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Burdock miR8175 improves insulin sensitivity in DIO mice by targeting PTP1B and PTPRF [II]

ABSTRACT: The incidence of type 2 diabetes (T2DM) induced by obesity is rapidly increasing. Although there are many drugs developed for type 2 diabetes, but the anti-diabetic effect of homology of medicine and food is also very popular with the majority of people. Burdock is one such food, but the molecular mechanism of anti-diabetic effect is unclear, limiting its further promotion. In recent years, studies have shown that plant mirnas can regulate host gene expression through dietary absorption, so plant miRNAs have become one of the main active ingredients in traditional Chinese medicine. Here, we report that miR8175, a plant miRNA from burdock root, has effective antidiabetic activity. miR8175 is highly enriched in burdock decoction. After administration of burdock decoction or synthetic miR8175 by gavage, significantly elevated levels of miR8175 in mouse serum and liver can be observed. Furthermore, both burdock decoction and miR8175 can significantly improve the impaired glucose metabolism of diabetic mice induced by a high-fat diet (HFD). Our results demonstrate that burdock decoction and miR8175 enhance the insulin sensitivity of the hepatic insulin signaling pathway by targeting PTPRF and PTP1B, which may be the reason for the improvement in metabolism.

ORGANISM(S): Arctium lappa

PROVIDER: GSE248826 | GEO | 2024/05/01

REPOSITORIES: GEO

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Burdock miR8175 improves insulin sensitivity in DIO mice by targeting PTP1B and PTPRF [I]

Project description:The incidence of type 2 diabetes (T2DM) induced by obesity is rapidly increasing. Although there are many drugs developed for type 2 diabetes, but the anti-diabetic effect of homology of medicine and food is also very popular with the majority of people. Burdock is one such food, but the molecular mechanism of anti-diabetic effect is unclear, limiting its further promotion. In recent years, studies have shown that plant mirnas can regulate host gene expression through dietary absorption, so plant miRNAs have become one of the main active ingredients in traditional Chinese medicine. Here, we report that miR8175, a plant miRNA from burdock root, has effective antidiabetic activity. miR8175 is highly enriched in burdock decoction. After administration of burdock decoction or synthetic miR8175 by gavage, significantly elevated levels of miR8175 in mouse serum and liver can be observed. Furthermore, both burdock decoction and miR8175 can significantly improve the impaired glucose metabolism of diabetic mice induced by a high-fat diet (HFD). Our results demonstrate that burdock decoction and miR8175 enhance the insulin sensitivity of the hepatic insulin signaling pathway by targeting PTPRF and PTP1B, which may be the reason for the improvement in metabolism.

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Project description:Acute Lung Injury (ALI) can cause Acute Respiratory Distress Syndrome (ARDS), a lethal condition with limited treatment options and currently a common global cause of death due to COVID-19-induced ALI. ARDS secondary to Transfusion-Related Acute Lung Injury (TRALI) has been recapitulated pre-clinically by anti-MHC-I antibody administration to LPS-primed mice. In this model, we demonstrated that inhibitors of PTP1B, a protein tyrosine phosphatase that regulates signaling pathways of fundamental importance to homeostasis and inflammation, prevented lung injury and increased survival. Treatment with PTP1B inhibitors attenuated the aberrant neutrophil function that drives ALI, and was associated with release of myeloperoxidase, suppression of Neutrophil Extracellular Trap (NET) formation, and inhibition of neutrophil migration. Mechanistically, reduced signaling through the CXCR4 chemokine receptor, particularly to the activation of mTOR, was essential for these effects, linking PTP1B in hibition to promoting an aged neutrophil phenotype. Considering dysregulated activation of neutrophils is implicated in sepsis and can cause collateral tissue damage, we demonstrated also that PTP1B inhibitors improved survival and ameliorated lung injury in the LPS-induced sepsis model. Our data highlight PTP1B inhibition for prevention of TRALI and ARDS from multiple etiologies.

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CaMKIIdelta is required for diabetic hyperglycemia but not nephropathy

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