ArticleThe Biochemical journal1998
Thyroid hormone regulation of the Na+/glucose cotransporter SGLT1 in Caco-2 cells.
Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 47 citations in OpenAlex.
- Thyroid Hormones Regulate Postprandial Glucose Metabolism by Regulating SGLT1 Expression in the Small Intestine in Rats and Mice.International journal of molecular sciences · 2025Article
- Design of Nanohydrogels for Targeted Intracellular Drug Transport to the Trans-Golgi Network.Advanced healthcare materials · 2023Article
- Relationship between subclinical hypothyroidism and distal-symmetric diabetic polyneuropathy in type 2 diabetes mellitus referred to Kosar Hospital in Semnan and related indicators in 2019-2020.Journal of family medicine and primary care · 2022Article
- Glucose transport in lymphocytes.Pflugers Archiv : European journal of physiology · 2020Review
- Diabetes mellitus and thyroid diseases.Diabetology international · 2018Article
- Tumor suppressor gene adenomatous polyposis coli downregulates intestinal transport.Pflugers Archiv : European journal of physiology · 2011Article
- Article
- The molecular basis of lactose intolerance.Science progress · 2009Review
- The molecular basis of lactose intolerance.Science progress · 2005Review
- Decreased activity and expression of intestinal oligopeptide transporter PEPT1 in rats with hyperthyroidism in vivo.Pharmaceutical research · 2004Article
- Small bowel review: normal physiology part 1.Digestive diseases and sciences · 2001Review
- SGLT gene expression in primary lung cancers and their metastatic lesions.Japanese journal of cancer research : Gann · 2001Article
- Glucose and thyroid hormone co-regulate the expression of the intestinal fructose transporter GLUT5.The Biochemical journal · 1999Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The expression of the Na+/glucose cotransporter (SGLT1) in response to thyroid hormone [3,5,3'-tri-iodo-l-thyronine (T3)] was investigated in the enterocytic model cell line Caco-2/TC7. In differentiated cells, T3 treatment induces an average 10-fold increase in glucose consumption as well as a T3 dose-dependent increase in SGLT1 mRNA abundance. Only cells grown on glucose-containing media, but not on the non-metabolizable glucose analogue alpha-methylglucose (AMG), could respond to T3-treatment. The Vmax parameter of AMG transport was enhanced 6-fold by T3 treatment, whereas the protein abundance of SGLT1 was unchanged. The role of Na+ recycling in the T3-related activation of SGLT1 activity was suggested by both the large increase in Na+/K+ATPase protein abundance and the inhibition, down to control levels, of AMG uptake in ouabain-treated cells. Further investigations aimed at identifying the presence of a second cotransporter that could be expressed erroneously in the colon cancer cell line were unsuccessful: T3-treatment did not modify the sugar-specificity profile of AMG transport and did not induce the expression of SGLT2 as assessed by reverse transcription-PCR. Our results show that T3 can stimulate the SGLT1 cotransport activity in Caco-2 cells. Both transcriptional and translational levels of regulation are involved. Finally, glucose metabolism is required for SGLT1 expression, a result that contrasts with the in vivo situation and may be related to the fetal phenotype of the cells.
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