, although its primary role is the regulation of fat stores by controlling lipolysis and lipogenesis, this hormone also has implications in other physiological processes within WAT, such as apoptosis, browning and inflammation. Although a massive number of questions related to leptin actions have been answered, the necessity for further clarification facilitates constantly renewing interest in this hormone and its pathways. In this review, leptin actions in white adipose tissue will be summarized in the context of obesity. Full article

(This article belongs to the Special Issue Leptin)

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24 pages, 1248 KiB

Open AccessReview

Role of Leptin in Inflammation and Vice Versa

by Antonio Pérez-Pérez, Flora Sánchez-Jiménez, Teresa Vilariño-García and Víctor Sánchez-Margalet

Int. J. Mol. Sci. 2020, 21(16), 5887; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21165887 - 16 Aug 2020

Cited by 123 | Viewed by 12232

Abstract

Inflammation is an essential immune response for the maintenance of tissue homeostasis. In a general sense, acute and chronic inflammation are different types of adaptive response that are called into action when other homeostatic mechanisms are insufficient. Although considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and tissue injury, the causes and mechanisms of systemic chronic inflammation are much less known. The pathogenic capacity of this type of inflammation is puzzling and represents a common link of the multifactorial diseases, such as cardiovascular diseases and type 2 diabetes. In recent years, interest has been raised by the discovery of novel mediators of inflammation, such as microRNAs and adipokines, with different effects on target tissues. In the present review, we discuss the data emerged from research of leptin in obesity as an inflammatory mediator sustaining multifactorial diseases and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses. On the other direction, chronic inflammation, either from autoimmune or infectious diseases, or impaired microbiota (dysbiosis) may impair the leptin response inducing resistance to the weight control, and therefore it may be a cause of obesity. Thus, we are reviewing the published data regarding the role of leptin in inflammation, and the other way around, the role of inflammation on the development of leptin resistance and obesity Full article

(This article belongs to the Special Issue Leptin)

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