Background: Lack of vitamin D (VD) has been associated with colorectal cancer (CRC). VD has anti-inflammatory effects and regulates several cellular pathways by means of its receptor, including epigenetic modifications. Adipose tissue dysfunction has been related to low-grade inflammation, which is related to diseases like cancer. The aim of this study was to explore the relationship between serum 25-hydroxyvitamin D (25(OH)D), adipose tissue gene expression of VD receptor (VDR), pro-inflammatory markers, and the epigenetic factor DNA methyltransferase 3a (DNMT3A) as well as VDR promoter methylation in CRC.
Methods: Blood and visceral adipose tissue from 57 CRC and 50 healthy control subjects were collected. CRC subjects had lower serum 25(OH)D levels and higher VDR gene expression, and these were negatively correlated in the CRC group.
Results: Adipose tissue , , and gene expression were higher in the CRC subjects than in the control subjects. 25(OH)D correlated negatively with and CRP. In turn, CRP correlated positively with , , , and gene expression as well as that correlated positively with and . mRNA was negatively correlated with serum 25(OH)D and positively correlated with DNA methylation. DNA methylation at position 4 had lower levels in the CRC group. Global methylation at dinucleotide 3 was lower in the CRC group.
Conclusion: Our results suggest that adipose tissue may be a key factor in CRC development. The low 25(OH)D levels and high adipose tissue expression in CRC may, at least in part, mediate this relationship by modifying adipose tissue DNA methylation and promoting inflammation.
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http://dx.doi.org/10.1186/s13148-018-0493-0 | DOI Listing |
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Department of Pharmaceutical Sciences & Technology, BIT Mesra, Ranchi, 835215, India.
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Department of Biomedical Engineering, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Although the role of low-level laser therapy (LLLT) and human adipose-derived stem cells (hADSC) in accelerating diabetic wound healing has been proven, their synergistic effect is still debated. This study aimed to evaluate the individual and combined effects of LLLT and hADSC on wound healing and on biomechanical parameters in type 2 diabetic rabbits. In this experimental study, 40 rabbits with type 2 diabetes (induced by streptozotocin (STZ)) were included.
View Article and Find Full Text PDFAging (Albany NY)
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Department of Pathology, Yale University School of Medicine, New Haven, CT 06519, USA.
Studies of the aging transcriptome focus on genes that change with age. But what can we learn from age-invariant genes-those that remain unchanged throughout the aging process? These genes also have a practical application: they can serve as reference genes in expression studies. Reference genes have mostly been identified and validated in young organisms, and no systematic investigation has been done across the lifespan.
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Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai 200233, China.
Type 2 diabetes mellitus (T2DM) is closely associated with obesity, while interactions between the two diseases remain to be fully elucidated. To this point, we offer this perspective to introduce a set of new insights into the interpretation of T2DM spanning the etiology, pathogenesis, and treatment approaches. These include a definition of T2DM as an energy surplus-induced diabetes characterized by the gradual decline of β cell insulin secretion function, which ultimately aims to prevent the onset of severe obesity through mechanisms of weight loss.
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February 2025
Hubei Key Laboratory of Cell Homeostasis, Department of Biochemistry, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, Hubei 430072, China.
Graphical Abstract Lipoprotein lipase (LPL) mediates peripheral tissue triglyceride (TG) uptake. Hepatic ANGPTL3 (A3) and ANGPTL8 (A8) form a complex and inhibit LPL activity in the white adipose tissue (WAT) via systematic circulation. ANGPTL4 (A4) is expressed in WAT and inhibits LPL activity locally.
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