1. Academic Validation
  2. Dihydromyricetin Ameliorates Inflammation-Induced Insulin Resistance via Phospholipase C-CaMKK-AMPK Signal Pathway

Dihydromyricetin Ameliorates Inflammation-Induced Insulin Resistance via Phospholipase C-CaMKK-AMPK Signal Pathway

  • Oxid Med Cell Longev. 2021 Oct 5;2021:8542809. doi: 10.1155/2021/8542809.
Lianjie Hou 1 2 Fangyi Jiang 1 Bo Huang 1 Weijie Zheng 1 Yufei Jiang 1 Gengyuan Cai 1 Dewu Liu 1 Ching Yuan Hu 3 Chong Wang 1
Affiliations

Affiliations

  • 1 Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, China.
  • 2 The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan City People's Hospital, Qingyuan, 511518 Guangdong, China.
  • 3 Department of Human Nutrition, Food and Animal Sciences, College of Tropical Agriculture and Human Resources, University of Hawaii at Manoa, USA.
Abstract

Patients with metabolic syndrome have a higher risk of type II diabetes and Cardiovascular Disease. The metabolic syndrome has become an urgent public health problem. Insulin resistance is the common pathophysiological basis of metabolic syndrome. The higher incidence of Insulin resistance in obese groups is due to increased levels of inflammatory factors during obesity. Therefore, developing a therapeutic strategy for Insulin resistance has great significance for the treatment of the metabolic syndrome. Dihydromyricetin, as a bioactive polyphenol, has been used for anti-inflammatory, antitumor, and improving Insulin sensitivity. However, the target of DHM and molecular mechanism of DHM for preventing inflammation-induced Insulin resistance is still unclear. In this study, we first confirmed the role of dihydromyricetin in inflammation-induced Insulin resistance in vivo and in vitro. Then, we demonstrated that dihydromyricetin resisted inflammation-induced Insulin resistance by activating Ca2+-CaMKK-AMPK using signal pathway blockers, Ca2+ probes, and immunofluorescence. Finally, we clarified that dihydromyricetin activated Ca2+-CaMKK-AMPK signaling pathway by interacting with the Phospholipase C (PLC), its target protein, using drug affinity responsive target stability (DARTS) assay. Our results not only demonstrated that dihydromyricetin resisted inflammation-induced Insulin resistance via the PLC-CaMKK-AMPK signal pathway but also discovered that the target protein of dihydromyricetin is the PLC. Our results provided experimental data for the development of dihydromyricetin as a functional food and new therapeutic strategies for treating or preventing PLC.

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