Lecture 33: Neurocircuitry of Metabolism 5 Flashcards

1
Q

If the levels of leptin and insulin are elevated in the blood how is this going to effect AgRP and POMC and their physiological output?

A

increased leptin and insulin will inhibit AgRP and activate POMC neurons
this will promote energy expenditure, repress HGP and reduce food intake

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2
Q

What is lost in obesity?

A

the plasticity of the brain window

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3
Q

How are AgRP neurons affected when fasted? How are these neurons affected during refeeding?

A

AgRP neurons are activated when fasted as they induce feeding behaviour
AgRP neuronal firing is then diminished upon refeeding

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4
Q

When is the feeding induced suppression of AgRP neurons lost?

A

in obesity

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5
Q

What do you predict will happen if AgRP neurons are always turned on?

A

increased food intake, increased adiposity, increased blood glucose levels

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6
Q

What occurs during cellular leptin resistance?

A

neurons in the ARC become resistant to the effects of leptin in the blood

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6
Q

What happens when neurons in the ARC become resistant to the effects of leptin in the blood?

A

this attenuates alpha-MSH release and downstream activation of other hypothalamic nuclei (including the PVH)

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7
Q

What is the role of protein tyrosine phosphatases?

A

dephosphorylate tyrosine residues on proteins and, therefore, control cellular signalling along with protein tyrosine kinases

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8
Q

What is the role of PTP1B?

A

negatively regulates LepR signalling

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9
Q

What is the role of TCPTP?

A

negatively regulates IR signalling

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10
Q

What is the significance of PTP1B and TCPTP in obesity?

A

expression of PTP1B and TCPTP is significantly increased in the ARC in obesity

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11
Q

If the levels of TCPTP and PTP1B are elevated in ARC neurons what’s going to happen to physiological outputs such as WAT browning and HGP?

A

WAT browning will decrease and HGP will increase

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