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Search Results (307)

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Keywords = adiponectin receptor

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19 pages, 1487 KiB  
Review
AdipoRon as a Novel Therapeutic Agent for Depression: A Comprehensive Review of Preclinical Evidence
by Lucas Fornari Laurindo, Victória Dogani Rodrigues, Rodrigo Haber Mellen, Rafael Santos de Argollo Haber, Vitor Engrácia Valenti, Lívia Fornari Laurindo, Eduardo Federighi Baisi Chagas, Camila Marcondes de Oliveira, Rosa Direito, Maria Angélica Miglino and Sandra Maria Barbalho
Biomedicines 2025, 13(8), 1867; https://doi.org/10.3390/biomedicines13081867 - 31 Jul 2025
Viewed by 109
Abstract
Background/Objectives: Depression is a mood disorder that causes persistent sadness and loss of interest, and its etiology involves a condition known as hypoadiponectinemia, which is prevalent in depressive individuals compared with healthy individuals and causes neuroinflammation. The use of intact adiponectin protein to [...] Read more.
Background/Objectives: Depression is a mood disorder that causes persistent sadness and loss of interest, and its etiology involves a condition known as hypoadiponectinemia, which is prevalent in depressive individuals compared with healthy individuals and causes neuroinflammation. The use of intact adiponectin protein to target neuroinflammation in depressive moods is complex due to the difficulties associated with using the intact protein. AdipoRon, a synthetic oral peptide that targets the AdipoR1 and AdipoR2 receptors for adiponectin, has emerged in this context. Its most prominent effects include reduced inflammation and the attenuation of oxidative stress. To the best of our knowledge, no comprehensive review has addressed these results so far. To fill this literature gap, we present a comprehensive review examining the effectiveness of AdipoRon in treating depression. Methods: Only preclinical models are included due to the absence of clinical studies. Results: Analyzing the included studies shows that AdipoRon demonstrates contrasting effects against depression. However, most of the evidence underscores AdipoRon-based adiponectin replacement therapies as potential candidates for future treatment against this critical psychiatric condition due to their anti-neuroinflammatory potential, ultimately inhibiting several neuroinflammatory pathways. Conclusions: Future research endeavors must address several limitations due to the heterogeneity of the studies’ methodologies and results. Full article
(This article belongs to the Section Neurobiology and Clinical Neuroscience)
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11 pages, 243 KiB  
Review
Adipokines: Do They Affect the Osteochondral Unit?
by Sergio Rosini, Gianantonio Saviola, Stefano Rosini, Eleonora Baldissarro and Luigi Molfetta
Rheumato 2025, 5(3), 9; https://doi.org/10.3390/rheumato5030009 - 22 Jul 2025
Viewed by 164
Abstract
Obesity, characterized by excessive or abnormal accumulation of body fat, is associated with a range of metabolic and inflammatory diseases, including osteoarthritis (OA). In obese individuals, adipose tissue expansion—via adipocyte hypertrophy or hyperplasia—is accompanied by altered secretion of adipokines such as leptin and [...] Read more.
Obesity, characterized by excessive or abnormal accumulation of body fat, is associated with a range of metabolic and inflammatory diseases, including osteoarthritis (OA). In obese individuals, adipose tissue expansion—via adipocyte hypertrophy or hyperplasia—is accompanied by altered secretion of adipokines such as leptin and adiponectin, which play significant roles in immune modulation, metabolism, and skeletal homeostasis. Leptin, acting through the hypothalamus, regulates the sympathetic nervous system and modulates hormonal axes, influencing bone metabolism and cartilage integrity. Elevated leptin concentrations in the synovial fluid, and the presence of its receptors on cartilage surfaces, suggest its direct role in cartilage degradation and OA progression. Conversely, adiponectin exerts anti-inflammatory effects, modulates osteoblast and macrophage activity, and appears to have a protective function in joint metabolism. These findings underscore the complex interplay between the adipose tissue, adipokines, and the osteochondral unit, highlighting the importance of their balance in maintaining joint health. Full article
25 pages, 1538 KiB  
Review
Lipid Hormones at the Intersection of Metabolic Imbalances and Endocrine Disorders
by Maria-Zinaida Dobre, Bogdana Virgolici and Ruxandra Cioarcă-Nedelcu
Curr. Issues Mol. Biol. 2025, 47(7), 565; https://doi.org/10.3390/cimb47070565 - 18 Jul 2025
Viewed by 466
Abstract
Lipid hormone imbalances involving glucocorticoids, thyroid hormones (THs), and sex hormones have widespread metabolic consequences, contributing to the global increase in obesity and insulin resistance. This review examines the complex role of disrupted lipid hormone pathways in the development of metabolic disorders, particularly [...] Read more.
Lipid hormone imbalances involving glucocorticoids, thyroid hormones (THs), and sex hormones have widespread metabolic consequences, contributing to the global increase in obesity and insulin resistance. This review examines the complex role of disrupted lipid hormone pathways in the development of metabolic disorders, particularly metabolic dysfunction-associated steatotic liver disease (MASLD). Endocrine disorders such as hypercortisolism, hypothyroidism, and polycystic ovary syndrome (PCOS) are closely linked to MASLD through shared metabolic pathways. Mechanisms include glucocorticoid-induced gluconeogenesis and lipolysis, impaired lipid clearance in hypothyroidism, and the hyperandrogenism-induced downregulation of hepatic low-density lipoprotein (LDL) receptors. PCOS-related factors—such as central obesity, adipocyte hypertrophy, low adiponectin levels, and genetic predisposition—further promote hepatic steatosis. Thyroid dysfunction may also impair the hepatic deiodination of T4, contributing to lipid accumulation and inflammation. Given the overlapping pathophysiology among endocrine, hepatic, and reproductive disorders, multidisciplinary collaboration is essential to optimize diagnosis, treatment, and long-term cardiometabolic outcomes. Full article
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17 pages, 1758 KiB  
Article
Bioactive Polysaccharides from Fermented Dendrobium officinale: Structural Insights and Their Role in Skin Barrier Repair
by Wanshuai Wang, Anqi Zou, Qingtao Yu, Zhe Wang, Daotong Tan, Kaiye Yang, Chao Cai and Guangli Yu
Molecules 2025, 30(13), 2875; https://doi.org/10.3390/molecules30132875 - 6 Jul 2025
Viewed by 600
Abstract
Dendrobium, a prominent genus in the Orchidaceae family, has generated significant research attention due to its demonstrated biological potential, particularly its notable anti-inflammatory and antioxidant activities. In this study, two fractions of fermented Dendrobium officinale polysaccharides (FDOPs) were successfully isolated through a [...] Read more.
Dendrobium, a prominent genus in the Orchidaceae family, has generated significant research attention due to its demonstrated biological potential, particularly its notable anti-inflammatory and antioxidant activities. In this study, two fractions of fermented Dendrobium officinale polysaccharides (FDOPs) were successfully isolated through a multi-stage purification strategy including gradient ethanol precipitation, gel column chromatography, and ion exchange chromatography with Lactobacillus reuteri CCFM863. Structural characterization revealed that both Dendrobium officinale polysaccharide fractions consisted of (1→4)-β-D-Manp, (1→4)-β-D-Glcp, and (1→4)-α-D-Glcp residues. The anti-inflammatory efficacy and keratinocyte-protective potential of FDOPs (FDOP-1A and FDOP-2A) were investigated by using lipopolysaccharide (LPS)-induced RAW264.7 and HaCaT cells models, which showed significant inhibitions on the inflammatory factors of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), nitric oxide (NO), and interleukin-1 beta (IL-1β); recovered levels of filaggrin (FLG), aquaporin 3 (AQP3), transient receptor potential vanilloid 4 (TRPV4), cathelicidin antimicrobial peptide (CAMP)/LL-37, and adiponectin (ADIPOQ); and the reduced protein expression of the TLR4/IκB-α/NF-κB/NLRP3 pathway. Notably, the FDOPs exhibited a remarkable reactive oxygen species (ROS) scavenging capacity, demonstrating superior antioxidant activity. Therefore, FDOPs show dual anti-inflammatory and antioxidant properties, making them suitable as active ingredients for modulating epidermal inflammation and promoting skin barrier repair. Full article
(This article belongs to the Special Issue Biotechnology and Biomass Valorization)
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20 pages, 5017 KiB  
Article
Poly-L-Lactic Acid Filler Increases Adipogenesis and Adiponectin in Aged Subcutaneous Tissue
by Seyeon Oh, Nala Shin, Sang Ju Lee, Kuk Hui Son and Kyunghee Byun
Polymers 2025, 17(13), 1826; https://doi.org/10.3390/polym17131826 - 30 Jun 2025
Viewed by 540
Abstract
Poly-L-lactic acid (PLLA) filler, which increases volume and collagen synthesis, is used for skin rejuvenation. Subcutaneous adipose tissue (SAT) contains precursors that differentiate into mature adipocytes that secrete adiponectin, which modulates SAT function and increases adipogenesis. During aging, adiponectin and precursor cell functions [...] Read more.
Poly-L-lactic acid (PLLA) filler, which increases volume and collagen synthesis, is used for skin rejuvenation. Subcutaneous adipose tissue (SAT) contains precursors that differentiate into mature adipocytes that secrete adiponectin, which modulates SAT function and increases adipogenesis. During aging, adiponectin and precursor cell functions decrease, reducing adipogenesis and facial volume. Adiponectin also increases collagen synthesis by stimulating fibroblasts. After hydrogen peroxide treatment to induce senescent adipocytes (3T3-L1) and aged skin, follow-up PLLA treatment increased adipogenesis by stimulating the nuclear factor erythroid-2-related factor 2 (NRF2)/peroxisome proliferator-activated receptor gamma (PPARγ)/CCAAT/enhancer binding protein alpha (C/EBPα) pathway. This resulted in increased adiponectin secretion, which promoted collagen synthesis and mitigated the loss of SAT volume. In the senescent adipocyte, PLLA increased NRF2/PPARγ/C/EBPα, adipogenesis factors (fatty acid binding protein 4, lipoprotein lipase, and cluster of differentiation 36), lipogenesis factors (ATP citrate lyase, acetyl-CoA carboxylase, and fatty acid synthase), adiponectin, and lipid droplet size. Treatment of senescent fibroblasts with conditioned medium from PLLA-treated adipocytes increased collagen1 and 3 and decreased matrix metalloproteinase1 and 3 expressions. Similarly, PLLA increased NRF2/PPARγ/C/EBPα, adipogenesis, and lipogenesis factors in aged mouse SAT. Also, PLLA increased adiponectin and adipocyte numbers without hypertrophy and increased collagen accumulation and dermal thickness. In summary, PLLA increased adipogenesis and adiponectin, which increased the volume of SAT and collagen synthesis, thereby rejuvenating aged skin. Full article
(This article belongs to the Section Biobased and Biodegradable Polymers)
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25 pages, 937 KiB  
Review
T-Cadherin (CDH13) and Non-Coding RNAs: The Crosstalk Between Health and Disease
by Kseniya Rubina, Artem Maier, Polina Klimovich, Veronika Sysoeva, Daniil Romashin, Ekaterina Semina and Vsevolod Tkachuk
Int. J. Mol. Sci. 2025, 26(13), 6127; https://doi.org/10.3390/ijms26136127 - 26 Jun 2025
Viewed by 619
Abstract
T-cadherin (CDH13) is an atypical, glycosyl-phosphatidylinositol-anchored cadherin with functions ranging from axon guidance and vascular patterning to adipokine signaling and cell-fate specification. Originally identified as a homophilic cue for migrating neural crest cells, projecting axons, and growing blood vessels, it later [...] Read more.
T-cadherin (CDH13) is an atypical, glycosyl-phosphatidylinositol-anchored cadherin with functions ranging from axon guidance and vascular patterning to adipokine signaling and cell-fate specification. Originally identified as a homophilic cue for migrating neural crest cells, projecting axons, and growing blood vessels, it later emerged as a dual metabolic receptor for cardioprotective high-molecular-weight adiponectin and atherogenic low-density lipoproteins. We recently showed that mesenchymal stem/stromal cells lacking T-cadherin are predisposed to adipogenesis, underscoring its role in lineage choice. Emerging evidence indicates that CDH13 expression and function are fine-tuned by non-coding RNAs (ncRNAs). MiR-199b-5p, miR-377-3p, miR-23a/27a/24-2, and the miR-142 family directly bind CDH13 3′-UTR or its epigenetic regulators, affecting transcription or accelerating decay. Long non-coding RNAs (lncRNAs), including antisense transcripts CDH13-AS1/AS2, brain-restricted FEDORA, and context-dependent LINC00707 and UPAT, either sponge these miRNAs or recruit DNMT/TET enzymes to the CDH13 promoter. Circular RNAs (circRNAs), i.e.circCDH13 and circ_0000119, can add a third level of complexity by sequestering miRNA repressors or boosting DNMT1. Collectively, this ncRNA circuitry regulates T-cadherin across cardiovascular, metabolic, oncogenic, and neurodegenerative conditions. This review integrates both experimentally validated data and in silico predictions to map the ncRNA-CDH13 crosstalk between health and disease, opening new avenues for biomarker discovery and RNA-based therapeutics. Full article
(This article belongs to the Special Issue Regulation by Non-Coding RNAs 2025)
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10 pages, 231 KiB  
Review
From Menopause to Molecular Dysregulation: Proteomic Insights into Obesity-Related Pathways—A Narrative Review
by Basant E. Katamesh, Jithinraj Edakkanambeth Varayil, Nina Pillai and Ann Vincent
Biomedicines 2025, 13(7), 1558; https://doi.org/10.3390/biomedicines13071558 - 25 Jun 2025
Viewed by 425
Abstract
Peri- and postmenopausal women often experience unexplained weight gain despite maintaining consistent dietary and lifestyle habits. While the biological mechanisms underlying this phenomenon remain poorly understood, physiological and pathophysiological changes during the menopausal transition are likely contributors. Proteomic profiling holds potential for revealing [...] Read more.
Peri- and postmenopausal women often experience unexplained weight gain despite maintaining consistent dietary and lifestyle habits. While the biological mechanisms underlying this phenomenon remain poorly understood, physiological and pathophysiological changes during the menopausal transition are likely contributors. Proteomic profiling holds potential for revealing key molecular pathways involved in the pathogenesis of obesity in this population. This review synthesizes current evidence on proteomic alterations linked to overweight and obesity in peri- and postmenopausal women. A structured literature search was performed across Ovid MEDLINE®, EMBASE, the Cochrane Library, and Scopus for studies published between October 2010 and March 2025. Eligible studies included original research involving overweight or obese peri- or postmenopausal women that reported proteomic data. Extracted information encompassed study design, participant characteristics, sample types, and proteomic findings. Identified proteins were cross-referenced with a prior review of consistently dysregulated proteins in obesity. Five studies met the inclusion criteria, collectively revealing consistent proteomic patterns associated with inflammation, metabolic dysfunction, and endothelial dysregulation. These included C-reactive protein, Tissue necrotic factor-alpha, interleukins, adiponectin, and endocan. Notably, one study demonstrated that weight loss led to reductions in IL-6, IL-1 receptor antagonist, and CRP, suggesting that obesity-related inflammation may be at least partially reversible. This review provides preliminary evidence linking chronic inflammation, metabolic dysregulation, and vascular stress to obesity in peri- and postmenopausal women. These proteomic signatures enhance understanding of menopausal weight gain and highlight the potential of proteomics to guide personalized interventions. However, larger, well-designed prospective studies are needed to confirm these associations and clarify causal pathways. Full article
(This article belongs to the Section Endocrinology and Metabolism Research)
43 pages, 1769 KiB  
Review
The Role of LAIR1 as a Regulatory Receptor of Antitumor Immune Cell Responses and Tumor Cell Growth and Expansion
by Alessandro Poggi, Serena Matis, Chiara Rosa Maria Uras, Lizzia Raffaghello, Roberto Benelli and Maria Raffaella Zocchi
Biomolecules 2025, 15(6), 866; https://doi.org/10.3390/biom15060866 - 13 Jun 2025
Viewed by 805
Abstract
It is becoming evident that the therapeutic effect of reawakening the immune response is to limit tumor cell growth and expansion. The use of immune checkpoint inhibitors, like blocking antibodies against programmed cell death receptor (PD) 1 and/or cytotoxic T lymphocyte antigen (CTLA) [...] Read more.
It is becoming evident that the therapeutic effect of reawakening the immune response is to limit tumor cell growth and expansion. The use of immune checkpoint inhibitors, like blocking antibodies against programmed cell death receptor (PD) 1 and/or cytotoxic T lymphocyte antigen (CTLA) 4 alone or in combination with other drugs, has led to unexpected positive results in some tumors but not all. Several other molecules inhibiting lymphocyte antitumor effector subsets have been discovered in the last 30 years. Herein, we focus on the leukocyte-associated immunoglobulin (Ig)-like receptor 1 (LAIR1/CD305). LAIR1 represents a typical immunoregulatory molecule expressed on almost all leukocytes, unlike other regulatory receptors expressed on discrete leukocyte subsets. It bears two immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in the intracytoplasmic protein domain involved in the downregulation of signals mediated by activating receptors. LAIR1 binds to several ligands, such as collagen I and III, complement component 1Q, surfactant protein D, adiponectin, and repetitive interspersed families of polypeptides expressed by erythrocytes infected with Plasmodium malariae. This would suggest LAIR1 involvement in several cell-to-cell interactions and possibly in metabolic regulation. The presence of both cellular and soluble forms of LAIR would indicate a fine regulation of the immunoregulatory activity, as happens for the soluble/exosome-associated forms of PD1 and CTLA4 molecules. As a consequence, LAIR1 appears to play a role in some autoimmune diseases and the immune response against tumor cells. The finding of LAIR1 expression on hematological malignancies, but also on some solid tumors, could open a rationale for the targeting of this molecule to treat neoplasia, either alone or in combination with other therapeutic options. Full article
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17 pages, 6100 KiB  
Article
Effects of Modified Messenger RNA of Adiponectin Delivered by Lipid Nanoparticles on Adipogenesis and Bone Metabolism In Vitro and In Vivo
by Ying Xie, Qian Ma, Jinghao Wang, Zoe Xiaofang Zhu, Rady E. El-Araby, Maxwell Tu, Zhongyu Li, Xiaoyang Xu, Qisheng Tu and Jake Chen
Cells 2025, 14(12), 891; https://doi.org/10.3390/cells14120891 - 13 Jun 2025
Viewed by 831
Abstract
Adiponectin (APN) is a secreted adipokine that plays a key role in modulating energy and bone metabolism, as well as regulating inflammatory responses. The overexpression of APN has been proposed as a potential therapeutic strategy for treating obesity and related disorders. Lipid nanoparticles [...] Read more.
Adiponectin (APN) is a secreted adipokine that plays a key role in modulating energy and bone metabolism, as well as regulating inflammatory responses. The overexpression of APN has been proposed as a potential therapeutic strategy for treating obesity and related disorders. Lipid nanoparticles (LNPs) are promising vectors for transporting messenger ribonucleic acid (mRNA) molecules. This study tested whether delivering a stabilized version of adiponectin mRNA (APN mRNA) using lipid nanoparticles could reduce fat formation and promote bone repair in vitro and in vivo. We demonstrated that transfection with APN-LNP upregulated the mRNA and protein expression of APN, while inhibiting adipogenesis in 3T3-L1 adipocytes. APN-LNP enhanced osteogenic gene expression in MC3T3-E1 cells in a dose-dependent manner. It also reduced matrix metalloproteinase 9 expression in receptor activator of nuclear factor-kappaB ligand (RANKL)-stimulated RAW264.7 cells, suggesting an anti-resorptive effect. In vivo, a femoral fracture model was established to explore the application of APN-LNP in promoting bone healing in diet-induced obese mice. Micro-computed tomography and histology analysis indicated that intravenous injection with APN-LNP promoted bone healing. Fasting blood glucose and body weight were decreased in the APN-LNP group. Moreover, APN-LNP increased bone sialoprotein and runt-related transcription factor 2 expression in contralateral femurs, as well as interleukin-10 expression in white adipose tissues. Thus, our study provides promising preclinical data on the potential use of APN-LNP for treating bone disorders in obesity. Full article
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28 pages, 1260 KiB  
Review
Unravelling the Adiponectin Hallmark and Exploring the Therapeutic Potential of Its Receptor Agonists in Cancer Metabolic Reprogramming
by Sanober Kafeel, Giuseppina Palmiero, Alessia Salzillo, Angela Ragone, Silvio Naviglio and Luigi Sapio
Biomolecules 2025, 15(6), 820; https://doi.org/10.3390/biom15060820 - 5 Jun 2025
Viewed by 830
Abstract
As the most abundant fat-derived hormone, adiponectin plays an essential role in regulating energy homeostasis. Current evidence proposes the serum levels of adiponectin as a risk factor and a diagnostic/prognostic biomarker in cancer. Moreover, distinctive antineoplastic features have also been reported as a [...] Read more.
As the most abundant fat-derived hormone, adiponectin plays an essential role in regulating energy homeostasis. Current evidence proposes the serum levels of adiponectin as a risk factor and a diagnostic/prognostic biomarker in cancer. Moreover, distinctive antineoplastic features have also been reported as a result of adiponectin supplementation in preclinical models. Mapping of the cancer-associated metabolic changes has elucidated a highly adaptable and interconnected system that allows malignant cells to sustain their growth and survival. Along with the pyruvate into acetyl-CoA conversion, downregulation of both lactate dehydrogenase and glycolysis-related genes depicts the main adiponectin-induced perturbations affecting glucose metabolism in cancer. Meanwhile, a multi-level approach involving lipid trafficking, catabolism, and de novo synthesis has been attributed to adiponectin in malignancies. The adiponectin receptor agonist AdipoRon has recently been recognized as a promising antineoplastic compound. Remarkably, AdipoRon-mediated changes in cancer metabolism occur together with its antiproliferative potential. This review aimed at recapitulating the modulatory effects of adiponectin, as well as those of its synthetic receptor agonists, in driving metabolic alterations in cancerous cells. A critical discussion is also conducted to deduce whether the adiponectin axis could serve as a putative target to address the metabolic reprogramming in cancer progression. Full article
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18 pages, 4414 KiB  
Article
Effects of Sleeve Gastrectomy and Treadmill Exercise on Skeletal Muscle and Ectopic Fat in High-Fat Diet-Induced Obese Rats
by Takaaki Noguchi, Yuichi Yoshida, Koro Gotoh, Satoshi Nagai, Kentaro Sada, Naoki Matsuda, Miho Suzuki, Akiko Kudo, Shotaro Miyamoto, Yoshinori Ozeki, Takashi Ozaki, Takeshi Nakata, Akihiro Fukuda, Takayuki Masaki and Hirotaka Shibata
Int. J. Mol. Sci. 2025, 26(11), 5294; https://doi.org/10.3390/ijms26115294 - 30 May 2025
Viewed by 588
Abstract
A high-fat diet (HFD) can lead to obesity and skeletal muscle atrophy. Sleeve gastrectomy (SG) improves obesity and increases skeletal muscle mass. This study examined whether SG prevented skeletal muscle atrophy in a diet-induced rat obesity rat model. First, 8-week-old male Sprague-Dawley rats [...] Read more.
A high-fat diet (HFD) can lead to obesity and skeletal muscle atrophy. Sleeve gastrectomy (SG) improves obesity and increases skeletal muscle mass. This study examined whether SG prevented skeletal muscle atrophy in a diet-induced rat obesity rat model. First, 8-week-old male Sprague-Dawley rats underwent surgical (sham-operated or SG) and dietary (standard, high-fat diet, or same pair feeding as SG [PF]) interventions without exercise. In the second experiment, treadmill exercise was added for 4 weeks post-SG (SG + Ex). In the third experiment, rats received an adiponectin receptor agonist (AdipoRon) injection. The HFD induced weight gain and decreased muscle fiber area. SG + Ex reversed these levels, followed by increases in adiponectin in the blood and skeletal muscle and myoblast determination protein 1 (MyoD) and decreased peri-muscular adipose tissue (PMAT) mass, but SG alone did not. No similar changes were observed in the PF group, with or without exercise. Injection of AdipoRon had a similar effect on skeletal muscle and PMAT as SG + Ex. The combination of SG and exercise, but not calorie restriction alone, had better impacts on skeletal muscle and PMAT than SG or exercise alone. Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
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11 pages, 1137 KiB  
Article
Evaluation of Adipokine Status and Leptin Receptor Gene Polymorphism in Patients with Severe Asthma
by Saule Maimysheva, Lyudmila Karazhanova, Andrey Orekhov, Assel Chinybayeva and Bolat Ashirov
Diagnostics 2025, 15(9), 1154; https://doi.org/10.3390/diagnostics15091154 - 1 May 2025
Viewed by 454
Abstract
Background: Severe and difficult-to-control asthma occurs in 3–10% of patients in developed countries. The aim of our study was to investigate the association of the prognostic role of leptin and adiponectin, as well as the leptin receptor gene polymorphism Gln223Arg, in patients [...] Read more.
Background: Severe and difficult-to-control asthma occurs in 3–10% of patients in developed countries. The aim of our study was to investigate the association of the prognostic role of leptin and adiponectin, as well as the leptin receptor gene polymorphism Gln223Arg, in patients with difficult-to-control and severe asthma. Methods: The present study included 200 patients with asthma hospitalized in the Department of Pulmonology between January 2018 and December 2021. In all patients, in addition to routine clinical investigations, adiponectin, leptin and their ratio were analyzed, as well as levels of pro-inflammatory cytokines (IL-6, IL-8 and TNF-alpha). External respiratory function was also assessed. LEPR Gln223Arg single-nucleotide polymorphisms were genotyped by real-time PCR method. Results: Patients were randomized into two groups, depending on the severity of asthma: an uncontrolled asthma group and a controlled asthma group, according to the GINA criteria. Among patients with uncontrolled asthma, 101 subjects (74.3%) had metabolic syndrome (p < 0.001). There was an inverse association of the adiponectin/leptin ratio with the eosinophil count (B = −0.305, p < 0.001), IL-6 (B = −0.026, p < 0.001), IL-8 (B = −0.062, p < 0.001) and TNF-alpha (B = −0.047, p < 0.001) and a direct correlation with the level of FEV1 (B = 0.121, p < 0.001) and FVC (B = 0.104, p < 0.001). A probable association of homozygous A/A allele with increased risk of uncontrolled asthma was shown (p = 0.007). Conclusions: Leptin receptor polymorphism with A/A genotype may be associated with a higher probability of developing severe and difficult-to-control asthma. Full article
(This article belongs to the Section Clinical Diagnosis and Prognosis)
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17 pages, 3030 KiB  
Article
Pharmacological Blocking of Adiponectin Receptors Induces Alzheimer’s Disease-like Neuropathology and Impairs Hippocampal Function
by Hui-Hui Guo, Hai-Ning Ou, Jia-Sui Yu, Suk-Yu Yau and Hector Wing-Hong Tsang
Biomedicines 2025, 13(5), 1056; https://doi.org/10.3390/biomedicines13051056 - 27 Apr 2025
Viewed by 615
Abstract
Background/Objectives: Previous studies have shown that adiponectin deficiency or blocking adiponectin receptors (AdipoRs) in the brain can lead to an Alzheimer’s disease (AD)-like neuropathology. While AdipoRs are abundantly expressed in peripheral tissues, the effects of blocking these receptors in the peripheral tissues [...] Read more.
Background/Objectives: Previous studies have shown that adiponectin deficiency or blocking adiponectin receptors (AdipoRs) in the brain can lead to an Alzheimer’s disease (AD)-like neuropathology. While AdipoRs are abundantly expressed in peripheral tissues, the effects of blocking these receptors in the peripheral tissues on the brain are unclear. This study investigates the impacts of blocking AdipoRs with a peripheral administration of ADP400, an antagonist peptide that targets AdipoRs on cognitive performance, hippocampal adult neurogenesis, and AD-like neuropathology in mice. Methods: Adult mice were intraperitoneally administered with ADP400 peptide that blocks peripheral AdipoRs continuously for 21 days, followed by a battery of behavioral test for mood and memory performance. Results: ADP400-treated mice exhibited impaired memory performance and increased anxiety-like behaviors. Molecular analyses revealed heightened hyperphosphorylation of tau and increased β-amyloid levels, alongside decreased expression of AdipoRs and PP2A in the hippocampus, suggesting a critical role of AdipoRs in AD-like neuropathology. Furthermore, ADP400 treatment significantly reduced hippocampal adult neurogenesis, as indicated by decreased BrdU, Ki67, and DCX staining. Inhibiting peripheral adiponectin receptors could lead to tau hyperphosphorylation and accumulated β-amyloid levels. Conclusions: These findings highlight the critical role of peripheral manipulation of adiponectin receptors in modulating cognitive function and adult neurogenesis, offering insights into potential therapeutic strategies for AD and related cognitive disorders. Full article
(This article belongs to the Special Issue Recent Advances in Adipokines—2nd Edition)
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21 pages, 8479 KiB  
Article
Hepatoprotective and Antiatherosclerotic Effects of Oleoylethanolamide-Based Dietary Supplement in Dietary-Induced Obesity in Mice
by Darya Ivashkevich, Arina Ponomarenko, Igor Manzhulo, Anastasia Egoraeva and Inessa Dyuizen
Pathophysiology 2025, 32(2), 16; https://doi.org/10.3390/pathophysiology32020016 - 18 Apr 2025
Viewed by 636
Abstract
Background: Metabolic effects of oleoylethanolamide-based dietary supplement (OEA-DS) were studied in a model of dietary-induced obesity in mice. Obesity was induced by a 2-month high-fat, high-cholesterol diet, resulting in significant morphological changes in liver tissues and elevated cholesterol levels in the animals’ blood [...] Read more.
Background: Metabolic effects of oleoylethanolamide-based dietary supplement (OEA-DS) were studied in a model of dietary-induced obesity in mice. Obesity was induced by a 2-month high-fat, high-cholesterol diet, resulting in significant morphological changes in liver tissues and elevated cholesterol levels in the animals’ blood serum. Elevated levels of proinflammatory cytokines, oxidative stress, and hepatocyte apoptosis were also observed in the liver tissue. The aim of this study was to examine the mechanisms through which an OEA-based dietary supplement (OEA-DS) exerts a comprehensive influence on multiple aspects of the pathogenesis of MASLD, thereby demonstrating a robust hepatoprotective effect. Methods: mice were fed a high-fat, high-cholesterol diet with or without OEA-DS supplementation. Liver tissues and blood serum were analyzed for cholesterol levels, inflammatory markers (CD68, Iba-1, CD163, IL-1β, IL-6, TNFα), apoptotic markers (Bad, Bax, Bcl-2), nuclear receptors (PPAR-α, PPAR-γ, AdipoR1), and enzymes involved in lipolysis (Acox1, Cpt1a) and cholesterol metabolism (Ldlr, Furin, Pcsk9). Immunohistochemistry, Western blotting, and RT-PCR were used to assess protein expression and gene transcription. Results: administration of OEA-DS normalized cholesterol levels, decreased expression of inflammatory markers (CD68 and Iba-1), pro-apoptotic markers (Bad, Bax) and levels of pro-inflammatory cytokines (IL-1β, IL-6, TNFα). In parallel, the expression of nuclear receptors PPAR-α and PPAR-γ, adiponectin receptor 1 (AdipoR1), and anti-inflammatory (CD163) and anti-apoptotic (Bcl-2) markers have risen. OEA-DS administration induced the expression of liver lipolysis enzymes (Acox1, Cpt1a) and cholesterol metabolism factors (Ldlr, Furin), while simultaneously reducing the transcription of the proatherogenic factor Pcsk9. Conclusions: The results of this study suggest a complex action of OEA-DS in obesity-associated liver damage, which includes reduction of systemic inflammation. Full article
(This article belongs to the Section Metabolic Disorders)
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15 pages, 3827 KiB  
Article
Luteolin Relieves Metabolic Dysfunction-Associated Fatty Liver Disease Caused by a High-Fat Diet in Rats Through Modulating the AdipoR1/AMPK/PPARγ Signaling Pathway
by Pongsakorn Taweesap, Prapassorn Potue, Juthamas Khamseekaew, Metee Iampanichakul, Banyaphon Jan-O, Poungrat Pakdeechote and Putcharawipa Maneesai
Int. J. Mol. Sci. 2025, 26(8), 3804; https://doi.org/10.3390/ijms26083804 - 17 Apr 2025
Cited by 2 | Viewed by 888
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a significant global public health issue. Luteolin possesses several beneficial biological properties, including antioxidation and anti-inflammation. This study investigated luteolin’s effect and potential mechanisms on MAFLD in high-fat diet (HFD)-fed rats. Rats were administered an HFD [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a significant global public health issue. Luteolin possesses several beneficial biological properties, including antioxidation and anti-inflammation. This study investigated luteolin’s effect and potential mechanisms on MAFLD in high-fat diet (HFD)-fed rats. Rats were administered an HFD supplemented with fructose for 12 weeks to induce MAFLD. After that, the HFD-fed rats were given either luteolin (50 or 100 mg/kg/day) or metformin (100 mg/kg/day) for 4 weeks. Luteolin improved metabolic parameters induced by the HFD, since it decreased body weight, blood pressure, fasting blood glucose, serum insulin, free fatty acids, cholesterol, and triglyceride levels (p < 0.05). Luteolin reduced hepatic injury and inflammatory markers in HFD-fed rats (p < 0.05). Additionally, HFD-fed rats treated with luteolin showed reduced malondialdehyde and raised catalase activity in plasma (p < 0.05). Luteolin attenuated hepatic steatosis compared to the untreated rats (p < 0.05). Luteolin also increased plasma adiponectin levels accompanied by upregulation of adiponectin receptor 1 (AdipoR1), AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor γ (PPAR-γ) protein expression in liver (p < 0.05). These findings revealed that luteolin ameliorated HFD-induced MAFLD in rats, possibly by reducing metabolic alterations and oxidative stress and restoring AdipoR1, AMPK, and PPARγ protein expression in HFD-fed rats. Full article
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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