Search

Your search keyword '"Abulizi, Abudukadier"' showing total 4 results
Start Over Author "Abulizi, Abudukadier" Publisher american diabetes association
4 results on '"Abulizi, Abudukadier"'

1. 369-OR: [1,2-13C2]-L-Glutamine Mass Isotopomers Map Hepatic Mitochondrial Metabolism without Tracer Interference

Author

SIEBEL, STEPHAN, primary, CARDONE, REBECCA L., additional, ABULIZI, ABUDUKADIER, additional, RAAISA, RAAISA, additional, WILLIAMS, RICHARD M., additional, SEHGAL, RAGHAV, additional, BUTRICO, GINA MARIE, additional, CLINE, GARY, additional, ROTHMAN, DOUGLAS L., additional, MASON, GRAEME F., additional, and KIBBEY, RICHARD, additional

Published
2020
Full Text
View/download PDF

3. Tetrahydrobiopterin Has a Glucose-Lowering Effect by Suppressing Hepatic Gluconeogenesis in an Endothelial Nitric Oxide Synthase–Dependent Manner in Diabetic Mice

Author

Yuichi Sato, Yoshihito Fujita, Akiko Ohashi, Akio Obara, Shimpei Fujimoto, Masaya Hosokawa, Yasuhiko Nakamura, Masahito Ogura, Hiroyuki Hasegawa, Nobuya Inagaki, Abulizi Abudukadier, and Toru Fukushima

Subjects
Male, medicine.medical_specialty, Nitric Oxide Synthase Type III, Endocrinology, Diabetes and Metabolism, Immunoblotting, Biopterin, Diabetes Mellitus, Experimental, chemistry.chemical_compound, Mice, Insulin resistance, Enos, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Animals, Hypoglycemic Agents, RNA, Small Interfering, Cells, Cultured, Original Research, biology, Reverse Transcriptase Polymerase Chain Reaction, Gluconeogenesis, AMPK, Endothelial Cells, Tetrahydrobiopterin, biology.organism_classification, medicine.disease, Immunohistochemistry, Mice, Inbred C57BL, Endocrinology, Metabolism, chemistry, Liver, Hepatocytes, medicine.drug
Abstract

Endothelial nitric oxide synthase (eNOS) dysfunction induces insulin resistance and glucose intolerance. Tetrahydrobiopterin (BH4) is an essential cofactor of eNOS that regulates eNOS activity. In the diabetic state, BH4 is oxidized to 7,8-dihydrobiopterin, which leads to eNOS dysfunction owing to eNOS uncoupling. The current study investigates the effects of BH4 on glucose metabolism and insulin sensitivity in diabetic mice. Single administration of BH4 lowered fasting blood glucose levels in wild-type mice with streptozotocin (STZ)-induced diabetes and alleviated eNOS dysfunction by increasing eNOS dimerization in the liver of these mice. Liver has a critical role in glucose-lowering effects of BH4 through suppression of hepatic gluconeogenesis. BH4 activated AMP kinase (AMPK), and the suppressing effect of BH4 on gluconeogenesis was AMPK-dependent. In addition, the glucose-lowering effect and activation of AMPK by BH4 did not appear in mice with STZ-induced diabetes lacking eNOS. Consecutive administration of BH4 in ob/ob mice ameliorated glucose intolerance and insulin resistance. Taken together, BH4 suppresses hepatic gluconeogenesis in an eNOS-dependent manner, and BH4 has a glucose-lowering effect as well as an insulin-sensitizing effect in diabetic mice. BH4 has potential in the treatment of type 2 diabetes.

Published
2013

4. Tetrahydrobiopterin Has a Glucose-Lowering Effect by Suppressing Hepatic Gluconeogenesis in an Endothelial Nitric Oxide Synthase--Dependent Manner in Diabetic Mice.

Author

Abulizi Abudukadier, Yoshihito Fujita, Akio Obara, Akiko Ohashi, Toru Fukushima, Yuichi Sato, Masahito Ogura, Yasuhiko Nakamura, Shimpei Fujimoto, Masaya Hosokawa, Hiroyuki Hasegawa, and Nobuya Inagaki

Subjects
*TETRAHYDROBIOPTERIN, *GLUCONEOGENESIS, *NITRIC-oxide synthases, *DIABETES, *INSULIN resistance, *GLUCOSE intolerance, *GLUCOSE metabolism
Abstract

Endothelial nitric oxide synthase (eNOS) dysfunction induces insulin resistance and glucose intolerance. Tetrahydrobiopterin (BH4) is an essential cofactor of eNOS that regulates eNOS activity. In the diabetic state, BH4 is oxidized to 7,8-dihydrobiopterin, which leads to eNOS dysfunction owing to eNOS uncoupling. The current study investigates the effects of BH4 on glucose metabolism and insulin sensitivity in diabetic mice. Single administration of BH4 lowered fasting blood glucose levels in wild-type mice with streptozotocin (STZ)-induced diabetes and alleviated eNOS dysfunction by increasing eNOS dimerization in the liver of these mice. Liver has a critical role in glucose-lowering effects of BH4 through suppression of hepatic gluconeogenesis. BH4 activated AMP kinase (AMPK), and the suppressing effect of BH4 on gluconeogenesis was AMPK-dependent. In addition, the glucose-lowering effect and activation of AMPK by BH4 did not appear in mice with STZ-induced diabetes lacking eNOS. Consecutive administration of BH4 in ob/ob mice ameliorated glucose intolerance and insulin resistance. Taken together, BH4 suppresses hepatic gluconeo-genesis in an eNOS-dependent manner, and BH4 has a glucose-lowering effect as well as an insulin-sensitizing effect in diabetic mice. BH4 has potential in the treatment of type 2 diabetes. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results