ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2019
Intestinal serine protease inhibition increases FGF21 and improves metabolism in obese mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice.PloS one · 2025Article
- COVID-19: Diabetes Perspective-Pathophysiology and Management.Pathogens (Basel, Switzerland) · 2023Review
- Targeting FGF21 in cardiovascular and metabolic diseases: from mechanism to medicine.International journal of biological sciences · 2023Review
- COVID-19 and diabetes mellitus: from pathophysiology to clinical management.Nature reviews. Endocrinology · 2021Review
- Discovery and characterization of a small-molecule enteropeptidase inhibitor, SCO-792.Pharmacology research & perspectives · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypsin is the major serine protease responsible for intestinal protein digestion. An inhibitor, camostat (CS), reduced weight gain, hyperglycemia, and dyslipidemia in obese rats; however, the mechanisms for these are largely unknown. We reasoned that CS creates an apparent dietary protein restriction, which is known to increase hepatic fibroblast growth factor 21 (FGF21). Therefore, metabolic responses to CS and a gut-restricted CS metabolite, FOY-251, were measured in mice. Food intake, body weight, blood glucose, branched-chain amino acids (LC/MS), hormone levels (ELISA), liver pathology (histology), and transcriptional changes (qRT-PCR) were measured in
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