MicroRNAs (miRNAs) are short non-coding RNA that post-transcriptionally regulates gene expression. Some miRNAs have been proposed to be associated with obesity. However, miRNAs, which are related to the development of obesity in vivo remains unknown. Here in, we found the up-regulation of miR-335 in obesity using microarray analysis for miRNA. The expressions of miR-335 in liver and white adipose tissue (WAT) were up-regulated in obese mice including ob/ob, db/db, and KKAy mice. Increased miR-335 expressions were associated with an elevated body, liver and WAT weight, and hepatic triglyceride and cholesterol. Furthermore, miR-335 levels were closely correlated with expression levels of adipocyte differentiation markers such as PPARgamma, aP2, and FAS in 3T3-L1 adipocyte. These findings provide the first evidence that the up-regulated expressions of miR-335 in liver and WAT of obese mice might contribute to the pathophysiology of obesity.
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http://dx.doi.org/10.1016/j.bbrc.2009.05.058 | DOI Listing |
IBRO Neurosci Rep
June 2025
Université de la Réunion, INSERM, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Saint-Pierre 97410, France.
It is well recognized that type II Diabetes (T2D) and overweight/obesity are established risk factors for stroke, worsening also their consequences. However, the underlying mechanisms by which these disorders aggravate outcomes are not yet clear limiting the therapeutic opportunities. To fill this gap, we characterized, for the first time, the effects of T2D and obesity on the brain repair mechanisms occurring 7 days after stroke, notably glial scarring.
View Article and Find Full Text PDFJ Gastrointest Oncol
December 2024
Medical Physics Unit, Department of Oncology, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Background: Orthotopic models offer a more accurate representation of colorectal cancer (CRC) compared to subcutaneous models. Despite promising results from the reported intra-rectal models, establishing a standardized method for CRC research remains challenging due to model variability, hindering comprehensive studies on CRC pathogenesis and treatment modalities, such as brachytherapy. This study aimed to establish a standardized workflow for an orthotopic intra-rectal animal model to induce the growth of colorectal adenocarcinoma in male and female mice.
View Article and Find Full Text PDFMol Metab
January 2025
Institut Numecan, INRAE, INSERM, Univ Rennes, Rennes, France. Electronic address:
Background: Obesity and overweight are associated with low-grade inflammation induced by adipose tissue expansion and perpetuated by altered intestinal homeostasis, including increased epithelial permeability. Intestinal epithelium functions are supported by intestinal epithelial cells (IEC) mitochondria function.
Methods And Results: Here, we report that diet-induced obesity (DIO) in mice induces lipid metabolism adaptations favoring lipid storage in IEC together with reduced number, altered dynamics and diminished oxidative phosphorylation activity of IEC mitochondria.
Biomed Pharmacother
January 2025
Jagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology, Department of General Biochemistry, Gronostajowa 7, Kraków 30-387, Poland. Electronic address:
Sterile inflammation contributes to the development of many liver diseases including non-alcoholic fatty liver disease. Tumor necrosis factor alpha (TNFα) is a key cytokine driving liver inflammation primarily through pro-inflammatory activation of liver sinusoidal endothelial cells (LSEC). The knowledge of whether modulating LSEC activation can alleviate liver inflammation is scarce.
View Article and Find Full Text PDFJCI Insight
January 2025
Division of Nephrology, The University of Alabama at Birmingham, Birmingham, United States of America.
Disrupted feeding and fasting cycles as well as chronic high fat diet (HFD)-induced obesity are associated with cardiovascular disease risk factors. We designed studies that determined whether two weeks of time-restricted feeding (TRF) intervention in mice fed a chronic HFD would reduce cardiovascular disease risk factors. Mice were fed a normal diet (ND; 10% fat) ad libitum or HFD (45% fat) for 18 weeks ad libitum to establish diet-induced obesity.
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