ArticleInternational journal of molecular sciences2021
Liver-Specific Overexpression of Prostasin Attenuates High-Fat Diet-Induced Metabolic Dysregulation in Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- High-fat diet score reveals total and cardiovascular mortality and identifies protein biomarkers in large cohorts.Journal of advanced research · 2026Article
- Article
- Bile acid regulation of xenobiotic nuclear receptors on the expressions of orosomucoids in the liver.American journal of physiology. Endocrinology and metabolism · 2025Article
- RNA-seq analysis reveals transcriptome changes in livers fromBiochemistry and biophysics reports · 2025Article
- Autologous Paracrine Prostasin-Matriptase Serine Protease Interaction in Lymphoid Cancer Cells.Cells · 2025Article
- GPI-anchored serine proteases: essential roles in development, homeostasis, and disease.Biological chemistry · 2025Review
- Thyroid-Stimulating Hormone Regulates the Glucose Metabolism in Hepatocytes via Toll-Like Receptor 4/Tollip Pathway.International journal of endocrinology · 2025Article
- Transcriptome Analysis Revealed Potential Genes of Skeletal Muscle Thermogenesis in Mashen Pigs and Large White Pigs under Cold Stress.International journal of molecular sciences · 2023Article
- Plasma prostasin: a novel risk marker for incidence of diabetes and cancer mortality.Diabetologia · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The liver has a most indispensable role in glucose and lipid metabolism where we see some of the most serious worldwide health problems. The serine protease prostasin (PRSS8) cleaves toll-like receptor 4 (TLR4) and regulates hepatic insulin sensitivity under PRSS8 knockout condition. However, liver substrate proteins of PRSS8 other than TLR4 and the effect to glucose and lipid metabolism remain unclarified with hepatic elevation of PRSS8 expression. Here we show that high-fat-diet-fed liver-specific PRSS8 transgenic mice improved glucose tolerance and hepatic steatosis independent of body weight. PRSS8 amplified extracellular signal-regulated kinase phosphorylation associated with matrix metalloproteinase 14 activation in vivo and in vitro. Moreover, in humans, serum PRSS8 levels reduced more in type 2 diabetes mellitus (T2DM) patients than healthy controls and were lower in T2DM patients with increased maximum carotid artery intima media thickness (>1.1 mm). These results identify the regulatory mechanisms of PRSS8 overexpression over glucose and lipid metabolism, as well as excessive hepatic fat storage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.