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Z OLD ESA 1- Metabolism > Appetite > Flashcards

Flashcards in Appetite Deck (117):
1

What is the appetite control centre called?

Satiety centre

2

Where is the satiety centre located?

In the hypothalamus

3

What does the hypothalamus contain?

Several clusters of neurones referred to as nuclei

4

What nucleus plays a central role in controlling appetite?

The arcuate nucleus

5

How does the arcuate nucleus control appetite?

It receives a range of stimuli, and passes them on to higher brain function

6

Where is the arcuate nucleus located?

At the bottom of the hypothalamus

7

What is the advantage of the arcuate nucleus being at the bottom of the hypothalamus?

It is in an ideal position to pass things to the blood stream

8

Is the arcuate nucleus the only part of the brain that controls appetite?

No

9

What kind of signals are processed by the arcuate nucleus?

- Hormonal 
- Nutrient
- Neuronal

10

What processes the signals in the arcuate nucleus?

Primary neurones

11

What are the two types of primary neurone?

- Stimulatory 
- Inhibitory

12

What do the stimulatory neurones on the arcuate nucleus consist of?

#NAME?

13

What do the stimulatory neurones promote?

Hunger

14

What do the inhibitory neurones of the arcuate nucleus consist of?

#NAME?

15

What does POMC yield?

Several neurotransmitters including α-MSH and ß-endorphins

16

What do the inhibitory neurones of the arcuate nucleus promote?

Satiety

17

Where does α-MSH act?

At M4 receptors

18

What do primary neurones synapse with?

Secondary neurones in other regions of the hypothalamus

19

What happens to the signals in the secondary neurones?

They integrate to alter feeding behaviour

20

Where to hormonal signals to the hypothalamus come from?

The gut

21

What kind of hormone is ghrelin?

Peptide

22

Where is ghrelin released from?

Stomach wall

23

When is ghrelin released?

When stomach is empty

24

What does ghrelin do?

Stimulates excitatory primary neurones in arcuate nucelus, stimulating appetite

25

What does the filling of the stomach do?

Inhibits ghrelin release

26

What kind of hormone is PYY?

Peptide

27

How many amino acids is PYY?

36

28

Where is PYY released from?

Cells in the ileum and colon

29

When is PYY released?

In response to feeding

30

What does PYY do?

Inhibits the excitatory primary neurones of the arcuate nucleus and stimulates the inhibitory neurones, suppressing appetite

31

What happens when PYY is injected into mice?

It makes them anorexic

32

What happens to the PYY response in obesity?

It is blunted following food intake

33

What hormonal signals are sent from the body to the hypothalamus?

- Leptin 
- Insulin
- Amylin

34

What kind of hormone is leptin?

Peptide

35

Where is leptin released from?

Adipocytes

36

What effects does leptin have in the arcuate nucleus?

- Stimulates the inhibitory (POMC) neurones 
- Inhibits the excitatory  (AgRP/NPY) neurones

37

What is the overall effect of leptin?

Suppresses appetite

38

What does leptin induce the expression of?

Uncoupling proteins in the mitochondria

39

What is the result of the expression of uncoupling proteins in the mitochondria due to leptin?

Energy is dissipated as heat

40

What effect does insulin have on appetite?

Suppresses it

41

How does insulin suppress appetite?

Similar mechanism to leptin (but less significant effect)

42

What kind of hormone is amylin?

Peptide

43

Where is amylin secreted from?

ß-cells in pancreas

44

What is the role of amylin?

Not fully understood, but known to suppress appetite, decrease glucagon secretion and slow gastric emptying

45

What is pramlintide?

A amylin analouge

46

What is pramlintide used for?

Treatment of type 2 diabetes, as suppresses appetite

47

Which neurones are orexigenic?

Stimulatory neurones

48

Which neurones are anorexigenic?

Inhibitory neurone

49

Other than primary neurones, what feeds into the secondary neurones?

Hedonic inputs

50

When was leptin discovered?

After studying inbred strain of obese mice (ob/ob)

51

How was the effect of leptin found in the obese mice?

Used positional cloning to show that ob/ob mice have loss of function of leptin gene

52

Have the findings of the obese mice been replicated in humans?

Yes, but incredibly rare

53

How do patients found to have defective leptin respond to leptin injections?

Remarkably well

54

What effect does leptin have on ‘common obesity’ patients?

Little

55

What is metabolic syndrome also known as?

- Syndrome X
- Insulin resistance syndrome
- Cardiometabolic syndrome
- Reaven’s syndrome

56

What is a syndrome?

A group or recognisable pattern of symptoms or abnormalities that indicate a particular trait or disease

57

What is metabolic syndrome?

Rather than a disease per se, it’s a cluster of the most dangerous risk factors associated with cardiovascular disease;
- abdominal obesity
- high blood pressure
- insulin resistance
- raised fasting blood glucose
- dyslipidaemia (HDL cholesterol and increased triglycerides)

58

What is the significance in the presence of multiple risk factors in metabolic syndrome?

Any one of them alone is detrimental to health, but combined they represent a very serious health risk

59

What is the prevalence of metabolic syndrome?

- Very common (~20-25% of adults)
- Present in more than 40% of adults >40
- Prevalence increasing

60

How do prevalence rates of metabolic syndrome vary?

Among races and gender

61

How is metabolic syndrome diagnosed?

#NAME?

62

What does the IDF definition of metabolic syndrome require?

Central obesity, plus 2 of 4 factors

63

What is the aetiology of metabolic syndrome?

Exact cause unknown, but insulin resistance and central obesity significant factors

64

What is meant by insulin resistance?

When cells become less sensitive and eventually resistant to insulin

65

What can happen to signalling pathways downstream to insulin in insulin resistance?

They can become desensitised

66

What do high plasma glucose levels leads to?

More insulin production

67

What does the increased insulin production due to high plasma glucose levels lead to?

The ß-cells eventually becoming unable to cope, eventually wearing out

68

What is the eventual result of hyperglycaemia?

Type 2 diabetes

69

What does hyperglycaemia cause even before type 2 diabetes sets in?

Extensive damage to vasculature

70

What does obesity in general contribute to?

- Hypertension
- High cholesterol 
- Hyperglycaemia

71

What does obesity pose a significant risk for?

- Type 2 diabetes 
- Coronary heart disease

72

What is more indicative of metabolic syndrome?

#NAME?

73

What is the primary intervention for metabolic syndrome?

- Promote healthy lifestyle 
- Moderate calorie restriction
- Moderate increase in physical activity 
- Change to healthy diet

74

What calorie restriction is aimed for in primary intervention for metabolic syndrome?

Aim for 5-10% reduction in body mass in a year

75

What physical activity is involved in primary intervention for metabolic syndrome?

Walking regularly, light sport activity if possible

76

What is meant by healthy diet in primary intervention for metabolic syndrome?

- Avoiding sugar rich drinks 
- More fruit and veg
- Lower fat intake

77

When is secondary intervention needed for metabolic syndrome?

When lifestyle change is not enough

78

What happens in secondary intervention for metabolic syndrome?

Drug treatment may be required

79

What drug treatments are used for metabolic syndrome?

- Statins
- Antihypertensive drugs, e.g. ACE inhibitors 
- Possibly anti diabetic drugs

80

What do statins do?

Reduce LDL cholesterol

81

What do antihypertensive drugs do?

Reduce blood pressure

82

When was the Barker hypothesis published?

1991

83

What was the Barker hypothesis based on?

Several studies of large cohorts of adult men

84

What did Barkers statistical analysis show?

Strongest associations between incidence of adult disease and birth weight

85

What diseases did Barker find to have associations with birth weight?

- Metabolic syndrome
- Coronary heart disease
- Stroke 
- Hypertension
- Type 2 diabetes

86

When did the Dutch famine occur?

1944

87

Where did the Dutch famine occur?

In occupied Netherlands

88

What did subsequent epidemiological studies of the Dutch famine find?

#NAME?

89

What did the low birth weights of the children’s children suggest?

Trans generational passage

90

Where have similar findings to the Dutch famine been found?

- Nigerian civil war famine 
- China famine

91

What is thought to play a role in the passage of information?

Epigenetics

92

What are epigenetic mechanisms affected by?

- Development
- Environmental chemicals 
- Drugs/pharmaceuticals 
- Ageing 
- Diet

93

What developmental stages can affect epigenetics?

Both in utero and in childhood

94

What can epigenetics cause modification by?

- DNA methylation 
- Histone modification

95

What is being modified in DNA methylation

The DNA itself

96

What happens in DNA methylation?

A methyl group can tag DNA, and activate or repress genes

97

What kind of molecule is a methyl group?

An epigenetic factor

98

Where are methyl groups found?

In some dietary sources

99

Call all of a DNA molecule be methylated?

No, only certain regions

100

What does methylation of DNA determine?

Traits

101

Why does DNA methylation contribute to epigenetics?

Because the methylation pattern is passed on from one generation to the next

102

What are histones?

Proteins in which DNA can wind for compaction and gene regulation

103

What do histones determine?

The accessibility of a particular region of DNA to transcription machinery

104

What happens in the histone means the DNA is inaccessible?

The gene is inactive

105

Where to epigenetic factors bind to histones?

To ‘tails’

106

What does epigenetic factor binding to histone tails do?

Alters the extent to which DNA is wrapped around the histone, and the availability of DNA to be activated

107

Give two examples of histone modification types

- Phosphorylation 
- Methylation

108

What is meant by the thrifty phenotype hypothesis and fetal programming?

If a woman experiences low nutrition during pregnancy, this programs’ a child for a similar life

109

What does foetal programming seem to involve?

Insulin and leptin resistance

110

What is the purpose of foetal programming?

Optimises the offsprings chance of survival in harsh environment- evolutionary favourable mechanism

111

What is the problem with foetal programming?

If the offspring lives a ‘life of plenty’, with high calories and low exercise, the adaptations in metabolism can result in obesity, diabetes and metabolic syndrome

112

Where does the tendency for obesity in offspring also appear?

After excess nutritional intake during pregnancy

113

What does embryological or neonatal nutritional imbalance lead to?

- Hormonal changes 
- Metabolic changes
- Altered cellular differentiation

114

What do the changes due to embryological nutritional imbalance lead to?

Epigenetic regulation

115

What is the result of epigenetic regulation?

Long term effects on gene transmission, causing an increased risk of disease

116

What are the clinical implications of the Developmental Origins of Adult Health and Aisease (DOHaD) hypothesis?

- Potentially provides better understanding of origins of some adult disease states
- Highlights importance of antenatal care in adequate and appropriate nutrition 
- Potential socioeconomic issues

117

What socioeconomic issues does DOHaD raise?

Women at greatest risk for poor nutrition during pregnancy may be least likely to present for antenatal care