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Flashcards in S2: Control of Food Intake Deck (31)
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1
Q

Define satiety

A

State of being full after eating food

2
Q

Define appetite

A

Describes the desire to satisfy the body’s need of food; often a hunger stimulated response

3
Q

Define Hunger

A

Discomfort caused by lack of food and the desire to eat – a strong craving for food

4
Q

Define Aphagia

A

The inability or refusal to swallow

5
Q

Define hyperphagia/polyphagia

A

An abnormal desire for food (extreme unsatisfied drive to eat)

6
Q

What provide cues to tell use when to start and stop eating?

A

Hunger, satiation and satiety are cues that tell us when to start and stop eating.

7
Q

What controls food intake?

A

Hypothalamic control: Balance between stimulating and inhibiting forces in the hypothalamus regulates feeding

8
Q

Reasons for differences in BMI

A
  • Genes - 70%

- How much we eat and its compositions

9
Q

List the factors that influence appetite

A

External e.g. food availability, variety of food, social eating

Sensory factors: The combination of taste, smell, sight and sometimes sound a food

Emotional state: stress, anxiety, depression

Social factors: e.g. in asian culture rice is a staple

Physiological regulation: Our desire for food is driven by the evolutionary need to supply our bodies with nutrients and energy so that we can survive, propagate and pass our genes onto our offsping

10
Q

What two neurotransmitters in the hypothalamus control feeding behaviour?

A
  • Orexigenic neurotransmitters: ↑appetite

* Anorexigenic neurotransmitters: ↓ appetite

11
Q

What is the role of the lateral hypothalamus (LH) in the control of food intake?

A

It is the hunger centre.

LH and VMN have the ability to restrain feeding if required

  • Lesion - increase appetite , with weight gain that tends to persist
12
Q

Where is the satiety centre?

A

Ventromedial nucleus (VMN)

13
Q

What is the role of the Dorsomedial Nucleus (DMN) in the control of food intake?

A

It is the hunger centre (along with the lateral hypothalamus).

It modulates energy intake and releases NPY (neuropeptide y) into DMN which increases feeding

14
Q

List anorexigenic factors that decrease appetite

A

5-HT (5-HT2C and 5-HT1A), dopamine, GABA

15
Q

What is the dinural variation in food intake?

A
  • Carbohydrates metabolised during the day
  • Fats metabolised at night
  • Hypothalamus responds to the switch between carbohydrate and fat metabolism
16
Q

Role of the prefrontal cortex in the executive control of food intake

A
  • Integration of sensory information from inside and outside the body;
  • Receive emotional and cognitive information from the limbic system
  • Helps one make choices by translating all of the homeostatic and environmental information into adaptive behavioural response
17
Q

Role of the limbic system in the executive control of food intake

A

Complex system of nerves and networks in the brain; areas concerned with instinct and mood. May control emotions, pleasure (fear, anger, etc.)
- So cortico-limbic mechanisms of reward appear to be under executive control

• The satiation of feeding behaviour is associated with motor planning and execution

18
Q

List various molecules that increase appetite

A

Opioids, somatostatin, growth hormone releasing hormone

19
Q

Why does the brain have a glucostat?

A

The brain has a glucostat, it can measure the amount of glucose that is reaching it because it relies on it so heavily.

the concentration of glucose in the blood will stimulate glucoreceptors in the hypothalamus. This means we have to take glucose up.
Decreased blood glucose will up-regulate hunger while increased blood glucose will up-regulate satiety.

20
Q

Why do diabetics feel hungry despite increased glucose?

A

Diabetics feel hungry despite increased glucose. This is because blood glucose is not entering the cells, so the body isn’t sensing this.

21
Q

How does the temperature of environment affect appetite?

A

Cold environments simulate feeding while hot environments inhibit appetite. This is useful as allows to put fat on when cold.

22
Q

List afferent inputs of food intake

A
  • Distension of a full stomach inhibits appetite, contraction of an empty one stimulates appetite both via afferents
  • Denervation of intestine and stomach seems to have no effect on food intake, tells us there are other things going on
  • Deposition of fat may control appetite, as fat tissue has ability to release leptin (more fat = more leptin)

Hormones and factors are released coincident (at same time) with a meal play a role in regulating food intake.
Fat ingestion causes CCK release and slowing of gastric emptying giving a feeling of fullness.

23
Q

How does injection of CCK in the brain reduce appetite?

A

Fat ingestion causes CCK release and slowing of gastric emptying giving a feeling of fullness.

Hence CCK (from I cells in the intestine or nerve endings) inhibit further food intake; this can be described as a satiety factor

24
Q

Describe leptin

A

Comes from white adipose tissue and can be said to be a lipostat, meaning it signals fat stores in adipose tissue, in other words the more leptin you have the more fat you have hanging around.

Leptin controls fat stores by operating a feedback mechanism between adipose tissue and brain, increased adipose tissue size = increased leptin secretion

Leptin increases the expression of anorexigenic factors.

Leptin also stimulates metabolic rate and INHIBITS neuropeptide Y, neuropeptide Y is a stimulant of feeding. So inhibiting it, causes inhibition of feeding.

25
Q

What does resistance of leptin lead to?

A

Some people may become resistant to the effects of leptin, leading to binge eating despite having enough leptin around and an adequate/growing of adipose tissue (obese).

26
Q

Why is acts to counteract leptin?

A

Ghrelin

27
Q

What acts to work with leptin?

A

Synergistic Interaction between Leptin and CCK to reduce short-term food intake in lean mice

When you put leptin and CCK together you get a synergistic effect -> the effects of both agents together are much greater than either on its own.

28
Q

Describe Ghrelin

A

Ghrelin (is an orexin)
->
Is fasting acting and stimulates food intake

  • It is released by the stomach, pancreas, adrenals in response to nutritional status
  • Circulating levels of ghrelin will increase before meals (preprandially) and decrease after a meal

Ghrelin increases central orexins, for example neuropeptide Y and cannabinoids.
It also suppresses the ability of leptin to stimulate anorexigenic factors.

Ghrelin secretion can also be inhibited by leptin

29
Q

What does loss of ghrelin activity usually indicate?

A

A loss of ghrelin activity often demonstrates a success of gastric bypass

30
Q

Describe Obestatin

A
  • Produced by epithelial cells of the stomach
  • Encoded by ghrelin gene but acts in opposing direction to ghrelin

It suppresses food intake (suppresses appetite, so decreases body weight gain)
So it antagonises ghrelin induced food intake (and growth hormone secretion)

31
Q

What stimulates leptin/ghrelin release?

A

Info is sent to the hypothalamus -> stomach feels distended -> leptin/ghrelin released etc. central molecules will then influence our food intake