Troxerutin attenuates insulin resistance via pancreatic IL-22/JAK1/STAT3 signaling activation in dihydrotestosterone-induced polycystic ovary syndrome rats

Am J Physiol Endocrinol Metab. 2022 Nov 1;323(5):E405-E417. doi: 10.1152/ajpendo.00150.2022. Epub 2022 Sep 14.

Abstract

Polycystic ovary syndrome (PCOS) is an extremely common endocrine-metabolic disorder and the main cause of infertility in premenopausal women, thus targeted treatments are sorely needed. Accumulative evidence showed that exogenous supplementation of IL-22 in PCOS mice may be of significant positive effect on insulin resistance (IR), a root causative factor for this condition, but much remained unknown about its mechanism. According to our previous study, troxerutin, a common anticoagulant and thrombolytic agent in clinic, alleviated various PCOS-like phenotypes in dihydrotestosterone (DHT)-treated rat model with unclear mechanism. Here, glucose tolerance tests (GTTs), insulin tolerance tests (ITTs), and homeostatic model assessment of insulin resistance (HOMA-IR) analyses revealed that troxerutin treatment in DHT-treated rats also significantly improved insulin resistance and enhanced serum IL-22 levels, which thereby activated IL-22R1/Janus kinase 1 (JAK1)/signal transducer and activator of transcription-3 (STAT3) signaling pathway in pancreatic islet. This protective effect of troxerutin on insulin resistance improvement was blocked by an inhibitor of p-STAT3, S3I-201. Troxerutin administration to DHT rats decreased the relative abundance of Bifidobacterium and enhanced secondary bile acid profiles, which were positively correlated with serum IL-22 concentration. Conclusively, the present study reported that troxerutin is an endogenous enhancer of IL-22 and the effect of troxerutin on insulin resistance improvement was via IL-22R1/JAK1/STAT3 signaling activation in a DHT-induced PCOS rat model. These insights may be translated into a primary therapeutic agent for PCOS with insulin resistance and hyperandrogenism.NEW & NOTEWORTHY Troxerutin decreased the relative abundance of Bifidobacterium, along with enhancement of secondary bile acids/IL-22 system, which thereby activated its downstream IL-22R1/JAK1/STAT3 signaling pathway in pancreatic β cells, subsequently attenuated insulin resistance (IR), hyperandrogenism and PCOS-like phenotypes in DHT-induced PCOS rat models. Troxerutin is an endogenous IL-22 enhancer and may be of therapeutic value for PCOS with insulin resistance.

Keywords: STAT3; insulin resistance; interleukin-22; polycystic ovary syndrome; troxerutin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticoagulants
  • Bile Acids and Salts / pharmacology
  • Dihydrotestosterone / pharmacology
  • Female
  • Fibrinolytic Agents
  • Humans
  • Hyperandrogenism*
  • Insulin / metabolism
  • Insulin Resistance* / physiology
  • Interleukin-22
  • Janus Kinase 1 / metabolism
  • Janus Kinase 1 / pharmacology
  • Mice
  • Polycystic Ovary Syndrome* / chemically induced
  • Polycystic Ovary Syndrome* / drug therapy
  • Rats
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction

Substances

  • Anticoagulants
  • Bile Acids and Salts
  • Dihydrotestosterone
  • Fibrinolytic Agents
  • Insulin
  • JAK1 protein, human
  • Janus Kinase 1
  • STAT3 protein, human
  • STAT3 Transcription Factor
  • troxerutin