ArticleLaboratory investigation; a journal of technical methods and pathology2016
Regulation of intestinal SGLT1 by catestatin in hyperleptinemic type 2 diabetic mice.
Article in Laboratory investigation; a journal of technical methods and pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Meta-analysis of sotagliflozin, a dual sodium-glucose-cotransporter 1/2 inhibitor, for heart failure in type 2 diabetes.ESC heart failure · 2025Pooled it
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- Inhibition of protein kinase C-α and activation of ezrin byAmerican journal of physiology. Endocrinology and metabolism · 2023Article
- A Lipidomics- and Transcriptomics-Based Analysis of the Intestine of Genetically Obese (Cells · 2023Article
- Role of Catestatin in the Cardiovascular System and Metabolic Disorders.Frontiers in cardiovascular medicine · 2022Review
- Article
- Potential impacts of diabetes mellitus and anti-diabetes agents on expressions of sodium-glucose transporters (SGLTs) in mice.Endocrine · 2021Article
- Expression of SGLT1 in the Mouse Endometrial Epithelium and its Role in Early Embryonic Development and Implantation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Mechanisms of Glucose Absorption in the Small Intestine in Health and Metabolic Diseases and Their Role in Appetite Regulation.Nutrients · 2021Review
- Glucose transporters in the small intestine in health and disease.Pflugers Archiv : European journal of physiology · 2020Review
- An inducible intestinal epithelial cell-specific NHE3 knockout mouse model mimicking congenital sodium diarrhea.Clinical science (London, England : 1979) · 2020Article
- Article
- Adenylyl Cyclase 6 Expression Is Essential for Cholera Toxin-Induced Diarrhea.The Journal of infectious diseases · 2019Article
- What does sodium-glucose co-transporter 1 inhibition add: Prospects for dual inhibition.Diabetes, obesity & metabolism · 2019 · on this mapReview
- Sotagliflozin, the first dual SGLT inhibitor: current outlook and perspectives.Cardiovascular diabetology · 2019Review
- Development of SGLT1 and SGLT2 inhibitors.Diabetologia · 2018Review
- Renal tubule insulin receptor modestly promotes elevated blood pressure and markedly stimulates glucose reabsorption.JCI insight · 2018Article
- Therapeutic Potential of Ginsenosides as an Adjuvant Treatment for Diabetes.Frontiers in pharmacology · 2018Review
- Chronic Hyperinsulinaemic Hypoglycaemia in Rats Is Accompanied by Increased Body Weight, Hyperleptinaemia, and Decreased Neuronal Glucose Transporter Levels in the Brain.International journal of endocrinology · 2017Article
- Sodium-glucose cotransport.Current opinion in nephrology and hypertension · 2015Review
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
The small intestine is the major site for nutrient absorption that is critical in maintenance of euglycemia. Leptin, a key hormone involved in energy homeostasis, directly affects nutrient transport across the intestinal epithelium. Catestatin (CST), a 21-amino acid peptide derived from proprotein chromogranin A, has been shown to modulate leptin signaling. Therefore, we reasoned that leptin and CST could modulate intestinal Na(+)-glucose transporter 1 (SGLT1) expression in the context of obesity and diabetes. We found that hyperleptinemic db/db mice exhibit increased mucosal mass, associated with an enhanced proliferative response and decreased apoptosis in intestinal crypts, a finding absent in leptin-deficient ob/ob mice. Intestinal SGLT1 abundance was significantly decreased in hyperleptinemic but not leptin-deficient mice, indicating leptin regulation of SGLT1 expression. Phlorizin, a SGLT1/2 inhibitor, was without effect in an oral glucose tolerance test in db/db mice. The alterations in architecture and SGLT1 abundance were not accompanied by changes in the localization of intestinal alkaline phosphatase, indicating intact differentiation. Treatment of db/db mice with CST restored intestinal SGLT1 abundance and intestinal turnover, suggesting a cross-talk between leptin and CST, without affecting plasma leptin levels. Consistent with this hypothesis, we identified structural homology between CST and the AB-loop of leptin and protein-protein docking revealed binding of CST and leptin with the Ig-like binding site-III of the leptin receptor. In summary, downregulation of SGLT1 in an obese type 2 diabetic mouse model with hyperleptinemia is presumably mediated via the short form of the leptin receptor and reduces overt hyperglycemia.
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