T-1095, an inhibitor of renal Na+-glucose cotransporters, may provide a novel approach to treating diabetes
T-1095, an inhibitor of renal Na+-glucose cotransporters, may provide a novel approach to treating diabetes. A Oku , K Ueta , K Arakawa , T Ishihara , M Nawano , Y Kuronuma , M Matsumoto , A Saito , K Tsujihara , M Anai , T Asano , Y Kanai and H Endou Discovery Research Laboratory, Tanabe Seiyaku Co...
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Published in | Diabetes (New York, N.Y.) Vol. 48; no. 9; pp. 1794 - 1800 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.09.1999
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Subjects | |
Online Access | Get full text |
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Summary: | T-1095, an inhibitor of renal Na+-glucose cotransporters, may provide a novel approach to treating diabetes.
A Oku ,
K Ueta ,
K Arakawa ,
T Ishihara ,
M Nawano ,
Y Kuronuma ,
M Matsumoto ,
A Saito ,
K Tsujihara ,
M Anai ,
T Asano ,
Y Kanai and
H Endou
Discovery Research Laboratory, Tanabe Seiyaku Company Ltd., Saitama, Toda, Japan.
Abstract
T-1095A and T-1095 are synthetic agents derived from phlorizin, a specific inhibitor of Na+-glucose cotransporters (SGLTs).
Unlike phlorizin, T-1095 is absorbed into the circulation via oral administration, is metabolized to the active form, T-1095A,
and suppresses the activity of SGLTs in the kidney. Orally administered T-1095 increases urinary glucose excretion in diabetic
animals, thereby decreasing blood glucose levels. Indeed, the postprandial hyperglycemia after a meal load was shown to be
suppressed by this compound in streptozotocin (STZ)-induced diabetic rats. With long-term T-1095 treatment, both blood glucose
and HbA1c levels were reduced in STZ-induced diabetic rats and yellow KK mice. In addition, there was amelioration of abnormal
carbohydrate metabolism, i.e., hyperinsulinemia and hypertriglyceridemia, and of the development of microalbuminuria, in yellow
KK mice. Thus, T-1095 may be a useful antidiabetic drug, providing a novel therapeutic approach for diabetes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0012-1797 1939-327X |
DOI: | 10.2337/diabetes.48.9.1794 |