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During the last decades, artificial sweeteners have been extensively used because both consumers and food manufacturing companies have become interested in replacing table sugar in foods. These sweeteners are non-nutritive because they do not provide any calories. People suffering from a metabolic disease (obesity and/or diabetes) consume these substances instead of table sugar so as to control their dietary intake of carbohydrates, lower blood glucose levels and also to control their body weight. However, even though evidence of a clear relationship linking artificial sweetener use to weight gain and other metabolic health effects is limited, recent animal studies provide intriguing information that supports an active metabolic role of artificial sweeteners in the small intestine. It has been shown that this stimulation occurs by an increase in apical GLUT2 correlated with reciprocal regulation of sweet taste receptor heterodimer (T1R2/3). Preliminary data obtained in our laboratory have shown that the sweet taste receptor heterodimer (T1R2/3) is expressed in proximal tubule cells and that saccharin increases brush border membrane (BBM) levels of this protein. However, it is unclear whether saccharin can stimulate renal glucose absorption. The aim of this ongoing study is to assess the effect of a saccharin infusion on renal glucose transport.

FP446A MICROPUNCTURE STUDY OF THE EFFECT OF SACCHARIN INFUSION ON RENAL GLUCOSE TRANSPORT IN RATS