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System Neuroscience > Week 10: Regulation Of Metabolism And Feeding > Flashcards

Week 10: Regulation Of Metabolism And Feeding Flashcards

1
Q

Define Caloric homeostasis

A

Maintenence of energy balance in the body. Preserves cellular metabolism; we store energy for when food is scarce and bridge gaps between meals

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2
Q

Define Orexigenic

A

Appetite stimulating

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3
Q

Define Anorexigenic

A

Appetite inhibiting

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4
Q

Define Anabolic

A

Building/storing

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5
Q

Define Catabolic

A

Breaking down/ using

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6
Q

Define prandjal

A

Relating to meals

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7
Q

Define phagia

A

(Suffix) to eat

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8
Q

What is Adiposity?

A

Amount of body fat

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9
Q

What does Hunger and satiation govern?

A

Meal-by-meal eating behaviour

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10
Q

What does hypothalamic circuitry coordinate?

A

Daily food intake With long term, homeostatic, and feedback regulation of energy balance and body weight

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11
Q

What is Prandial or Fed state?

A

Insulin promotes use and storage (anabolic)

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12
Q

Postabsorptive or Fasted state?

A

Absence of insulin; mobilisation of stores (catabolic)

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13
Q

What does liver do?

A

Oxidizes many lipids Stores carbohydrates

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14
Q

What do most tissues e.g. muscles do?

A

Oxidise glucose or lipids

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15
Q

What does CNS do?

A

Oxidises mainly glucose

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16
Q

What does adipose tissue do?

A

Stores lipids

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17
Q

What is the cephalic phase?

A

Hypothalamus drives the parasympathetic NS stimulation of pancreatic insulin secretion

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18
Q

What is the GI phase?

A

Gut hormone stimulate insulin secretion

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19
Q

What is substrate phase?

A

Insulin secretion stimulated by metabolites (glucose)

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20
Q

What is the gastric signal?

A

Stomach distension - vagus nerve > nucleus tracts solitarius ( NTS)

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21
Q

What are the post-gastric signals (I.e. intestinal)

A

Cholecystokinin Glucagon-like peptide-1 (GLP-1) / peptide YY (PYY) Liver signals Increased plasma osmolality

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22
Q

Cholecystokinin

A

Enteroendocrine cells secrete CCK when fatty acids are detected - acts in vagus (synergises with stretch) - hormonal and neural

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23
Q

GLP-1/ PYY

A

Taste carbohydrates in gut, GLP-1 increases insulin secretion and both act centrally - hormonal

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24
Q

Liver signals

A

Detect absorbed nutrients/insulin - satiation signals via vagus - neural

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25
Q

Increased plasma osmolality

A

Sensors in brain (caudal brainstem) or viscera

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26
Q

When do meals terminate?

A

Before nutrient homeostasis occurrs

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27
Q

What happens when satiation signals disappear?

A

Hunger can re-emerge and another meal is initiated

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28
Q

What are the internal hunger and satiation signals?

A

Hunger pangs/ stretch Various blood chemicals relating to body state including insulin, glucose, CCK, GLP-1, ghrelin, osmolality

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29
Q

What are the internal contextual factors?

A

Mood; habit; memory

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30
Q

What are the external quality cues?

A

Appearance and smell of food

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31
Q

What are the external context cue ?

A

Safe time to eat Social setting Cultural factors Time of day

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32
Q

What are the internal hunger and satiation signals?

A

Hunger pangs/ stretch Various blood chemicals relating to body state including insulin, glucose, CCK, GLP-1, ghrelin, osmolality

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33
Q

What are the internal contextual factors?

A

Mood; habit; memory

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34
Q

What are the external quality cues?

A

Appearance and smell of food

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35
Q

What are the external context cue ?

A

Safe time to eat Social setting Cultural factors Time of day

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36
Q

What are two physiological functions of body weight?

A

Food intake Intestinal absorption

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37
Q

The brainstem mediated important reflexes via what route?

A

Dorsal Vagal Complex (DVC) Parabrachial nucleus (PBN)

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38
Q

What are higher centres required for?

A

Modification and integration of signals Learning, adipocyte factors and circadian rhythms (daily cycle)

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39
Q

What does the reflex arc act to modulate?

A

Absorption and incorporation of other metabolites

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40
Q

What is the NTS closely associated with?

A

Dorsal Medial vagus Area postrema

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41
Q

What does the reflex arc act to modulate?

A

Absorption and incorporation of other metabolites Allow more or less food to be absorbed at the hypothalamus levels

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42
Q

What is the NTS closely associated with?

A

Dorsal Medial vagus Area postrema

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43
Q

What is satiation signals associated with?

A

Body weight (adipocyte)

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44
Q

What does Adiposity influence?

A

Food intake indirectly

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45
Q

What is the main centre for control of body weight?

A

Hypothalamus

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46
Q

What is Leptin?

A

A satiation signal of Adiposity

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47
Q

What does Leptos mean?

A

Thin

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48
Q

What happens if there is a genetic mutation in the peptide ob/ob or its receptor db/db?

A

are obese

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49
Q

What happens to tissue if someone has more adipose tissue?

A

The tissue is less responsive to insulin

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50
Q

What effect does leptin and insulin have?

A

Catabolic effects on metabolism

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51
Q

What is Ghrelin?

A

Hunger signal

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52
Q

What is ghrelin and where is it secreted from?

A

Peptide and by the stomach during fasting

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53
Q

When is Ghrelin secreted?

A

Just prior to meals suggesting it has a role in the initiation of meals

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54
Q

What does Ghrelin affect?

A

Dopamine reward pathways

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55
Q

What does levels of Ghrelin correlate with?

A

Hunger scores

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56
Q

What is hyperphagia?

A

Abnormally great desire for food

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57
Q

What is hypophagia?

A

Reduction in food intake and eating behaviour

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58
Q

What is dorsomedial involved in?

A

Circadian rhythms Feeding (inhibition) Emotions

59
Q

What is ventromedial involved in?

A

Inhibits feeding (satiety centre)

60
Q

What is the Lateral hypothalamic area Involved in?

A

Eating, drinking

61
Q

What does VMH lesions disrupt?

A

Autonomic tone - decreasing sympathetic/ increasing parasympathetic, Vagal tone

62
Q

What does LHA lesion disrupt?

A

Sensorimotor integration - reward and motor systems

63
Q

What is the main centre for appetite regulation?

A

Arcuate nucleus

64
Q

What 2 neurones are key to regulation of food intake and metabolism?

A

Dopamine neurons GHRH

65
Q

What is the precursor for melanocortin peptides (alpha MSH)?

A

Pro-opiomelanocortin (POMC)

66
Q

Where does POMC act on?

A

Melanocortin receptors (e.g. MCR4)

67
Q

What does POMC play an important role in?

A

Inhibit feeding (anorexigenic effects)

68
Q

What does deficiency of POMC lead to?

A

Hyperphagia and obesity

69
Q

Where are melanocortin receptor 4 found in?

A

Numerous projection sites of Arcuate POMC neurons

70
Q

What is MCR4 expresses by?

A

PVH neurons which surpresses food intake

71
Q

What does melanocortin stimulation of MC4R cause?

A

Increase in energy expenditure and maintain glucose homeostasis

72
Q

What does genetic deletion of MC4R in life and human result in?

A

Severe hyperphagic obesity

73
Q

What is neuropeptide Y?

A

Orexigenic - effects lasts 1-2 hours

74
Q

What does agouti-related peptide have?

A

Longer acting Orexigenic effect; acts as a melanocortin receptor antagonist

75
Q

What does injection of NPY into the PVN cause?

A

Increased food intake and negatively controls sympathetic outflow Directly inhibits MC4R expressing cells

76
Q

What does ablation of NPY/AgRP In adults result in?

A

Profound decrease in food intake and body weight

77
Q

What are satiety signals?

A

Both hormonal and neural

78
Q

Where does bidirectional flow of information occur?

A

Brainstem and hypothalamus

79
Q

What does leptin/insulin in Arcuate nucleus stimulate?

A

POMC anorexigenic cells Inhibits NPY/ AGRP Orexigenic cells

80
Q

What does low level of insulin and leptin release?

A

NPY/AgRP/GABA cells from inhibitory satiety Control

81
Q

What stimulates feeding behaviour?

A

High Ghrelin levels from Vagal input and hypothalamic circuits

82
Q

What is Lateral hypothalamic area?

A

Orexigenic site - driving feeding as well as central to anabolic effects

83
Q

Where does the enteroendocrine peptides act on?

A

ARC system

84
Q

What are other satiety factors ?

A

GLP-1 and PYY

85
Q

What does GLP-1 and PYY act ?

A

Stimulate POMC and inhibit NPY cells

86
Q

What has therapeutic potential in obesity treatment?

A

GLP-1 agonists

87
Q

What does global deficiency of 5-HT2C or 5-HT1B receptors result in?

A

Hyperphagia Obesity Disturbed glucose homeostasis

88
Q

What is mood controlled by?

A

Serotonergic systems

89
Q

What is serotonergic systems?

A

Implication for interaction of mood with eating behaviours

90
Q

What does low level of insulin and leptin release?

A

NPY/AgRP/GABA cells from inhibitory satiety Control

91
Q

What stimulates feeding behaviour?

A

High Ghrelin levels from Vagal input and hypothalamic circuits

92
Q

What is Lateral hypothalamic area?

A

Orexigenic site - driving feeding as well as central to anabolic effects

93
Q

Where does the enteroendocrine peptides act on?

A

ARC system

94
Q

What are other satiety factors ?

A

GLP-1 and PYY

95
Q

What does GLP-1 and PYY act ?

A

Stimulate POMC and inhibit NPY cells

96
Q

What has therapeutic potential in obesity treatment?

A

GLP-1 agonists

97
Q

What does global deficiency of 5-HT2C or 5-HT1B receptors result in?

A

Hyperphagia Obesity Disturbed glucose homeostasis

98
Q

What is mood controlled by?

A

Serotonergic systems

99
Q

What is serotonergic systems?

A

Implication for interaction of mood with eating behaviours

100
Q

What is found in Paraventricular nucleus?

A

Oxytocin (OXY) Corticotropin releasing hormone (CRH) Both peptides are anorexigenic

101
Q

What does OXY mediate?

A

CRH effect and stress related decrease in eating

102
Q

What does CRH mediate ?

A

Increase in sympathetic activity

103
Q

What is involved in Lateral hypothalamic area?

A

Orexin Melanocortin concentrating hormone (MCH) - they are orexigenic

104
Q

What does orexin cause?

A

Wakefulness It’s decrease after eating inside drowsiness

105
Q

Where does area postrema lie?

A

Caudal end of the 4th ventricle adjacent to the nucleus of tractus solitarus, not connected to the hypothalamus

106
Q

Where does area postrema get information from?

A

Blood and transfers that information into dorsal vagal complex (DVC)

107
Q

What does area postrema detect?

A

Toxins

108
Q

What does dorsal motor nucleus of vagus control?

A

Parasympathetic output

109
Q

Where is the input from hypothalamus Via?

A

Paraventricular nucleus to sympathetic preganglionic neurons in spinal cord

110
Q

What is the main centre for appetite regulation?

A

Arcuate nucleus

111
Q

Where is arcuate nucleus found?

A

Median eminence

Connecting hypothalamus to pituitary gland

112
Q

What does dopamine neuron do?

A

Inhibit prolactin secretion

113
Q

What does GHRH cause ?

A

Pulsatile release and growth hormone secretion

114
Q

What are key regulation of food intake and metabolism?

A

Dopamine neurons

GHRH

115
Q

Where is the brainstem involved through?

A

Dorsal vagal complex

Parabrachial nuclei around superior cerebellar peduncle

116
Q

What does brainstem centre allow?

A

Reflexive eating behaviours
Distinguishing whether something is good or bad to eat
Recognise how much glucose and salt there are in the bloodstream

117
Q

Decerebrate rat

A

Do not have cortical input
Distinguish between bitter, salty, sweet flavours and eat accordingly
They don’t eat as much bitter - toxic substance

118
Q

Where does afferent input go to?

A

Nucleus tract of solitarus

119
Q

What does reflex arc act to modulate?

A

Absorption and incorporation of other metabolites

120
Q

What is NTS closely associated with?

A

Dorsal medial vagus

Area postrema

121
Q

Where is food mainly absorbed by body?

A

Small intestine (duodenum)

122
Q

What happens after we’ve eaten?

A

Glucose is absorbed into the blood
Travel to the liver
The liver store glucose as glycogen

123
Q

What is the role of insulin

A

Stimulate glucose uptake to liver by the blood indirectly
Insulin inhibit secretion of glucose to the blood from liver
Stimulate uptake of glucose to adipocyte to produce more triglyceride
Stimulate uptake glucose to skeletal muscles

124
Q

What does body absorb?

A

FA
AA
Monoglyceride
Stored as glycogen, protein and triglyceride

125
Q

Fed state

A

Gluconeogensis
Lipogensis
Protein synthesis

126
Q

What does liver have?

A

Short term capacity
Releases glucose by breaking down glycogen stores
Produced ketone bodies

127
Q

When is insulin released?

A

In the presence of glucose in the body

There are low levels of glucose before meals

128
Q

What is insulin release?

A

Biphasic

129
Q

What is cephalic Phase activated by?

A

Thought
Smell
Taste
Sight of food

130
Q

What is the cephalic phase mediated by?

A

Cholinergic/vagal mechanism Via parasympathetic

131
Q

What does meals generate?

A

Satiation signals

132
Q

What does stomach have and what does liver release?

A

Stomach - stretch receptors

Liver releases CCK, GLP-1

133
Q

What are adipocyte signal?

A

Leptin

Insulin

134
Q

What does receptors on stomach fire?

A

Signals to the brain which say that the stomach is full which inhibit feeding
Activating ventromedial hypothalamus

135
Q

What are CCK and GLP1 releases in proportion to?

A

Content of fat and protein

136
Q

What does leptin level indicate?

A

How much fat you have stored in adipose tissue

The more fat, the higher the leptin level

137
Q

What does sight, taste and smell override?

A

Biochemical signal and it can cause you to eat more quickly

138
Q

What is satiation signal associated with?

A

Body weight (adipocity)

139
Q

Scientific approach to obesity

A

Lack of will power
Lifestyle/environment
Biology/genes

140
Q

What does elevated extracellular glucose level activate?

A

POMC Neurons

141
Q

What does POMC neurons produce?

A

Anorectic peptide alpha-melanocyte by posttranscriptional processing of POMC

142
Q

What is alpha-MSH

A

Main peptide involved in appetite regulation

143
Q

What does alpha-MSH bind to?

A

Melanocortin receptor 3 and 4 on second order neurons and activate catabolic pathways
Reduced food intake
Increased energy expenditure

144
Q

What does endorphin modulate?

A

Reward system

System Neuroscience (17 decks)

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