What is it about?
In this study we evaluated whether intestinal expression of the glucose carriers SGLT1 and GLUT2 is altered in dysglycemic conditions characterized by post-load hyperglycemia such as impaired glucose tolerance (IGT) or normal glucose tolerance with 1h-post load glucose levels ≥155 mg/dl (NGT 1h-high). We demonstrated for the first time that subjects with NGT 1h-high and IGT have a significant increase in duodenal SGLT1 abundance, similarly to that observed in individuals with type 2 diabetes, in comparison to normal tolerant subjects with 1-hour post-load glucose <155 mg/dl. A significant increase in duodenal GLUT-2 expression was observed in subjects with type 2 diabetes, but not in individuals with dysglycemic conditions.
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Why is it important?
The results of our study suggest that dysregulated glucose absorption in the proximal gut due to up-regulation of SGTL-1 in individuals at risk to develop type 2 diabetes, such as those with 1-hour post-load glucose ≥155 mg/dl or IGT, may play an important pathophysiological role in causing these dysglycemic conditions.
Perspectives
The observation that subjects at risk for diabetes having post-prandial hyperglycemia as well as indiivduals with type 2 diabetes have higher duodenal levels of SGLT-1 highlights the potential for therapeutic intervention in type 2 diabetes and prediabetes conditions with pharmaceutical agents able to reduce the abundance and/or the activity of SGLT-1 transporter in the intestinal mucosa in order to counteract postprandial hyperglycemia and the progression to type 2 diabetes
teresa vanessa fiorentino
Universita degli Studi Magna Graecia di Catanzaro
Read the Original
This page is a summary of: Duodenal Sodium/Glucose Cotransporter 1 Expression Under Fasting Conditions Is Associated With Postload Hyperglycemia, The Journal of Clinical Endocrinology & Metabolism, September 2017, Endocrine Society,
DOI: 10.1210/jc.2017-00348.
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