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Biology
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Molecular Basis of Metabolic Homeostasis
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Molecular Basis of Metabolic Homeostasis

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 2176

Special Issue Editor

Dr. Verónica Miksztowicz

E-Mail Website
Guest Editor
Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial, Instituto de Investigaciones Biomédicas UCA-CONICET, Facultad de Medicina, Pontificia Universidad Católica Argentina, Buenos Aires 1113, Argentina
Interests: adipose tissue; bone; metabolism; GLP-1 agonists; mitochondria

Special Issue Information

Dear Colleagues,

Maintaining metabolic homeostasis is essential for cellular life, and it involves a tight regulation of temperature, food intake, energy expenditure, and glycemia. The adipose tissue, liver, and pancreas are traditionally considered organs of the endocrine system involved in regulating metabolic homeostasis, and an appropriate crosstalk between them is necessary for ensuring individual health.  The dysregulation of the molecular mechanisms associated with metabolic homeostasis led to the development of metabolic disorders, with obesity being one of the most prevalent metabolic disorders worldwide. Obesity, characterized by adipose tissue expansion, is a multifactorial inflammatory chronic disease that increases the risk of metabolic syndrome, diabetes, cancer, liver disease, and cardiovascular disease, among others.  Adipose tissue is a heterogeneous organ with a high degree of plasticity. It regulates many aspects of whole-body physiology, including food intake, maintenance of energy levels, insulin sensitivity, body temperature, and immune responses. Alterations of adipose tissue plasticity modify metabolic homeostasis, driving the progression of different diseases.

A better understanding of the mechanisms associated with metabolic homeostasis in adipose tissue and the impact of its deregulation on other organs is essential for the development of novel therapeutic approaches and strategies to improve metabolic diseases.

This Special Issue will focus on original research articles, brief reports, and review articles related to the metabolic processes necessary to maintain cellular and tissue homeostasis, including animal models and in vitro studies.

Dr. Verónica Miksztowicz
Guest Editor

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. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • metabolic homeostasis
  • adipose tissue
  • liver diseases
  • cardiovascular disease

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Published Papers (2 papers)

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Research

21 pages, 3892 KB  
Article
High Salt Intake Affects Visceral Adipose Tissue Homeostasis: Beneficial Effects of GLP-1 Agonists
by Vanessa Touceda, Leonardo Cacciagiú, Ignacio Barbani Moglie, Morena Wiszniewski, Valeria Sanchez, Romina C. De Lucca, Agustina Vidal, Paola Finocchietto, Silvia Friedman, Germán E. González and Verónica Miksztowicz
Biology 2025, 14(9), 1171; https://doi.org/10.3390/biology14091171 - 2 Sep 2025
Viewed by 436
Abstract
High salt (NaCl) intake has been associated with visceral adipose tissue (VAT) dysfunction independently of its impact on blood pressure. Liraglutide (LGT), a GLP-1 agonist, could be a potential therapeutic option. We investigated the impact of a chronic high-salt diet (HSD) on VAT [...] Read more.
High salt (NaCl) intake has been associated with visceral adipose tissue (VAT) dysfunction independently of its impact on blood pressure. Liraglutide (LGT), a GLP-1 agonist, could be a potential therapeutic option. We investigated the impact of a chronic high-salt diet (HSD) on VAT homeostasis and evaluated the potential protective effects of LGT, a GLP-1 receptor agonist. Male C57BL/6 mice were fed a standard diet (Control, C) or 8% NaCl (HSD) for 15 weeks and subsequently treated with LGT or vehicle for 5 weeks. In VAT, histological characteristics, collagen deposition, vascular density, mitochondrial dynamics, oxidative stress, and adipokine expression were evaluated. The HSD significantly decreased body weight, VAT mass, and adipocyte size (p < 0.05). Moreover, it impaired vascular density and induced interstitial fibrosis (p < 0.01). LGT treatment improved vascularization and VEGF expression and reduced fibrosis (p < 0.05 vs. the HSD). The HSD induced oxidative stress and mitochondrial fragmentation, which were attenuated by LGT (p < 0.001). Leptin levels were elevated by the HSD (p < 0.05) and normalized with LGT, while adiponectin levels increased. In conclusion, excessive salt consumption induces structural and metabolic dysfunction in VAT. LGT therapy mitigates several of these adverse effects, supporting its potential as a novel strategy for managing salt-sensitive adipose tissue dysfunction. Full article
(This article belongs to the Special Issue Molecular Basis of Metabolic Homeostasis)
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17 pages, 2001 KB  
Article
Farnesol Improves Endoplasmic Reticulum Stress and Hepatic Metabolic Dysfunction Induced by Tunicamycin in Mice
by Naqash Goswami, Lionel Kinkpe, Lun Hua, Yong Zhuo, Zhengfeng Fang, Lianqiang Che, Yan Lin, Shengyu Xu, Xuemei Jiang, Bin Feng and De Wu
Biology 2025, 14(2), 213; https://doi.org/10.3390/biology14020213 - 18 Feb 2025
Viewed by 1139
Abstract
Endoplasmic reticulum (ER) stress significantly affects liver metabolism, often leading to disorders such as hepatic steatosis. Tunicamycin (TM), a known ER stress inducer, is frequently used to model metabolic stress, but its specific effects on liver energy homeostasis remain unclear. This study investigates [...] Read more.
Endoplasmic reticulum (ER) stress significantly affects liver metabolism, often leading to disorders such as hepatic steatosis. Tunicamycin (TM), a known ER stress inducer, is frequently used to model metabolic stress, but its specific effects on liver energy homeostasis remain unclear. This study investigates how farnesol (FOH), a natural compound with antioxidant and anti-inflammatory properties, counteracts TM-induced ER stress and its associated metabolic disruptions in the liver. Using both primary hepatocytes and a mouse model, this study demonstrates that TM treatment caused upregulation of ER stress markers, including ATF4, and disrupted genes related to lipid metabolism and gluconeogenesis. Co-treatment with FOH reduced these stress markers and restored the expression of metabolic genes. In vivo, FOH treatment alleviated oxidative stress, reduced lipid accumulation, and restored normal glycogen and lipid metabolism. Histological analysis further confirmed that FOH preserved liver architecture and minimized cellular damage. FOH also stabilized serum lipid profiles and modulated key metabolic biomarkers, suggesting its protective role against TM-induced liver injury. These findings suggest that FOH has therapeutic potential in mitigating ER stress-related metabolic dysfunctions, offering promising insights for the treatment of liver diseases linked to metabolic stress. Full article
(This article belongs to the Special Issue Molecular Basis of Metabolic Homeostasis)
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