Background: Human Adenovirus D-36 (HAdV-D36) promotes adipogenesis in cellular and animal models and may contribute to the development of human obesity. Induction of PPARγ by HAdV-D36 seems to have a central role in the maintenance of adipogenic status. There is limited information about epigenetic mechanisms contributing to this process in human adipose tissue. This study evaluated the expression of lncRNAs (ADINR, GAS5 and MEG3) and miRNAs (miR-18a and miR-140) involved in the adipogenic process in visceral adipose tissue (VAT) of subjects with obesity with previous HAdV-D36 infection (seropositive) and unexposed (seronegative) subjects with obesity.
Methods: Individuals with obesity were grouped according to the presence of antibodies against HAdV-D36 (Seropositive: HAdV-D36[+], n = 29; and Seronegative: HAdV-D36[-], n = 28). Additionally, a group of individuals without obesity (n = 17) was selected as a control group. The HAdV-D36 serology was carried out by ELISA. Biopsies of VAT were obtained during an elective and clinically indicated surgery (bariatric or cholecystectomy). RNA extraction from VAT was performed and the expression of PPARG and non-coding RNAs was evaluated by qPCR.
Results: HAdV-D36[+] individuals had lower expression of anti-adipogenic lncRNAs GAS5 (p = 0.016) and MEG3 (p = 0.035) compared with HAdV-D36[-] subjects with obesity. HAdV-D36[+] subjects also presented increased expression of the adipogenic miRNA miR-18a (p = 0.042), which has been reported to be modulated by GAS5 through a RNA sponging mechanism during adipogenic differentiation. Additionally, an inverse correlation of GAS5 with PPARG expression was observed (r = -0.917, p = 0.01).
Conclusion: Our results suggest that HAdV-D36 is related to non-coding RNAs implicated in adipogenesis, representing a potential mechanism by which previous HAdV-D36 infection could be associated with the long-term maintenance of adipogenic status, probably through the GAS5/miR-18a axis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/s41366-024-01555-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Weight cycling exacerbates glucose intolerance and hepatic triglyceride storage in mice with a history of chronic high fat diet exposure.
J Transl Med
January 2025
Research Unit NeuroBiology of Diabetes, Helmholtz Munich, Ingolstädter Landstraße 1, 85764, Neuherberg, Germany.
Background: Obese subjects undergoing weight loss often fear the Yoyo dieting effect, which involves regaining or even surpassing their initial weight. To date, our understanding of such long-term obesity and weight cycling effects is still limited and often based on only short-term murine weight gain and loss studies. This study aimed to investigate the long-term impacts of weight cycling on glycemic control and metabolic health, focusing on adipose tissue, liver, and hypothalamus.
View Article and Find Full Text PDFWu-Mei-Wan enhances brown adipose tissue function and white adipose browning in obese mice via upregulation of HSF1.
Chin Med
January 2025
Department of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Background: This research aims to explore the anti-obesity potential of Wu-Mei-Wan (WMW), particularly its effects on adipose tissue regulation in obese mice induced by a high-fat diet (HFD). The study focuses on understanding the role of heat shock factor 1 (HSF1) in mediating these effects.
Methods: HFD-induced obese mice were treated with WMW.
Obesity-associated memory impairment and neuroinflammation precede widespread peripheral perturbations in aged rats.
Immun Ageing
January 2025
Institute for Behavioral Medicine Research, Ohio State University, 460 Medical Center Drive, Columbus, OH, 43210, USA.
Background: Obesity and metabolic syndrome are major public health concerns linked to cognitive decline with aging. Prior work from our lab has demonstrated that short-term high fat diet (HFD) rapidly impairs memory function via a neuroinflammatory mechanism. However, the degree to which these rapid inflammatory changes are unique to the brain is unknown.
View Article and Find Full Text PDFThe effects of the gut bacterial product, gassericin A, on obesity in mice.
Lipids Health Dis
January 2025
Department of Basic Sciences, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran.
Background: Obesity can arise from various physiological disorders. This research examined the impacts of the bacteriocin, gassericin A, which is generated by certain gut bacteria, using an in vivo model of obesity.
Methods: Fifty Swiss NIH mice were randomly assigned to five different groups.
Iron-Mediated Regulation in Adipose Tissue: A Comprehensive Review of Metabolism and Physiological Effects.
Curr Obes Rep
January 2025
Department of Endocrinology and Metabolism, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai, China.
Purpose Of Review: Review the latest data regarding the intersection of adipose tissue (AT) and iron to meet the needs of AT metabolism and the progression of related diseases.
Recent Findings: Iron is involved in fundamental biological metabolic processes and is precisely fine-tuned within the body to maintain cellular, tissue and even systemic iron homeostasis. AT not only serves as an energy storage depot but also represents the largest endocrine organ in the human body, maintaining systemic metabolic homeostasis.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!