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Physiology 2130 > Food Intake and Energy Homeostasis > Flashcards

Food Intake and Energy Homeostasis Flashcards

1
Q

What is BMI and what do we use it for?

A

Body Mass Index: used as a crude measure of obesity (kg/m2)

-measure to roughly determine if someone is obese or not

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2
Q

What is excluded from BMI measurement?

A

Doesn’t take into account muscle mass

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3
Q

What would be a better ratio to look at if we were to determine if someone is obese or not?

A

Ratio between Hips and git visceral fat to determine if you are at a risk of developing a condition that could kill you

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4
Q

How is obesity defined?

A

Having an abnormal or excess fat accumulation that presents a risk to an individuals health
(BMI 30+)

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5
Q

How prevalent is obesity in North America?

A

Obesity rates have increased 35% in the last 50 years

There is no sex discrimination when it comes to obesity

There has been a 80% increase in adult obesity rates

There has been a 300% increase in child obesity rates

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6
Q

What is energy balance?

A

Energy balance= energy intake-energy expenditure

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7
Q

How do we manipulate energy balance to lose or gain weight?

A

To lose we need to increase energy expenditure and decrease energy intake

To gain weight we need to increase energy intake and decrease energy expenditure

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8
Q

What are environmental/lifestyle factors that affect how much and what food we intake?

A

Taste& Smell- taking in energy when we dont need too

Availability- always aruond

Clock- daily schedule regardless if we need it

Social Habits and cues- events providing food when you have already eaten

Cost/reward optimization

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9
Q

What are individual predisposition/wirings that affect what food and how much we take in?

A

Genetic- predisposed to want to heart more. Hormones are released in excess or out of whack

Epigenetic: While in the womb, there was a change in condition that when you were born, you were more likely to eat more

Imprinted

Early Life events

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10
Q

What are the physiological events that affect how much and what to eat?

A

Internal Milieu nutrient sending (through organs)

Nutrient Partitioning

Energy Out

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11
Q

What can e do to these physiological process in our body?

A

We can over ride them in which we can then eat more than we need

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12
Q

What is the main physiological signal for food intake?

A

Negative feedback control system

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13
Q

What is an example of a negative feedback system control for food intake?

A

We are Hungry> We Eat> Increasing adipose tissue> Increasing leptin being released> Leptin is understood in the Satiety Centre (Arcuate Nucleus)> Tells body you are full> Stop eating> decrease adipose levels and leptin> Feeding centre turned on (lateral hypothalamus and Paraventricular nucleus)> Cycle repeats

  • Once the arcuate nuclei receives the signal from leptin, the feeding centre (lateral hypothalamus and paraventricular nuclei) are shut of
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14
Q

Why is the feeding centre shut off when leptin signals are circulating?

A

If you have too much leptin, the arcuate shuts off the the lateral hypothalamus and paraventricular nucleus because these 2 areas are related to hunger

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15
Q

What is the amount of adipose (fat) proportional too?

A

The amount of leptin hormone you have

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16
Q

What tissue releases the peptide leptin?

A

White adipose tissue releases leptin into circulation

17
Q

What does leptin trigger in the brain?

A

POMC Neurons
AgRP/NPY Neurons
-the amount of leptin affects each pathway differently

18
Q

Describe the POMC neural pathway?

A

Adipose releases Leptin. Triggers POMC neutrons to release alpha-MSH hormones. Which work at receptors MC4-R at the paraventricular nucleus. This can affect energy expenditure and therefore affect energy homeostasis

19
Q

Describe the AgRP/NPY neural pathway

A

Adipose releases Leptin. Triggers AgRP/NPY neutrons to release the hormone NPY-R. This hormone works on receptors in the dorsomedial hypothalamic nucleus. This can affect food intake

20
Q

What is the Lateral hypothalamus and what does it have an affect on in the neural pathways?

A

Is the feeding centre in the brain

-NPR-Y hormones have an affect in this nucleus and can influence food intake

21
Q

What happens when there is an acute increase in leptin?

A

Increase adipose
Increases Leptin
Activates POMC neurons (to shut down food intake)
MSH hormone turn on MC4-R Receptors
Energy Expenditure will increase beaqcuse we have too much
*At the same time the AgRP/NPY pathway is inhibited and affects how fast the hormones work

22
Q

If the POMC pathway is activated why is the AgRP/NPY pathway inactivated when there is an acute increase in leptin?

A

Neurons are shut down completely so they have no affect on the release of hormone and the receptor

23
Q

What happens when there is an acute decrease in leptin?

A

Decrease Adipose
Decrease in Leptin released
AgRP/NPY neurons activates
Neurons Stimulate NPY-R receptors in the Dorsalmedial hypothalamic nucleus
Food Intake increases
Shuts down communication between paraventricular nuclei to decrease energy expenditure
* at the same time the POMC pathway is inactivated which also leads to decreased energy expenditure

24
Q

How are the AgRP/NPY neurons activated?

A

They are not, they are tonically active (they are always on but can be inactivated/muted to see reduced effects)
-once the POMC pathway is removed, the AgRP/NPY neurons are able to go full force ahead

25
Q

What happens when there is a chronic increase in leptin?

A

The pathways will act the same way as if the person had decreased leptin levels in their system
-Leptin doesn’t exert the effects that leptin should at the POMC neurons

26
Q

How could someone become leptin resistant?

A

Decrease number of receptors
Decreased sensitivity of receptors
Not enough carrier proteins for leptin across BBB

27
Q

What is leptin resistance associated with?

A

Only neurons involved in feeding (POMC & AgRP), NOT in neurons in the SNS control throughout the brain

28
Q

What can leptin resistance lead to?

A

Obesity and hypertension because leptin is still present and exerting effects but something in the body is not seeing/registering that it is there. Body won’t take the appropriate actions and people will continue eating and BP will go up

29
Q

What is the normal function of the MC4-R receptor and what happens when it doesn’t work?

A

Normal: Able to receive input from alpha-MSH transmitter and increases energy expenditure

Not working: Pathway might still be working but MC4-R is not able to receive/interpret signals. Leads to a decrease in energy expenditure
-will retain more weight and not burn a lot of calories

30
Q

When the MC4-R recpeort isn’t working, is that due to environmental factors or genetics?

A

Genetic disorder of a non-functional MC4-R receptor and can result in obesity

31
Q

What is the lateral hypothalamic nucleus?

A

Houses the neurotransmitter orexin which regulates appetite

32
Q

What does chronic leptin resistance lead to?

A

Leads to constant SNS hypertension

33
Q

What is Orexin?

A

Neurotransmitter that stimulates food intake

-found in lateral hypothalamic neurons

34
Q

What is NPY?

A

Neurons and neurotransmitter that stimulates food

-found intake found in the the arcuate nucleus

35
Q

What is POMC?

A

Neurons that produce neurotransmitters Alpha-MSH which inhibits food intake and activates energy expenditure
-found in the arcuate nucleus

36
Q

What is the Paraventricular Nucleus?

A

Activates pathways for energy expenditure

-activates SNS as a results of increased alpha-MSH

37
Q

What is the Arcuate Nucleus?

A

Satiety centre which respond to leptin

38
Q

What is the Lateral Hypothalamus?

A

Feeding centre activates food intake

-responds to leptin

Physiology 2130 (44 decks)

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