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

Deadline for manuscript submissions: closed (20 March 2026) | Viewed by 28626

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Dr. Antonella Muscella

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Department of Biological and Environmental Science and Technologies (DiSTeBA), University of Salento, 73100 Lecce, Italy
Interests: signal transduction; hormones; apoptosis; autophagy; metabolism
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Special Issue Information

Dear Colleagues,

Cellular metabolism is a complex set of biochemical reactions that allow cells to produce energy, synthesize molecules, and maintain homeostasis.

This dynamic system responds to external factors such as nutrients, physical activity, and environmental conditions, adapting energy consumption and the synthesis of biomolecules according to the needs of the organism. Hormones, released by the endocrine glands, finely regulate cellular metabolism, influencing processes such as glycolysis, lipolysis, and protein synthesis.

Endocrine disorders, such as obesity, diabetes, hypo/hyperthyroidism, polycystic ovary syndrome (PCOS), Addison’s disease, and Cushing’s syndrome, profoundly alter metabolism, leading to imbalances in the management of glucose, fats, and proteins. For example, insulin resistance in diabetes prevents cells from using glucose, while thyroid dysfunction alters the basal metabolic rate. These metabolic alterations contribute to systemic complications, including chronic inflammation, cardiovascular dysfunction, and an increased risk of other chronic diseases.

Understanding the mechanisms underlying these hormonal signals may lead to new therapeutic strategies. Furthermore, recent advances in metabolomics and systems biology promise to provide new insights into dynamic metabolism, revealing potential biomarkers, therapeutic targets, and the possibility of personalized medicine to treat metabolic and endocrine disorders more effectively.

Dr. Antonella Muscella
Guest Editor

Manuscript Submission Information

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Keywords

cellular metabolism
homeostasis
endocrine disorders
hormonal signals
dynamic system

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Published Papers (7 papers)

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Research

Jump to: Review

21 pages, 1887 KB

Open AccessArticle

Triglyceride Accumulation in Adipocytes Modulated by Insulin Dynamics

by Tatiana Yu. Plyusnina, Yulia A. Chistyakova, Polina V. Fursova, Sergei S. Khruschev, Diana G. Kiseleva and Alexander M. Markin

Int. J. Mol. Sci. 2025, 26(24), 11805; https://doi.org/10.3390/ijms262411805 - 6 Dec 2025

Viewed by 894

Abstract

This study examined how meal frequency under isocaloric conditions affects triglyceride accumulation in adipocytes, focusing on the role of insulin dynamics. Using a mathematical model of carbohydrate–lipid metabolism, we simulated feeding regimens from one to eight meals/day while holding calories and macronutrient ratios constant. A simplified model allowed independent variation in insulin peak amplitude, width, and overlap Results show that, relative to thrice-daily feeding (the reference regimen with stable triglyceride content over one month), infrequent meals (1–2/day) reduce, while frequent meals (5–8/day) increase triglyceride accumulation—most strongly in healthy individuals and attenuated in type 2 diabetes, as parameterized from the literature. Crucially, fat accumulation correlates not with average insulin levels but with its dynamic profile. Metabolic flux analysis revealed that triglyceride accumulation is driven not by changes in synthesis rate but by suppression of lipolysis, which depends on the amplitude, duration, and degree of overlap of insulin peaks. Thus, fat mass is shaped not only by caloric intake but by meal timing, which defines the insulin signal’s temporal structure. These findings highlight that insulin dynamics—not mean concentration—govern lipid metabolism, urging dietary guidelines to account for meal pattern, not just composition or total energy. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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14 pages, 2028 KB

Open AccessArticle

Metabolically Healthy Obesity Is Characterized by a Distinct Proteome Signature

by Fayaz Ahmad Mir, Houari B. Abdesselem, Farhan Cyprian, Ahmad Iskandarani, Asmma Doudin, Mutasem AbdelRahim Shraim, Bader M. Alkhalaf, Meis Alkasem, Ibrahem Abdalhakam, Ilham Bensmail, Hamza A. Al Halabi, Shahrad Taheri and Abdul-Badi Abou-Samra

Int. J. Mol. Sci. 2025, 26(5), 2262; https://doi.org/10.3390/ijms26052262 - 4 Mar 2025

Cited by 2 | Viewed by 3092

Abstract

Obesity is commonly associated with metabolic diseases including type 2 diabetes, hypertension, and dyslipidemia. Moreover, individuals with obesity are at increased risk of cardiovascular disease. However, a subgroup of individuals within the obese population presents without concurrent metabolic disorders. Even though this group has a stable metabolic status and does not exhibit overt metabolic disease, this status may be transient; these individuals may have subclinical metabolic derangements. To investigate the latter hypothesis, an analysis of the proteome signature was conducted. Plasma samples from 27 subjects with obesity but without an associated metabolic disorder (obesity only (OBO)) and 15 lean healthy control (LHC) subjects were examined. Fasting samples were subjected to Olink proteomics analysis targeting 184 proteins enriched in cardiometabolic and inflammation pathways. Our results distinctly delineated two groups with distinct plasma protein expression profiles. Specifically, a total of 24 proteins were differentially expressed in individuals with obesity compared to LHC. Among these, 13 proteins were downregulated, whereas 11 proteins were upregulated. The pathways that were upregulated in the OBO group were related to chemoattractant activity, growth factor activity, G protein-coupled receptor binding, chemokine activity, and cytokine activity, whereas the pathways that were downregulated include regulation of T cell differentiation, leukocyte differentiation, reproductive system development, inflammatory response, neutrophil, lymphocyte, monocyte and leukocyte chemotaxis, and neutrophil migration. The study identifies several pathways that are altered in individuals with obesity compared to healthy control subjects. These findings provide valuable insights into the underlying mechanisms, potentially paving the way for the identification of therapeutic targets aimed at improving metabolic health in individuals with obesity. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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18 pages, 3127 KB

Open AccessArticle

Deciphering the Association: Critical HDL-C Levels and Their Impact on the Glycation Gap in People Living with HIV

by Elsa J. Anaya-Ambriz, Monserrat Alvarez-Zavala, Luz A. González-Hernández, Jaime F. Andrade-Villanueva, Sergio Zuñiga-Quiñones, Adriana Valle-Rodríguez, Tania E. Holguin-Aguirre and Karina Sánchez-Reyes

Int. J. Mol. Sci. 2025, 26(3), 914; https://doi.org/10.3390/ijms26030914 - 22 Jan 2025

Cited by 1 | Viewed by 1599

Abstract

People Living with HIV (PLWHIV) present an increased risk of developing non-communicable diseases, such as type 2 diabetes (T2D), making it crucial to optimize glycemic control and assess metabolic markers. HbA1c is considered the gold standard for evaluating glycemic control, while fructosamine (FA) offers advantages in assessing non-glycemic determinants. Discrepancies between HbA1c and FA are common and may be influenced by temporal factors. The Glycation Gap (G-gap) emerges as a tool to clarify these discrepancies. A cross-sectional analytical study was conducted involving PLWHIV with various glycemic statuses, as well as patients with T2D and controls. Sociodemographic data were collected along with blood samples to measure biochemical profiles and FA. HbA1c predicted from FA (pHbA1c) was calculated using a linear regression equation, facilitating G-gap determination. A positive correlation was found between G-gap and levels of VLDL-C and triglycerides (TG). Additionally, a negative correlation was observed between HDL-C levels < 40 mg/dL and a positive G-gap. These associations suggest that the G-gap may be a useful tool for metabolic evaluation in PLWHIV and a preventive method for identifying individuals at risk of developing chronic complications related to T2D. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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21 pages, 11820 KB

Open AccessArticle

The Impact of Resident Adipose Tissue Macrophages on Adipocyte Homeostasis and Dedifferentiation

by Julia Neugebauer, Nora Raulien, Lilli Arndt, Dagmar Akkermann, Constance Hobusch, Andreas Lindhorst, Janine Fröba and Martin Gericke

Int. J. Mol. Sci. 2024, 25(23), 13019; https://doi.org/10.3390/ijms252313019 - 4 Dec 2024

Cited by 2 | Viewed by 2839

Abstract

Obesity is concurrent with immunological dysregulation, resulting in chronic low-grade inflammation and cellular dysfunction. In pancreatic islets, this loss of function has been correlated with mature β-cells dedifferentiating into a precursor-like state through constant exposure to inflammatory stressors. As mature adipocytes likewise have the capability to dedifferentiate in vitro and in vivo, we wanted to analyze this cellular change in relation to adipose tissue (AT) inflammation and adipose tissue macrophage (ATM) activity. Using our organotypic AT explant culture method combined with a double-reporter mouse model for labeling ATMs and mature adipocytes, we were able to visualize and quantify dedifferentiated fat (DFAT) cells in AT explants. Preliminary testing showed increased dedifferentiation after tamoxifen (TAM) stimulation, making TAM-dependent lineage-tracing models unsuitable for quantification of naturally occurring DFAT cells. The regulatory role of ATMs in adipocyte dedifferentiation was shown through macrophage depletion using Plexxicon 5622 or clodronate liposomes, which significantly increased DFAT cell levels. Subsequent bulk RNA sequencing of macrophage-depleted explants revealed enrichment of the tumor necrosis factor α (TNFα) signaling pathway as well as downregulation of associated genes. Direct stimulation with TNFα decreased adipocyte dedifferentiation, while application of a TNFα-neutralizing antibody did not significantly alter DFAT cell levels. Our findings suggest a regulatory role of resident ATMs in maintaining the mature adipocyte phenotype and preventing excessive adipocyte dedifferentiation. The specific regulatory pathways as well as the impact that DFAT cells might have on ATMs, and vice versa, are subject to further investigation. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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15 pages, 1701 KB

Open AccessArticle

Lipidomics of Caco-2 Cells Under Simulated Microgravity Conditions

by Giulia Tolle, Gabriele Serreli, Monica Deiana, Loredana Moi, Patrizia Zavattari, Antonella Pantaleo, Cristina Manis, Mohammed Amine El Faqir and Pierluigi Caboni

Int. J. Mol. Sci. 2024, 25(23), 12638; https://doi.org/10.3390/ijms252312638 - 25 Nov 2024

Cited by 5 | Viewed by 2432

Abstract

Microgravity may profoundly impact the cardiovascular system, skeletal muscle system, and immune system of astronauts. At the cellular level, microgravity may also affect cell proliferation, differentiation, and growth, as well as lipid metabolism. In this work, we investigated lipid changes in Caco-2 cells cultured in a clinostat for 24 h under simulated microgravity conditions (SMC). Complex lipids were measured using a UHPLC-QTOF/MS platform, and the data were subjected to multivariate analysis. Under SMC, levels of ceramides Cer 18:0;O2/16:0, Cer 18:1;O2/16:0, Cer 18:1; O2/22:0, Cer 18:1;O2/24:0, and Cer 18:2;O2/24:0 were found to be upregulated, while sphingomyelins SM 16:1;O2/16:0, SM 16:1;O2/18:1, SM 18:1;O2/24:0, and SM 18:2;O2/24:0 were found to be downregulated. On the other hand, considering that sphingolipids are involved in the process of inflammation, we also treated Caco-2 cells with dextran sodium sulfate (DSS) to induce cell inflammation and lipopolysaccharide (LPS) to induce cell immune responses. As a result, we observed similar lipid dysregulation, indicating that SMC may exert a condition similar to inflammation. Our lipidomics strategy provides new insights into the altered metabolic pathway of ceramides and sphingomyelins of Caco-2 cells under SMC. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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Review

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30 pages, 3032 KB

Open AccessReview

Emerging Roles of Post-Translational Modifications in Metabolic Homeostasis and Type 2 Diabetes

by Yong Kyung Kim and Hyeongseok Kim

Int. J. Mol. Sci. 2025, 26(23), 11552; https://doi.org/10.3390/ijms262311552 - 28 Nov 2025

Cited by 2 | Viewed by 1932

Abstract

Post-translational modifications (PTMs) provide an integrated regulatory layer that couples nutrient and hormonal signals to whole-body energy homeostasis across metabolic organs. PTMs modulate protein activity, localization, stability, and metabolic networks in a tissue- and state-specific manner. Through network remodeling, PTMs integrate receptor signaling with chromatin and organelle function and align transcriptional control with mitochondrial function, proteostasis, and membrane trafficking. PTM crosstalk connects kinase cascades, nutrient-sensing pathways, and ubiquitin-family modifiers to orchestrate gluconeogenesis, lipolysis, glucose uptake, thermogenesis, and insulin secretion in response to nutrient cues. The metabolic state regulates PTM enzymes through changes in cofactors, redox tone, and compartmentalization, and PTM-dependent changes in transcription and signaling feedback to metabolic tone. In obesity and diabetes, dysregulated post translational modification networks disrupt insulin receptor signaling, disturb organelle quality control, and impair beta cell function, which promotes insulin resistance and beta cell failure. Consequently, PTMs organize metabolic information flow and modulate tissue responses to overnutrition and metabolic stress. A systems-level understanding of PTMs clarifies mechanisms of whole-body energy homeostasis and supports the discovery of new therapeutic targets in metabolic disease. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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27 pages, 3910 KB

Open AccessReview

Role of Fatty Acids β-Oxidation in the Metabolic Interactions Between Organs

by Alexander V. Panov, Vladimir I. Mayorov and Sergey I. Dikalov

Int. J. Mol. Sci. 2024, 25(23), 12740; https://doi.org/10.3390/ijms252312740 - 27 Nov 2024

Cited by 36 | Viewed by 15015

Abstract

In recent decades, several discoveries have been made that force us to reconsider old ideas about mitochondria and energy metabolism in the light of these discoveries. In this review, we discuss metabolic interaction between various organs, the metabolic significance of the primary substrates and their metabolic pathways, namely aerobic glycolysis, lactate shuttling, and fatty acids β-oxidation. We rely on the new ideas about the supramolecular structure of the mitochondrial respiratory chain (respirasome), the necessity of supporting substrates for fatty acids β-oxidation, and the reverse electron transfer via succinate dehydrogenase during β-oxidation. We conclude that ATP production during fatty acid β-oxidation has its upper limits and thus cannot support high energy demands alone. Meanwhile, β-oxidation creates conditions that significantly accelerate the cycle: glucose-aerobic glycolysis-lactate-gluconeogenesis-glucose. Therefore, glycolytic ATP production becomes an important energy source in high energy demand. In addition, lactate serves as a mitochondrial substrate after converting to pyruvate + H⁺ by the mitochondrial lactate dehydrogenase. All coupled metabolic pathways are irreversible, and the enzymes are organized into multienzyme structures. Full article

(This article belongs to the Special Issue Advances in Cell Metabolism in Endocrine Diseases)

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