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Z OLD ESA 1- Metabolism > Appetite > Flashcards

Appetite Flashcards

1
Q

What is the appetite control centre called?

A

Satiety centre

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2
Q

Where is the satiety centre located?

A

In the hypothalamus

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3
Q

What does the hypothalamus contain?

A

Several clusters of neurones referred to as nuclei

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4
Q

What nucleus plays a central role in controlling appetite?

A

The arcuate nucleus

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5
Q

How does the arcuate nucleus control appetite?

A

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

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6
Q

Where is the arcuate nucleus located?

A

At the bottom of the hypothalamus

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7
Q

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

A

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

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8
Q

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

A

No

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9
Q

What kind of signals are processed by the arcuate nucleus?

A
  • Hormonal
  • Nutrient
  • Neuronal
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10
Q

What processes the signals in the arcuate nucleus?

A

Primary neurones

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11
Q

What are the two types of primary neurone?

A
  • Stimulatory
  • Inhibitory
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12
Q

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

A

NAME?

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13
Q

What do the stimulatory neurones promote?

A

Hunger

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14
Q

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

A

NAME?

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15
Q

What does POMC yield?

A

Several neurotransmitters including α-MSH and ß-endorphins

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16
Q

What do the inhibitory neurones of the arcuate nucleus promote?

A

Satiety

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17
Q

Where does α-MSH act?

A

At M4 receptors

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18
Q

What do primary neurones synapse with?

A

Secondary neurones in other regions of the hypothalamus

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19
Q

What happens to the signals in the secondary neurones?

A

They integrate to alter feeding behaviour

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20
Q

Where to hormonal signals to the hypothalamus come from?

A

The gut

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21
Q

What kind of hormone is ghrelin?

A

Peptide

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22
Q

Where is ghrelin released from?

A

Stomach wall

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23
Q

When is ghrelin released?

A

When stomach is empty

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24
Q

What does ghrelin do?

A

Stimulates excitatory primary neurones in arcuate nucelus, stimulating appetite

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25
Q

What does the filling of the stomach do?

A

Inhibits ghrelin release

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26
Q

What kind of hormone is PYY?

A

Peptide

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27
Q

How many amino acids is PYY?

A

36

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28
Q

Where is PYY released from?

A

Cells in the ileum and colon

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29
Q

When is PYY released?

A

In response to feeding

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30
Q

What does PYY do?

A

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

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31
Q

What happens when PYY is injected into mice?

A

It makes them anorexic

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32
Q

What happens to the PYY response in obesity?

A

It is blunted following food intake

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33
Q

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

A
  • Leptin
  • Insulin
  • Amylin
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34
Q

What kind of hormone is leptin?

A

Peptide

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35
Q

Where is leptin released from?

A

Adipocytes

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36
Q

What effects does leptin have in the arcuate nucleus?

A
  • Stimulates the inhibitory (POMC) neurones
  • Inhibits the excitatory (AgRP/NPY) neurones
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37
Q

What is the overall effect of leptin?

A

Suppresses appetite

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38
Q

What does leptin induce the expression of?

A

Uncoupling proteins in the mitochondria

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39
Q

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

A

Energy is dissipated as heat

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40
Q

What effect does insulin have on appetite?

A

Suppresses it

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41
Q

How does insulin suppress appetite?

A

Similar mechanism to leptin (but less significant effect)

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42
Q

What kind of hormone is amylin?

A

Peptide

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43
Q

Where is amylin secreted from?

A

ß-cells in pancreas

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44
Q

What is the role of amylin?

A

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

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45
Q

What is pramlintide?

A

A amylin analouge

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46
Q

What is pramlintide used for?

A

Treatment of type 2 diabetes, as suppresses appetite

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47
Q

Which neurones are orexigenic?

A

Stimulatory neurones

48
Q

Which neurones are anorexigenic?

A

Inhibitory neurone

49
Q

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

A

Hedonic inputs

50
Q

When was leptin discovered?

A

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

51
Q

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

A

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

52
Q

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

A

Yes, but incredibly rare

53
Q

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

A

Remarkably well

54
Q

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

A

Little

55
Q

What is metabolic syndrome also known as?

A
  • Syndrome X
  • Insulin resistance syndrome
  • Cardiometabolic syndrome
  • Reaven’s syndrome
56
Q

What is a syndrome?

A

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

57
Q

What is metabolic syndrome?

A

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
Q

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

A

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

59
Q

What is the prevalence of metabolic syndrome?

A
  • Very common (~20-25% of adults)
  • Present in more than 40% of adults >40
  • Prevalence increasing
60
Q

How do prevalence rates of metabolic syndrome vary?

A

Among races and gender

61
Q

How is metabolic syndrome diagnosed?

A

NAME?

62
Q

What does the IDF definition of metabolic syndrome require?

A

Central obesity, plus 2 of 4 factors

63
Q

What is the aetiology of metabolic syndrome?

A

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

64
Q

What is meant by insulin resistance?

A

When cells become less sensitive and eventually resistant to insulin

65
Q

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

A

They can become desensitised

66
Q

What do high plasma glucose levels leads to?

A

More insulin production

67
Q

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

A

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

68
Q

What is the eventual result of hyperglycaemia?

A

Type 2 diabetes

69
Q

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

A

Extensive damage to vasculature

70
Q

What does obesity in general contribute to?

A
  • Hypertension
  • High cholesterol
  • Hyperglycaemia
71
Q

What does obesity pose a significant risk for?

A
  • Type 2 diabetes
  • Coronary heart disease
72
Q

What is more indicative of metabolic syndrome?

A

NAME?

73
Q

What is the primary intervention for metabolic syndrome?

A
  • Promote healthy lifestyle
  • Moderate calorie restriction
  • Moderate increase in physical activity
  • Change to healthy diet
74
Q

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

A

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

75
Q

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

A

Walking regularly, light sport activity if possible

76
Q

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

A
  • Avoiding sugar rich drinks
  • More fruit and veg
  • Lower fat intake
77
Q

When is secondary intervention needed for metabolic syndrome?

A

When lifestyle change is not enough

78
Q

What happens in secondary intervention for metabolic syndrome?

A

Drug treatment may be required

79
Q

What drug treatments are used for metabolic syndrome?

A
  • Statins
  • Antihypertensive drugs, e.g. ACE inhibitors
  • Possibly anti diabetic drugs
80
Q

What do statins do?

A

Reduce LDL cholesterol

81
Q

What do antihypertensive drugs do?

A

Reduce blood pressure

82
Q

When was the Barker hypothesis published?

A

1991

83
Q

What was the Barker hypothesis based on?

A

Several studies of large cohorts of adult men

84
Q

What did Barkers statistical analysis show?

A

Strongest associations between incidence of adult disease and birth weight

85
Q

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

A
  • Metabolic syndrome
  • Coronary heart disease
  • Stroke
  • Hypertension
  • Type 2 diabetes
86
Q

When did the Dutch famine occur?

A

1944

87
Q

Where did the Dutch famine occur?

A

In occupied Netherlands

88
Q

What did subsequent epidemiological studies of the Dutch famine find?

A

NAME?

89
Q

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

A

Trans generational passage

90
Q

Where have similar findings to the Dutch famine been found?

A
  • Nigerian civil war famine
  • China famine
91
Q

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

A

Epigenetics

92
Q

What are epigenetic mechanisms affected by?

A
  • Development
  • Environmental chemicals
  • Drugs/pharmaceuticals
  • Ageing
  • Diet
93
Q

What developmental stages can affect epigenetics?

A

Both in utero and in childhood

94
Q

What can epigenetics cause modification by?

A
  • DNA methylation
  • Histone modification
95
Q

What is being modified in DNA methylation

A

The DNA itself

96
Q

What happens in DNA methylation?

A

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

97
Q

What kind of molecule is a methyl group?

A

An epigenetic factor

98
Q

Where are methyl groups found?

A

In some dietary sources

99
Q

Call all of a DNA molecule be methylated?

A

No, only certain regions

100
Q

What does methylation of DNA determine?

A

Traits

101
Q

Why does DNA methylation contribute to epigenetics?

A

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

102
Q

What are histones?

A

Proteins in which DNA can wind for compaction and gene regulation

103
Q

What do histones determine?

A

The accessibility of a particular region of DNA to transcription machinery

104
Q

What happens in the histone means the DNA is inaccessible?

A

The gene is inactive

105
Q

Where to epigenetic factors bind to histones?

A

To ‘tails’

106
Q

What does epigenetic factor binding to histone tails do?

A

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

107
Q

Give two examples of histone modification types

A
  • Phosphorylation
  • Methylation
108
Q

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

A

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

109
Q

What does foetal programming seem to involve?

A

Insulin and leptin resistance

110
Q

What is the purpose of foetal programming?

A

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

111
Q

What is the problem with foetal programming?

A

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
Q

Where does the tendency for obesity in offspring also appear?

A

After excess nutritional intake during pregnancy

113
Q

What does embryological or neonatal nutritional imbalance lead to?

A
  • Hormonal changes
  • Metabolic changes
  • Altered cellular differentiation
114
Q

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

A

Epigenetic regulation

115
Q

What is the result of epigenetic regulation?

A

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

116
Q

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

A
  • 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
Q

What socioeconomic issues does DOHaD raise?

A

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

Z OLD ESA 1- Metabolism (17 decks)

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