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Molecular Mechanisms of Metabolic Syndrome
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Molecular Mechanisms of Metabolic Syndrome

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 (30 December 2023) | Viewed by 14177

Special Issue Editors

Dr. Cosmin Mihai Vesa

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Guest Editor
Department of Preclinical Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania
Interests: sustainability in public health; occupational medicine; environment-associated diseases; sick building syndrome; one health
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Dana Zaha

E-Mail Website
Guest Editor
Department of Preclinical Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania
Interests: laboratory analysis in metabolic disease; diabetes mellitus
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Simona Gabriela Bungau

E-Mail Website
Guest Editor
Department of Pharmacy, Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania
Interests: medicine; pharmacology; antidiabetic drugs; metabolism; public health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic syndrome represents a cluster of conditions such as obesity, high blood pressure, dyslipidemia, and hyperglycemia that greatly increase the cardiovascular risk of the individual but also increase the risk of development of oncologic diseases, autoimmune diseases, or neurodegenerative diseases. Complex molecular pathways in metabolic syndrome interconnect various organs, altering the cell molecular physiology. Insulin resistance represents the most explored mechanism in metabolic syndrome, but new research continues to discover and explore the role of adipokines, GLP-1, GIP, pro-inflammatory interleukins, miRNAs, and genetic mutations in metabolic syndrome. Research in this area can improve the therapy of metabolic syndrome and associated diseases such as atherosclerotic complications, cancer, or dementia that have very high prevalence among metabolic syndrome patients. This Special Issue aims to introduce a more in-depth understanding of the systemic influence of certain molecules and their effect on different signaling pathways involved in metabolic syndrome to target them or their actions.

Given the growing attention in this highly attractive field, we welcome those interested in this Special Issue. We would like you to find here the necessary opening for your original works or reviews, focused on the topic described above, with clinical or experimental in vivo or in vitro results. In the hope that you will approach this field with interest, we look forward to your research in the form of valuable scientific papers that will enrich this Special Issue.

Dr. Cosmin Mihai Vesa
Prof. Dr. Dana Zaha
Prof. Dr. Simona Gabriela Bungau
Guest Editors

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

  • metabolic syndrome
  • insulin resistance
  • adipokines
  • cardiovascular disease
  • molecular mechanism
  • molecular diagnostic
  • genetic sequencing
  • cytokines

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Published Papers (6 papers)

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Editorial

Jump to: Research, Review

2 pages, 173 KiB  
Editorial
Molecular Mechanisms of Metabolic Syndrome
by Cosmin Mihai Vesa, Dana Carmen Zaha and Simona Gabriela Bungău
Int. J. Mol. Sci. 2024, 25(10), 5452; https://doi.org/10.3390/ijms25105452 - 17 May 2024
Viewed by 1166
Abstract
Metabolic syndrome represents a cluster of conditions, such as abdominal obesity, hypertension, dyslipidemia, and hyperglycemia, that are highly prevalent in developed countries because of unhealthy lifestyles [...] Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)

Research

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11 pages, 1745 KiB  
Article
Nutrient Combinations Sensed by L-Cell Receptors Potentiate GLP-1 Secretion
by Nalini Sodum, Orvokki Mattila, Ravikant Sharma, Remi Kamakura, Vesa-Pekka Lehto, Jaroslaw Walkowiak, Karl-Heinz Herzig and Ghulam Shere Raza
Int. J. Mol. Sci. 2024, 25(2), 1087; https://doi.org/10.3390/ijms25021087 - 16 Jan 2024
Cited by 3 | Viewed by 2368
Abstract
Obesity is a risk factor for cardiometabolic diseases. Nutrients stimulate GLP-1 release; however, GLP-1 has a short half-life (<2 min), and only <10–15% reaches the systemic circulation. Human L-cells are localized in the distal ileum and colon, while most nutrients are absorbed in [...] Read more.
Obesity is a risk factor for cardiometabolic diseases. Nutrients stimulate GLP-1 release; however, GLP-1 has a short half-life (<2 min), and only <10–15% reaches the systemic circulation. Human L-cells are localized in the distal ileum and colon, while most nutrients are absorbed in the proximal intestine. We hypothesized that combinations of amino acids and fatty acids potentiate GLP-1 release via different L-cell receptors. GLP-1 secretion was studied in the mouse enteroendocrine STC-1 cells. Cells were pre-incubated with buffer for 1 h and treated with nutrients: alpha-linolenic acid (αLA), phenylalanine (Phe), tryptophan (Trp), and their combinations αLA+Phe and αLA+Trp with dipeptidyl peptidase-4 (DPP4) inhibitor. After 1 h GLP-1 in supernatants was measured and cell lysates taken for qPCR. αLA (12.5 µM) significantly stimulated GLP-1 secretion compared with the control. Phe (6.25–25 mM) and Trp (2.5–10 mM) showed a clear dose response for GLP-1 secretion. The combination of αLA (6.25 µM) and either Phe (12.5 mM) or Trp (5 mM) significantly increased GLP-1 secretion compared with αLA, Phe, or Trp individually. The combination of αLA and Trp upregulated GPR120 expression and potentiated GLP-1 secretion. These nutrient combinations could be used in sustained-delivery formulations to the colon to prolong GLP-1 release for diminishing appetite and preventing obesity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)
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20 pages, 2329 KiB  
Article
Exploring the Metabolic and Endocrine Preconditioning Associated with Thyroid Disorders: Risk Assessment and Association with Acne Severity
by Alexa Florina Bungau, Delia Mirela Tit, Simona Gabriela Bungau, Cosmin Mihai Vesa, Andrei-Flavius Radu, Ruxandra Cristina Marin, Laura Maria Endres and Lavinia-Cristina Moleriu
Int. J. Mol. Sci. 2024, 25(2), 721; https://doi.org/10.3390/ijms25020721 - 5 Jan 2024
Cited by 1 | Viewed by 2489
Abstract
Metabolic preconditioning, characterized by conditions like obesity and insulin resistance syndrome, disrupts hormonal balance. Elevated androgen levels stimulate excessive sebum production and follicular cell proliferation, leading to acne lesions. Similarly, thyroid hormone imbalances affect sebaceous gland activity, epidermal lipid composition, and skin cell [...] Read more.
Metabolic preconditioning, characterized by conditions like obesity and insulin resistance syndrome, disrupts hormonal balance. Elevated androgen levels stimulate excessive sebum production and follicular cell proliferation, leading to acne lesions. Similarly, thyroid hormone imbalances affect sebaceous gland activity, epidermal lipid composition, and skin cell turnover, impacting acne occurrence and severity. This study aimed to assess the potential contribution of metabolic and endocrine preconditions to acne development. A total of 389 patients diagnosed with acne were included and divided into three groups: the metabolic precondition group (MPG, N = 163, 41.9%), the endocrine precondition group (EPG, N = 162, 41.65%), and the control group (CG, N = 89, 22.88%). Data related to the degree of acne severity and comorbidities of interest were collected from the patients’ medical records. In the groups with concomitant diseases, moderate and severe acne were significantly more prevalent (56.44% and 41.10% in MPG, and 35.80% and 61.11% in EPG) compared to the control group (5.61% and 4.89%). The most prevalent preconditions observed were insulin resistance syndrome in MPG (63.8%) and autoimmune thyroiditis in EPG (95.06%). Significant age-related differences in acne severity were found across all study groups (p < 0.05). In MPG, the age variable was significantly higher in the presence of mild acne, while in EPG, the age variable was significantly lower for the mild acne group. A positive association was observed between the severity of acne and insulin resistance syndrome, obesity, autoimmune thyroiditis, and hypothyroidism (p < 0.05). Risk analysis indicated a significantly higher risk (RR > 1, 95% CI RR > 1, p < 0.001) of developing moderate and severe acne in the presence of these preconditions. The presence of both metabolic and endocrine preconditions significantly increased the likelihood of developing severe acne, leading to the hypothesis that both conditions may be contributing factors to the development of acne. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)
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14 pages, 2022 KiB  
Article
Plasma microRNA Profiling in Type 2 Diabetes Mellitus: A Pilot Study
by Ziravard N. Tonyan, Yury A. Barbitoff, Yulia A. Nasykhova, Maria M. Danilova, Polina Y. Kozyulina, Anastasiia A. Mikhailova, Olga L. Bulgakova, Margarita E. Vlasova, Nikita V. Golovkin and Andrey S. Glotov
Int. J. Mol. Sci. 2023, 24(24), 17406; https://doi.org/10.3390/ijms242417406 - 12 Dec 2023
Cited by 1 | Viewed by 1876
Abstract
Type 2 diabetes mellitus (T2D) is a chronic metabolic disease characterized by insulin resistance and β-cell dysfunction and leading to many micro- and macrovascular complications. In this study we analyzed the circulating miRNA expression profiles in plasma samples from 44 patients with T2D [...] Read more.
Type 2 diabetes mellitus (T2D) is a chronic metabolic disease characterized by insulin resistance and β-cell dysfunction and leading to many micro- and macrovascular complications. In this study we analyzed the circulating miRNA expression profiles in plasma samples from 44 patients with T2D and 22 healthy individuals using next generation sequencing and detected 229 differentially expressed miRNAs. An increased level of miR-5588-5p, miR-125b-2-3p, miR-1284, and a reduced level of miR-496 in T2D patients was verified. We also compared the expression landscapes in the same group of patients depending on body mass index and identified differential expression of miR-144-3p and miR-99a-5p in obese individuals. Identification and functional analysis of putative target genes was performed for miR-5588-5p, miR-125b-2-3p, miR-1284, and miR-496, showing chromatin modifying enzymes and apoptotic genes being among the significantly enriched pathways. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)
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18 pages, 1287 KiB  
Article
Identification of a Specific Plasma Sphingolipid Profile in a Group of Normal-Weight and Obese Subjects: A Novel Approach for a “Biochemical” Diagnosis of Metabolic Syndrome?
by Antonello E. Rigamonti, Michele Dei Cas, Diana Caroli, Alessandra De Col, Silvano G. Cella, Rita Paroni and Alessandro Sartorio
Int. J. Mol. Sci. 2023, 24(8), 7451; https://doi.org/10.3390/ijms24087451 - 18 Apr 2023
Cited by 2 | Viewed by 1995
Abstract
Metabolic syndrome is nosographically defined by using clinical diagnostic criteria such as those of the International Diabetes Federation (IDF) ones, including visceral adiposity, blood hypertension, insulin resistance and dyslipidemia. Due to the pathophysiological implications of the cardiometabolic risk of the obese subject, sphingolipids, [...] Read more.
Metabolic syndrome is nosographically defined by using clinical diagnostic criteria such as those of the International Diabetes Federation (IDF) ones, including visceral adiposity, blood hypertension, insulin resistance and dyslipidemia. Due to the pathophysiological implications of the cardiometabolic risk of the obese subject, sphingolipids, measured in the plasma, might be used to biochemically support the diagnosis of metabolic syndrome. A total of 84 participants, including normal-weight (NW) and obese subjects without (OB-SIMET−) and with (OB-SIMET+) metabolic syndrome, were included in the study, and sphingolipidomics, including ceramides (Cer), dihydroceramides (DHCer), hexosyl-ceramides (HexCer), lactosyl-ceramides (LacCer), sphingomyelins (SM) and GM3 ganglosides families, and sphingosine-1-phosphate (S1P) and its congeners, was performed in plasma. Only total DHCers and S1P were significantly higher in OB-SIMET+ than NW subjects (p < 0.05), while total Cers decreased in both obese groups, though statistical significance was reached only in OB-SIMET− (vs. NW) subjects (p < 0.05). When considering the comparisons of the single sphingolipid species in the obese groups (OB-SIMET− or OB-SIMET+) vs. NW subjects, Cer 24:0 was significantly decreased (p < 0.05), while Cer 24:1, DHCer 16:0, 18:0, 18:1 and 24:1, and SM 18:0, 18:1 and 24:1 were significantly increased (p < 0.05). Furthermore, taking into account the same groups for comparison, HexCer 22:0 and 24:0, and GM3 22:0 and 24:0 were significantly decreased (p < 0.05), while HexCer 24:1 and S1P were significantly increased (p < 0.05). After having analyzed all data via a PLS-DA-based approach, the subsequent determination of the VIP scores evidenced the existence of a specific cluster of 15 sphingolipids endowed with a high discriminating performance (i.e., VIP score > 1.0) among the three groups, including DHCer 18:0, DHCer 24:1, Cer 18:0, HexCer 22:0, GM3 24:0, Cer C24:1, SM 18:1, SM 18:0, DHCer 18:1, HexCer 24:0, SM 24:1, S1P, SM 16:0, HexCer 24:1 and LacCer 22:0. After having run a series of multiple linear regressions, modeled by inserting each sphingolipid having a VIP score > 1.0 as a dependent variable, and waist circumference (WC), systolic/diastolic blood pressures (SBP/DBP), homeostasis model assessment-estimated insulin resistance (HOMA-IR), high-density lipoprotein (HDL), triglycerides (TG) (surrogates of IDF criteria) and C-reactive protein (CRP) (a marker of inflammation) as independent variables, WC was significantly associated with DHCer 18:0, DHCer 24:1, Cer 18:0, HexCer 22:0, Cer 24:1, SM 18:1, and LacCer 22:0 (p < 0.05); SBP with Cer 18:0, Cer 24:1, and SM 18:0 (p < 0.05); HOMA-IR with DHCer 18:0, DHCer 24:1, Cer 18:0, Cer 24:1, SM 18:1, and SM 18:0 (p < 0.05); HDL with HexCer 22:0, and HexCer 24:0 (p < 0.05); TG with DHCer 18:1, DHCer 24:1, SM 18:1, and SM 16:0 (p < 0.05); CRP with DHCer 18:1, and SP1 (p < 0.05). In conclusion, a cluster of 15 sphingolipid species is able to discriminate, with high performance, NW, OB-SIMET− and OB-SIMET+ groups. Although (surrogates of) the IDF diagnostic criteria seem to predict only partially, but congruently, the observed sphingolipid signature, sphingolipidomics might represent a promising “biochemical” support for the clinical diagnosis of metabolic syndrome. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)
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Review

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20 pages, 821 KiB  
Review
Mitochondrial Dysfunction Associated with mtDNA in Metabolic Syndrome and Obesity
by Natalia Todosenko, Olga Khaziakhmatova, Vladimir Malashchenko, Kristina Yurova, Maria Bograya, Maria Beletskaya, Maria Vulf, Natalia Gazatova and Larisa Litvinova
Int. J. Mol. Sci. 2023, 24(15), 12012; https://doi.org/10.3390/ijms241512012 - 27 Jul 2023
Cited by 11 | Viewed by 2968
Abstract
Metabolic syndrome (MetS) is a precursor to the major health diseases associated with high mortality in industrialized countries: cardiovascular disease and diabetes. An important component of the pathogenesis of the metabolic syndrome is mitochondrial dysfunction, which is associated with tissue hypoxia, disruption of [...] Read more.
Metabolic syndrome (MetS) is a precursor to the major health diseases associated with high mortality in industrialized countries: cardiovascular disease and diabetes. An important component of the pathogenesis of the metabolic syndrome is mitochondrial dysfunction, which is associated with tissue hypoxia, disruption of mitochondrial integrity, increased production of reactive oxygen species, and a decrease in ATP, leading to a chronic inflammatory state that affects tissues and organ systems. The mitochondrial AAA + protease Lon (Lonp1) has a broad spectrum of activities. In addition to its classical function (degradation of misfolded or damaged proteins), enzymatic activity (proteolysis, chaperone activity, mitochondrial DNA (mtDNA)binding) has been demonstrated. At the same time, the spectrum of Lonp1 activity extends to the regulation of cellular processes inside mitochondria, as well as outside mitochondria (nuclear localization). This mitochondrial protease with enzymatic activity may be a promising molecular target for the development of targeted therapy for MetS and its components. The aim of this review is to elucidate the role of mtDNA in the pathogenesis of metabolic syndrome and its components as a key component of mitochondrial dysfunction and to describe the promising and little-studied AAA + LonP1 protease as a potential target in metabolic disorders. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Metabolic Syndrome)
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