Cell sub-journal: A miRNA can improve insulin sensitivity in obese mice

Previous studies have confirmed that anti-inflammatory M2-like macrophages play an important role in maintaining normal metabolic stability.
M2-like macrophages are active states of macrophages, have the ability to regulate tissue remodeling and inflammation subside, and play a key role in maintaining system insulin sensitivity and glucose stability.
recently, the University of California, San Diego, Jr. The Olefsky team published an online article in the journal Cell-Metabolism entitled "MiR-690, an exosomal-derived miRNA from M2-polarized phages, improves insulin sensitivity in mice" and found that MiR-690 is a miRNA from an M2-polarized macrophage exosome source that improves insulin sensitivity in obese mice.
through extensive pre-study studies, the team believes that anti-inflammatory M2-like macrophages secrete extracellular products containing tiny KERNs that increase insulin sensitivity, known as exos.
test results show that M2 exosomes can reduce glucose and insulin tolerance after 8 weeks of high-fat diet (HFD) and reduce obesity-induced insulin resistance.
in-body experiments, M2 Exos therapy also led to an increase in AKT phosphatization in fat cells, muscle cells and liver cells, reflecting Exos' insulin sensitivity.
, the team experimentally confirmed that the insulin sensitivity of the exosome worked through miR-690, rather than other ICT species or lipids and proteins.
miR-690 is an insulin-sensitive tiny ICT, and experiments have shown that anti-inflammatory M2-like bone marrow substituts express more miR-690, while M2 Exos is more abundant in the metabolic tissue of obese mice fed HFD for 4 weeks.
Compared to the obese control group, mice with miR-690 analogs had higher levels of akT phosphatization of insulin stimulation in their livers, skeletal muscles, and adipose tissues, indicating that miR-690 promotes insulin signaling and indicates its function as insulin-sensing miRNA.
, to better understand the regulatory role of miR-690, the team determined that the over-expression of miR-690 could lead to the upward of JAK/STAT and insulin signaling path paths, while inhibiting path pathbars such as glutathione metabolism.
then identified the target gene miR-690, Nadk, using target gene prediction algorithm TargetScan Mouse 7.2.
Nadk is a gene that encodes NAD-kinase, and numerous experiments have shown that Nadk knock-out can lead to greater activation of insulin signals; Cells treated with siRNA-Nadk and miR-690 Exos did not further improve insulin effectiveness compared to cells treated with -690 Exos, and these results confirmed that the miR-690-Nadk axis plays a role in regulating the insulin signals of cells.
, the researchers found that M2-polarized bone marrow-based macrophages (BMDMs) secrete miRNA-containing exosomes that improve glucose tolerance and insulin sensitivity when given to obese mice.
miR-690 is highly expressed in M2 BMDM Exo and also functions as an insulin booster in the body and outside the body.
Nadk is the real target mRNA for miR-690, and Nadk plays a role in regulating macrophage inflammation and insulin signaling.
data suggest that miR-690 may be a new insulin-sensitive molecule for metabolic diseases.