Which hormone mediates gluconeogenesis in infants after brown fat is depleted?

Cortisol is the hormone that plays a crucial role in mediating gluconeogenesis, especially in the context of infants after brown fat stores have been depleted. During periods of stress, illness, or nutritional deficiency, cortisol levels rise, stimulating the liver to convert non-carbohydrate sources, such as amino acids and glycerol, into glucose. This process is vital for maintaining blood glucose levels in infants, particularly since they have a limited glycogen reserve and rely heavily on gluconeogenesis to ensure adequate energy supply.

In the neonatal period, brown fat serves as a source of energy and is integral in thermogenesis, helping to keep the infant warm. Once these stores are used up, the body must rely more on gluconeogenesis to provide glucose, a critical energy source. Cortisol's action during this transition is essential, as it not only stimulates gluconeogenesis but also helps modulate metabolism under conditions of increased energy demand.

While insulin is primarily responsible for lowering blood glucose levels and facilitating glucose uptake, it does not promote gluconeogenesis. Adrenaline can stimulate gluconeogenesis but is typically associated with acute stress responses rather than the more sustained metabolic processes needed in the context of depleted brown fat. Prolactin mainly regulates lactation and