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Related Experiment Video

Updated: Nov 26, 2025

Glucose-Stimulated Insulin Secretion via Perfusion through the Mice Vasculature with an Intact Pancreas
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Circulating cathepsin S improves glycaemic control in mice.

Hamzeh Karimkhanloo1,2, Stacey N Keenan1, Emily W Sun3

  • 1Department of Physiology, University of Melbourne, Melbourne, Australia.

The Journal of Endocrinology
|December 8, 2020
PubMed
Summary

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Cathepsin S (CTSS) improves glucose tolerance by directly impacting liver glucose production and stimulating GLP-1 secretion. However, these benefits are lost in insulin-resistant states like obesity and type 2 diabetes.

Area of Science:

  • Biochemistry
  • Metabolic research
  • Endocrinology

Background:

  • Cathepsin S (CTSS), a cysteine protease, is implicated in metabolic dysregulation, with elevated levels observed in obesity and type 2 diabetes.
  • Previous research indicates CTSS deficiency improves glycemic control by reducing hepatic glucose production, but its circulating role in metabolism remains unclear.

Purpose of the Study:

  • To investigate the effects of recombinant CTSS on glucose and energy metabolism.
  • To elucidate the mechanisms by which CTSS influences glycemic control, including its impact on hepatocytes, myotubes, adipocytes, and incretin secretion.

Main Methods:

  • Administration of recombinant CTSS to cultured cells (hepatocytes, myotubes, adipocytes) and lean mice.
  • Assessment of glucose tolerance, plasma insulin levels, hepatic glucose output, and gene expression (G6pc, Pck1).
Keywords:
CTSSglucose metabolisminsulin sensitivitylipid metabolismliver

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  • Evaluation of CTSS effects on pancreatic beta-cell insulin secretion and intestinal GLP-1 secretion, including experiments with GLP-1 receptor antagonists and in insulin-resistant mouse models (high-fat-fed and db/db mice).

    • Main Results:

    • CTSS administration improved glucose tolerance and increased plasma insulin in lean mice.
    • CTSS reduced hepatic glucose output by suppressing G6pc and Pck1 mRNA expression in hepatocytes but had no effect on myotubes or adipocytes.
    • CTSS stimulated GLP-1 secretion from intestinal tissues and maintained glycemic benefits even with GLP-1 receptor blockade; however, these effects were abrogated in insulin-resistant mice.

    Conclusions:

    • CTSS plays a role in regulating glycemic control through direct effects on hepatocytes and GLP-1 secretion.
    • The beneficial effects of CTSS on glycemic control are lost in states of insulin resistance, highlighting a potential therapeutic limitation.