NBB 402W Lecture Notes - Lecture 2: Proopiomelanocortin, University Of California, San Francisco, Palatability

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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
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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.

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