Sci Adv | 邓成团队揭示蜥蜴GCGR受体的非经典产热机制
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TL;DR - A Science Advances study identifies constitutively active glucagon receptors (GCGRs) in lizard liver as a molecular driver of cold-induced thermogenesis. The finding revises the view that ectotherms rely almost entirely on external heat and reveals a mechanism for adaptation to cold environments.
- Cold exposure increased hepatic GCGR expression in thermoregulating lizard species, correlating positively with their ability to maintain body temperatures above ambient levels.
- Lizard GCGR activates Gs–cAMP signaling without glucagon, promoting glycogen and lipid breakdown, lipid oxidation, and expression of thermogenic genes such as FGF21.
- GCGR knockdown or inhibition lowered lizard body temperature and metabolic gene expression, supporting the pathway’s necessity.
- Expressing bearded-dragon GCGR increased cold-exposed lizards’ and mice’s body temperature and metabolic rate, including in glucagon-deficient mice, demonstrating ligand-independent activity.
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Sci Adv | 邓成团队揭示蜥蜴GCGR受体的非经典产热机制
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TL;DR - A Science Advances study identifies constitutively active glucagon receptors (GCGRs) in lizard liver as a molecular driver of cold-induced thermogenesis. The finding revises the view that ectotherms rely almost entirely on external heat and reveals a mechanism for adaptation to cold environments.
- Cold exposure increased hepatic GCGR expression in thermoregulating lizard species, correlating positively with their ability to maintain body temperatures above ambient levels.
- Lizard GCGR activates Gs–cAMP signaling without glucagon, promoting glycogen and lipid breakdown, lipid oxidation, and expression of thermogenic genes such as FGF21.
- GCGR knockdown or inhibition lowered lizard body temperature and metabolic gene expression, supporting the pathway’s necessity.
- Expressing bearded-dragon GCGR increased cold-exposed lizards’ and mice’s body temperature and metabolic rate, including in glucagon-deficient mice, demonstrating ligand-independent activity.