Appetite And Hunger Flashcards

1
Q

Theories of hunger

Keesey and Powley (1986) set point theory

A

Return the body to optimum level of bodily resources
Hunger is a result of an energy deficit.
Each individual has an optimum level of energy resources which is their set point, homeostasis is returning to at set point.
Energy level - hunger - meal initiated

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2
Q

Hunger is evolutionary unlikely because…

A

1) need a system that can predict not just respond

2) need to cope with inconsistent resources in environment

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3
Q

Evolutionary unlikely …

Not supported

A

Reduction in blood glucose needed to start a meal is substantial and drinking a high calorie drink prior to meal does not stop the meal.
Lowe (1993) beliefs about the content of the drink has more of an effect

Ignores the environment

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4
Q

Theories of hunger

1) anticipation

A

Animals are driven to eat by the expected pleasure of eating
Expected pleasure = positive incentive reward

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5
Q

Theories of hunger

2) craving

A

Eating and the perception of hunger are initiated by craving, enables you to take advantage of good food when it is available

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6
Q

Theories of hunger

Multiple factors:

A
Flavour of the food 
Knowledge about food
Time since last meal 
Blood glucose levels
Amount of food in gut
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7
Q

Learned tastes, sclafani (1990) Dwyer, Haselgrove and Jones (2011)

A

Flavour A - glucose
Flavour B - nothing
Rats prefer flavour A

flavour A - LiCl
Flavour B - nothing
Rats avoid flavour A

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8
Q

Galef (1995) food preferences can be…

A

Socially acquired

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9
Q

Learning to eat vitamins and minerals

Fudim (1978)

A

Associating salt with flavours
Almond and salt. Banana and sugar.
Nothing - prefer banana and sugar
Injection of formalin to induce a salt need - prefer almond and salt

You can learn tastes of what you need

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10
Q

Learning to eat vitamins and minerals

Harris (1933)

A

Thiamine depleted rats learned to choose a complete diet and avoid a thiamine depleted diet
However this effect was weakened when there was a choice between 10 different diets

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11
Q

When do we eat ?

Collier (1986)

A

Many mammals eat many small meals throughout the day

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12
Q

Initiating a meal;

Woods (1991) pre meal hunger

A

Eating stresses the body and moves it away from homeostasis
Signals for a meal evokes a cephalic phase where you eat a meal under certain circumstances
Hunger is the body preparing for homeostasis disruption

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13
Q

Initiating a meal

Weingarten (1983)

A

Conditioned hunger in rats
Buzzer+light = food
Are more when buzzer and light was presented

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14
Q

Digestion process;

A

1) chewing. Mix with saliva
2) saliva lubricates food. This begins digestion
3) swallowing - asophagus to stomach
4) HCl breaks food down. Popsin - protein = amino acids
5) stomach empties via pyloric sphirictor to duodenum - intestine where absorption takes place
6) digestive enzymes - proteins - amino acid
Starch - sugars
Bloodstream - liver
7) fats broken by bile and carried by duodenum into the lympathetic system
8) absorbed into large intestine or ejected via anus

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15
Q

The ventral medial hypothalamus is the …

A

Satiety centre

Hetherington and Ranson (1940) lesions to the ventramedial lead to hyperphagia (overeating and obesity)

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16
Q

VMH syndrome

A

1) the dynamic phase. Excessive eating and weight gain
2) the static phase where body weight is maintained

They will not work for food and are fussy eaters

17
Q

The lateral hypothalamus is a …

A

Feeding centre

Anand and Brobeck (1951) lesions here lead to aphagia - no eating

18
Q

LH syndrome

Teitelbaum and Epstein (1962)

A

1) aphagia and adipsia (no drinking)

2) recovery possible through tune feeding. Milk soaked cookies and dry food pellets

19
Q

The theory of the hypothalamus crumbled because…

A

1) VMH lesions damaged PVN which produces hyperphagia and obesity
2) hypothalamus regulates metabolism not eating.
VMH lesions increases blood insulin which has two consequences; increased lipogenesis, the production of fat, and decreased lipolysis, the break down of fat
3) LH lesions produce motor disturbances and lack of responsiveness

20
Q

The stomach

Cannon and Washburn (1912)

A

Contractions from an empty stomach correlates to feeling of hunger.
However, patients without a stomach still get hungry
Therefore the stomach is sufficient but not necessary for hunger

21
Q

The stomach

Koopmans (1981)

A

Extra stomach and a length of intestine transplanted into rats
Food injected into the stomach lead to decrease eating
The transplanted stomach had no nerves that workd so satiety signal must reach the brain through blood flow

22
Q

Peptides are short chains on amino acids

Gibbs, young and Smith (1973)

A

The satiety peptide is Cholehstokinin (CCK)
When this was injected into the gut of a hungry rat, eating decreased.
However it may induce illness

23
Q

Leptin

Seeley and Woods (2003)

A

Leptin receptor is in mouse brains - spontaneous mutation meant they lacked the peptide leptin. They are more but calories turned into fat more efficiently and there was no feedback signal to decrease appetite and enable fat metabolism

Injections of leptin into obese mice lead to decreased eating and weight