Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Ursula H. Neumann"'
Autor:
Ursula H. Neumann, Jessica S.S. Ho, Sam Chen, Yuen Yi C. Tam, Pieter R. Cullis, Timothy J. Kieffer
Publikováno v:
Molecular Metabolism, Vol 6, Iss 10, Pp 1161-1172 (2017)
Objective: Hyperglucagonemia is present in many forms of diabetes and contributes to hyperglycemia, and glucagon suppression can ameliorate diabetes in mice. Leptin, a glucagon suppressor, can also reverse diabetes in rodents. Lipid nanoparticle (LNP
Externí odkaz:
https://doaj.org/article/532b74c5d2db4fb3b5861d93c654d0c4
Publikováno v:
Molecular Metabolism, Vol 6, Iss 9, Pp 1052-1065 (2017)
Background: The hormone leptin is an important regulator of metabolic homeostasis, able to inhibit food intake and increase energy expenditure. Leptin can also independently lower blood glucose levels, particularly in hyperglycemic models of leptin o
Externí odkaz:
https://doaj.org/article/3e561b5b01694290bc4720cafb90aebc
Autor:
Ursula H. Neumann, Jessica S.S. Ho, Majid Mojibian, Scott D. Covey, Maureen J. Charron, Timothy J. Kieffer
Publikováno v:
Molecular Metabolism, Vol 5, Iss 8, Pp 731-736 (2016)
Objective: It has been thought that the depletion of insulin is responsible for the catabolic consequences of diabetes; however, evidence suggests that glucagon also plays a role in diabetes pathogenesis. Glucagon suppression by glucagon receptor (Gc
Externí odkaz:
https://doaj.org/article/a6195303ae054eafa5699dc6e31e513a
Autor:
Timothy J. Kieffer, Sam Chen, Jessica S.S. Ho, Pieter R. Cullis, Yuen Yi C. Tam, Ursula H. Neumann
Publikováno v:
Molecular Metabolism, Vol 6, Iss 10, Pp 1161-1172 (2017)
Molecular Metabolism
Molecular Metabolism
Objective Hyperglucagonemia is present in many forms of diabetes and contributes to hyperglycemia, and glucagon suppression can ameliorate diabetes in mice. Leptin, a glucagon suppressor, can also reverse diabetes in rodents. Lipid nanoparticle (LNP)
Publikováno v:
Endocrinology. 157:1007-1012
Leptin can reverse hyperglycemia in rodent models of type 1 diabetes. However, these models have used chemical or immune mediated β-cell destruction where insulin depletion is incomplete. Thus it is unknown which actions of leptin are entirely insul
Publikováno v:
American journal of physiology. Endocrinology and metabolism. 315(6)
It was long thought that the only hormone capable of reversing the catabolic consequences of diabetes was insulin. However, various studies have demonstrated that the adipocyte-derived hormone leptin can robustly lower blood glucose levels in rodent
Publikováno v:
Molecular Metabolism
Molecular Metabolism, Vol 6, Iss 9, Pp 1052-1065 (2017)
Molecular Metabolism, Vol 6, Iss 9, Pp 1052-1065 (2017)
Background: The hormone leptin is an important regulator of metabolic homeostasis, able to inhibit food intake and increase energy expenditure. Leptin can also independently lower blood glucose levels, particularly in hyperglycemic models of leptin o
Autor:
Timothy J. Kieffer, Scott D. Covey, Ursula H. Neumann, Brian Rodrigues, Frank K. Huynh, Ying Wang
Publikováno v:
Hepatology. 57:543-554
Obesity is highly associated with dyslipidemia and cardiovascular disease. However, the mechanism behind this association is not completely understood. The hormone leptin may be a molecular link between obesity and dysregulation of lipid metabolism.
Autor:
Scott D. Covey, Jasna Levi, Sarah L. Gray, Heather C. Denroche, Madeleine Speck, Timothy J. Kieffer, Ursula H. Neumann, Frank K. Huynh, Peter J. Voshol, Streamson C. Chua
Publikováno v:
Diabetes
OBJECTIVE The liver plays a critical role in integrating and controlling glucose metabolism. Thus, it is important that the liver receive and react to signals from other tissues regarding the nutrient status of the body. Leptin, which is produced and
Autor:
Timothy J. Kieffer, Pieter R. Cullis, Yuen Yi C. Tam, Ursula H. Neumann, Sam Chen, Scott D. Covey, Robert K. Baker
Publikováno v:
Endocrinology. 155(3)
The ability of leptin to improve metabolic abnormalities in models of leptin deficiency, lipodystrophy, and even type 1 diabetes is of significant interest. However, the mechanism by which leptin mediates these effects remains ill-defined. Leptin was