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Hunger and appetite are associated with fluctuations in glucose levels through mechanisms that remain incompletely understood. Hunger elicits epigastric sensations (“hunger pain”) that coincide with rhythmic gastric contractions, which intensify during hypoglycemia. These observations led to the glucostatic hypothesis, which proposed that glucose availability and utilization regulate food intake. Subsequent studies demonstrated that dynamic changes in blood glucose levels precede meal initiation and influence feeding behavior. Together, these findings provided early evidence for a physiological link between glycemia and appetite regulation.

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IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism

Mengjie Wang, Piotr J. Czernik, Beata Lecka-Czernik, Jennifer W. Hill

IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism

Leptin receptor (LepRb)-expressing neurons integrate metabolic and reproductive signals, yet the role of insulin-like growth factor 1 receptor (IGF1R) signaling within these neurons remains unclear. Because IGF-1 and insulin can partially activate each other’s receptors, we generated mice lacking IGF1R selectively in LepRb neurons (IGF1RLepRb) as well as mice lacking both IGF1R and insulin receptor (IR) in LepRb neurons (IGF1R/IRLepRb). These models were used to assess body growth, skeletal development, reproductive function, energy balance, and metabolic homeostasis. Deletion of IGF1R alone in LepRb neurons delayed pubertal onset, impaired adult fertility, and accelerated reproductive aging, accompanied by transient postnatal growth retardation. IGF1R deficiency also altered trabecular and cortical bone structural parameters in both sexes, supporting a role for IGF1R signaling in coordinating growth, skeletal physiology, and reproductive function. Despite reduced food intake and increased energy expenditure in females after adjusting for lean mass, IGF1R deletion caused only modest metabolic alterations, with transient decreases in body weight and largely unchanged body composition and locomotor activity. In contrast, combined deletion of IGF1R and IR in LepRb neurons resulted in marked metabolic disturbances, including increased adiposity, reduced lean mass, lower energy expenditure, decreased locomotor activity, and impaired insulin sensitivity in males. These findings indicate cooperative roles of IGF1R and IR signaling within LepRb neurons in regulating body composition, energy balance, and glucose homeostasis. Together, our results demonstrate that IGF1R signaling in LepRb neurons primarily regulates reproductive development, skeletal physiology, and growth, whereas combined IGF1R and IR signaling is required for maintaining metabolic homeostasis. These findings identify LepRb neurons as an important neuroendocrine hub integrating IGF and insulin signaling to coordinate growth, reproduction, and metabolism in a sex-dependent manner.

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IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism

Mengjie Wang, Piotr J. Czernik, Beata Lecka-Czernik, Jennifer W. Hill

IGF-1 and insulin receptors in LepRb neurons jointly regulate body growth, bone mass, reproduction, and metabolism

Leptin receptor (LepRb)-expressing neurons integrate metabolic and reproductive signals, yet the role of insulin-like growth factor 1 receptor (IGF1R) signaling within these neurons remains unclear. Because IGF-1 and insulin can partially activate each other’s receptors, we generated mice lacking IGF1R selectively in LepRb neurons (IGF1RLepRb) as well as mice lacking both IGF1R and insulin receptor (IR) in LepRb neurons (IGF1R/IRLepRb). These models were used to assess body growth, skeletal development, reproductive function, energy balance, and metabolic homeostasis. Deletion of IGF1R alone in LepRb neurons delayed pubertal onset, impaired adult fertility, and accelerated reproductive aging, accompanied by transient postnatal growth retardation. IGF1R deficiency also altered trabecular and cortical bone structural parameters in both sexes, supporting a role for IGF1R signaling in coordinating growth, skeletal physiology, and reproductive function. Despite reduced food intake and increased energy expenditure in females after adjusting for lean mass, IGF1R deletion caused only modest metabolic alterations, with transient decreases in body weight and largely unchanged body composition and locomotor activity. In contrast, combined deletion of IGF1R and IR in LepRb neurons resulted in marked metabolic disturbances, including increased adiposity, reduced lean mass, lower energy expenditure, decreased locomotor activity, and impaired insulin sensitivity in males. These findings indicate cooperative roles of IGF1R and IR signaling within LepRb neurons in regulating body composition, energy balance, and glucose homeostasis. Together, our results demonstrate that IGF1R signaling in LepRb neurons primarily regulates reproductive development, skeletal physiology, and growth, whereas combined IGF1R and IR signaling is required for maintaining metabolic homeostasis. These findings identify LepRb neurons as an important neuroendocrine hub integrating IGF and insulin signaling to coordinate growth, reproduction, and metabolism in a sex-dependent manner.

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13th
Helmholtz Diabetes Conference 
Munich, 21-23. Sep 2026                                                                                                                             

2024 impact factor: 6.6

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