Monica Dentice, PhD - "The Thyroid Hormone signalling in Skeletal Muscle and its central role in energy homeostasis"
- When Feb 04, 2025 from 12:00 PM to 01:15 PM (Europe/Berlin / UTC100)
- Where Tigem Auditorium Angelo Maramai
- Contact Name Carmine Settembre
- Contact Phone 08119230659
-
Add event to calendar
iCal

- https://www.tigem.it/newsroom/seminars/monica-dentice-phd-the-thyroid-hormone-signalling-in-skeletal-muscle-and-its-central-role-in-energy-homeostasis
- Monica Dentice, PhD - "The Thyroid Hormone signalling in Skeletal Muscle and its central role in energy homeostasis"
- 2025-02-04T12:00:00+01:00
- 2025-02-04T13:15:00+01:00
Monica Dentice, PhD
Professore Associato
Dipartimento di Medicina Clinica e Chirurgia
Università degli Studi di Napoli “Federico II”
Short CV
Abstract
Thyroid Hormones (THs) are key modulators of energy metabolism and cross-talk with other endocrine and metabolic factors. It is well established that thyroid hormone status correlates with body weight and energy expenditure. In the Skeletal Muscle (SKM), THs are critical bioenergetic regulators by controlling lipid and protein synthesis and catabolism, key enzymes of muscular energetic pathways and myogenic genes expression. Therefore, a lack or an excess of THs unbalance the muscular energetic equilibrium leading to severe metabolic failures.
It is well known that the adipokine leptin can increase hypothalamic control of TH synthesis, as an adaptive metabolic response that regulate body weight. In this study, we found that TH signal is heightened in overweight humans and is lost with obesity. In mice, systemic and intracerebroventricular leptin injection induces the expression of type 2 deiodinase (D2), the TH activating enzyme, in skeletal muscle. Mechanistically, leptin enhances the transcription of D2 by a STAT3- and a-MSH/cAMP-dependent regulation. Notably, mice lacking D2 or with a mutation in the TH receptor do not exhibit the metabolic effects of leptin, such as increased insulin sensitivity and oxygen consumption, indicating that leptin's peripheral metabolic effects in skeletal muscle are mediated by TH. These findings emphasize the crucial role of leptin in integrating metabolic activation induced by TH, while also contributing to appetite suppression in response to perceived fat stores.
Professore Associato
Dipartimento di Medicina Clinica e Chirurgia
Università degli Studi di Napoli “Federico II”
Short CV
Abstract
Thyroid Hormones (THs) are key modulators of energy metabolism and cross-talk with other endocrine and metabolic factors. It is well established that thyroid hormone status correlates with body weight and energy expenditure. In the Skeletal Muscle (SKM), THs are critical bioenergetic regulators by controlling lipid and protein synthesis and catabolism, key enzymes of muscular energetic pathways and myogenic genes expression. Therefore, a lack or an excess of THs unbalance the muscular energetic equilibrium leading to severe metabolic failures.
It is well known that the adipokine leptin can increase hypothalamic control of TH synthesis, as an adaptive metabolic response that regulate body weight. In this study, we found that TH signal is heightened in overweight humans and is lost with obesity. In mice, systemic and intracerebroventricular leptin injection induces the expression of type 2 deiodinase (D2), the TH activating enzyme, in skeletal muscle. Mechanistically, leptin enhances the transcription of D2 by a STAT3- and a-MSH/cAMP-dependent regulation. Notably, mice lacking D2 or with a mutation in the TH receptor do not exhibit the metabolic effects of leptin, such as increased insulin sensitivity and oxygen consumption, indicating that leptin's peripheral metabolic effects in skeletal muscle are mediated by TH. These findings emphasize the crucial role of leptin in integrating metabolic activation induced by TH, while also contributing to appetite suppression in response to perceived fat stores.