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Your search keyword '"Mighiu, A."' showing total 6 results
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6 results on '"Mighiu, A."'

1. Health state utilities for beta-thalassemia: a time trade-off study

Author

Martin, Antony P., primary, Ferri Grazzi, Enrico, additional, Mighiu, Claudia, additional, Chevli, Manoj, additional, Shah, Farrukh, additional, Maher, Louise, additional, Shaikh, Anum, additional, Sagar, Aliah, additional, Hubberstey, Hayley, additional, Franks, Bethany, additional, Ramos-Goñi, Juan M., additional, Oppe, Mark, additional, and Tang, Derek, additional

Published
2022
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2. Impact of progressive familial intrahepatic cholestasis on caregivers: caregiver-reported outcomes from the multinational PICTURE study

Author

Mighiu, Claudia, primary, O’Hara, Sonia, additional, Ferri Grazzi, Enrico, additional, Murray, Karen F., additional, Schattenberg, Jörn M., additional, Ventura, Emily, additional, Karakaidos, Melanie, additional, Taylor, Alison, additional, Brrang, Harpreet, additional, Dhawan, Anil, additional, Willemse, Jose, additional, and Finnegan, Alan, additional

Published
2022
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3. Hypothalamic glucagon signaling inhibits hepatic glucose production

Author

Maureen J. Charron, Madhu Chari, Nikita R Christian, Jessica T.Y. Yue, Beatrice M. Filippi, Clair S. Yang, Carol K.L. Lam, Tony K.T. Lam, Patricia I. Mighiu, and Mona A. Abraham

Subjects
Male, endocrine system, medicine.medical_specialty, medicine.medical_treatment, Hypothalamus, Diet, High-Fat, Glucagon, Glucagon-Like Peptide-1 Receptor, Article, General Biochemistry, Genetics and Molecular Biology, Rats, Sprague-Dawley, Mice, Internal medicine, Diabetes mellitus, Receptors, Glucagon, medicine, Animals, Receptor, Chemistry, Kinase, Insulin, digestive, oral, and skin physiology, Gluconeogenesis, General Medicine, medicine.disease, Cyclic AMP-Dependent Protein Kinases, Rats, Glucose, Endocrinology, Liver, Knockout mouse, Glucagon receptor, hormones, hormone substitutes, and hormone antagonists, Signal Transduction
Abstract

Glucagon activates hepatic protein kinase A (PKA) to increase glucose production, but the gluco-stimulatory effect is transient even in the presence of continuous intravenous glucagon infusion. Continuous intravenous infusion of insulin, however, inhibits glucose production through its sustained actions in both the liver and the mediobasal hypothalamus (MBH). In a pancreatic clamp setting, MBH infusion with glucagon activated MBH PKA and inhibited hepatic glucose production (HGP) in rats, as did central glucagon infusion in mice. Inhibition of glucagon receptor-PKA signaling in the MBH and hepatic vagotomy each negated the effect of MBH glucagon in rats, whereas the central effect of glucagon was diminished in glucagon receptor knockout mice. A sustained rise in plasma glucagon concentrations transiently increased HGP, and this transiency was abolished in rats with negated MBH glucagon action. In a nonclamp setting, MBH glucagon infusion improved glucose tolerance, and inhibition of glucagon receptor-PKA signaling in the MBH enhanced the ability of intravenous glucagon injection to increase plasma glucose concentrations. We also detected a similar enhancement of glucose concentrations that was associated with a disruption in MBH glucagon signaling in rats fed a high-fat diet. We show that hypothalamic glucagon signaling inhibits HGP and suggest that hypothalamic glucagon resistance contributes to hyperglycemia in diabetes and obesity.

Published
2013
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