NBB 402W Lecture Notes - Lecture 2: Proopiomelanocortin, University Of California, San Francisco, Palatability
UCSF Researchers Redefine Role of Brain's 'Hunger Circuit'
• Hunger circuit : 2 groups of cells
◦ AgRP and POMC neurons -- senses long-term changes in body's
hormone and nutrient levels
Responds immediately to presence of food
◦ AgRP -- activation directly drives eating; motivate animals to seek and
obtain food
◦ Work in opposition; when one is active the other is not
• Hypothalamus --> arcuate nucleus --> AgRP and POMC neurons in that
nucleus
• Hunger circuit thoery:
◦ Hunger --> gradual changes in hormone levels --> trigger AgRP neurons
--> drives us to eat
◦ Satiated --> circulating nutrients (glucose) --> POMC neurons -->
suppress desire to eat
• What happened in the neurons actually
◦ Seconds after food given, AgRP activity decreased and POMC activity
rose
◦ Expected it to take more time and slowly change activity
◦ Circuit could be quickly 'reset' -- POMC activity dampened and AgRP
neurons firing again if food taken away
◦ Magnitude of transition correlated with palatability of food offered
Stronger reversal with preferred foods
◦ Depended on accessibility of food
Slower transition if food could be smelled but not seen
• AgRP rapidly inactivated by sight and smell; slow changes from hormones
and nutrients
◦ 'anticipatory aspects'
• This circuit may be manipulating decision to go get food but not necessarily
the eating of food --- does not really help in reducing obesity
Introduction
• Summary/Goals
◦ Introduce metabolic syndromes due to high-fat/high-carb diets
◦ Homeostatic circuitry on feeding; discusses limbic brain regions and reward
driven feeding behavior
Document Summary
Ucsf researchers redefine role of brain"s "hunger circuit: hunger circuit : 2 groups of cells. Agrp and pomc neurons -- senses long-term changes in body"s hormone and nutrient levels. Agrp -- activation directly drives eating; motivate animals to seek and obtain food: hypothalamus --> arcuate nucleus --> agrp and pomc neurons in that. Work in opposition; when one is active the other is not nucleus: hunger circuit thoery: Hunger --> gradual changes in hormone levels --> trigger agrp neurons. Satiated --> circulating nutrients (glucose) --> pomc neurons --> suppress desire to eat: what happened in the neurons actually. Seconds after food given, agrp activity decreased and pomc activity rose. Expected it to take more time and slowly change activity. Circuit could be quickly "reset" -- pomc activity dampened and agrp neurons firing again if food taken away. Magnitude of transition correlated with palatability of food offered.