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Biosci Biotechnol Biochem ; 87(2): 163-170, 2023 Jan 24.
Article in English | MEDLINE | ID: mdl-36413460

ABSTRACT

Glucotoxicity, impaired insulin secretion, suppression of insulin gene expression, and apoptosis, in pancreatic ß-cells caused by chronic hyperglycemia is a key component of the pathogenesis of type 2 diabetes. Recently, it has been reported that rare sugar d-allulose has antihyperglycemic and antihyperlipidemic effects in diabetic rats. However, the direct effects of rare sugars including d-allulose on pancreatic ß-cell function are unclear. In this study, we investigated whether chronic exposure to ketohexoses causes glucotoxicity, suppression of insulin gene expression, and apoptosis, in INS-1 rat pancreatic insulinoma cells. d-Fructose, d-tagatose, l-allulose, and l-sorbose treatment for 1-week reduced insulin gene expression, whereas d-allulose, d-sorbose, l-fructose, and l-tagatose did not. All ketohexoses were transported into INS-1 cells, but were not metabolized. In addition, the ketohexoses did not induce apoptosis and did not affect glucose metabolism. These results suggest that long-term administration of d-allulose, d-sorbose, l-fructose, and l-tagatose does not affect pancreatic ß-cell function.


Subject(s)
Diabetes Mellitus, Experimental , Diabetes Mellitus, Type 2 , Insulinoma , Pancreatic Neoplasms , Rats , Animals , Sorbose , Fructose , Insulin/metabolism , Sugars , Glucose/metabolism
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