Exosome-derived miR-548ag drives hepatic lipid accumulation via upregulating FASN through inhibition of DNMT3B.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease worldwide. This study investigates the role of serum miR-548ag in regulating lipid metabolism and its contribution to MASLD in obesity. We found that miR-548ag levels were significantly elevated in the serum of both obese and MASLD patients and positively correlated with body mass index, fasting plasma glucose, triglycerides, total cholesterol, LDL, HDL, aspartate aminotransferase, and alanine aminotransferase levels.

TransmiR v3.0: an updated transcription factor-microRNA regulation database.

microRNAs (miRNAs) are active in various biological processes by mediating gene expression, and the full investigation of miRNA transcription is crucial for understanding the mechanisms underlying miRNA deregulation in pathological conditions. Here an updated TransmiR v3.0 database is presented with more comprehensive miRNA transcription regulation information, which contains 5095 transcription factor (TF) -miRNA regulations curated from 2285 papers and >6 million TF-miRNA regulations derived from ChIP-seq data.

miR-548ag promotes DPP4 expression in hepatocytes through activation of TLR(7/8)/NF-κB pathway.

Objective: In our previous study, we identified a notable increase in miR-548ag content after obesity, which contributes to the progression of Type 2 diabetes Mellitus(T2DM) through the up-regulation of Dipeptidyl Peptidase-4(DPP4) expression within the liver. However, the precise molecular mechanisms underlying the upregulation of DPP4 by miR-548ag remain elusive. Mature miRNAs rich in GU sequences can activate the TLR(7/8)/NF-κB signalling pathway, which transcriptionally activates DPP4 expression.

Association of saturated fatty acids with cancer risk: a systematic review and meta-analysis.

Objective: Extensive research has explored the link between saturated fatty acids (SFAs) and cardiovascular diseases, alongside other biological dysfunctions. Yet, their association with cancer risk remains a topic of debate among scholars. The present study aimed to elucidate this association through a robust meta-analysis.

KLF7 promotes adipocyte inflammation and glucose metabolism disorder by activating the PKCζ/NF-κB pathway.

In the obesity context, inflammatory cytokines secreted by adipocytes lead to insulin resistance and are key to metabolic syndrome development. In our previous study, we found that the transcription factor KLF7 promoted the expression of p-p65 and IL-6 in adipocytes. However, the specific molecular mechanism remained unclear.

Stress-inducible IL-6 is regulated by KLF7 in brown adipocytes.

Stress-inducible interleukin 6 (IL-6) is generated in brown adipocytes via beta-3 adrenergic receptor (ADRB3) signaling, which is necessary in stress hyperglycemia, the kind of metabolic adaptation enabling "fight or flight" response by means of liver gluconeogenesis. Nevertheless, the mechanism of ADRB3 signaling mediates IL-6 in brown adipocytes remains unclear. As a result, it is critical to understand how brown adipocytes produce IL-6 via ADRB3 signaling.

Hepatic Glucose Metabolism Disorder Induced by Adipose Tissue-Derived miR-548ag via DPP4 Upregulation.

The present study aimed to explore the molecular mechanism underlying the regulation of glucose metabolism by miR-548ag. For the first time, we found that miR-548ag expression was elevated in the abdominal adipose tissue and serum of subjects with obesity and type 2 diabetes mellitus (T2DM). The conditional knockout of adipose tissue notably reduced the expression and content of miR-548ag in mouse adipose tissue, serum, and liver tissue.