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Psyc 342 > hormones and feeding behaviour > Flashcards

hormones and feeding behaviour Flashcards

1
Q

motivation

A

behaviour in pursuit of a goal

fundamental element of our interaction with the world and with each other

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2
Q

motivation to obtain basic needs

A

food, water, sex and social interaction

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3
Q

regulation of motivated behaviours is achieved by the coordinated action of… which act within…

A

a) molecules
b) peptides
c) hormones
d) neurotransmitters

specific circuits that integrate multiple signals for complex decisions to be made

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4
Q

2 main reasons why we eat

A
  1. to meet the needs of the STRUCTURAL parts of the body (muscles, bones)
  2. to obtain ENERGY to fuel the body
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5
Q

energy balance

A

FOOD INTAKE to maintain HOMEOSTASIS

mammalian brain depends on GLUCOSE as main energy source

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6
Q

what in the adult brain have the highest energy demand?

A

neurons

they require CONTINUOUS delivery of glucose from blood

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7
Q

brain accounts for what percentage of body weight and consumes how much glucose-derived energy?

A

2% of body weight

consumes 20% of glucose-derived energy

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8
Q

what in the body is the main consumer of glucose?

A

the brain

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9
Q

2 primary systems that regulate food intake

A
  1. homeostatic
  2. hedonic
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10
Q

homeostatic regulation of food intake

A

controls energy balance by…

increasing motivation to eat following DEPLETION OF ENERGY stores

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11
Q

hedonic regulation of food intake

A

increases desire to consume foods that are HIGHLY PALATABLE

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12
Q

two time scales of energy balance

A
  1. short-term energy balance
  2. long-term energy balance
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13
Q

short term energy balance

A

acts primarily as determinant of satiety

to limit size of individual meals

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14
Q

long term energy balance

A

acts to keep body mass within a relatively fixed range

over weeks, moths, years

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15
Q

food intake is divorced from…

A

homeostatic processes

it relies on NON-HOMEOSTATIC processes like:
a) experience
b) habits
c) availability

ie. if rats receive a meal consistently at time 0, will begin to show ANTICIPATORY endocrine responses 1-2 hours in advance of the learned mealtime

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16
Q

fasting and refeeding

A

animals fluctuate between a well-fed and fasting state

correlated changes occur in secretion of:
a) hormones
b) neurotransmitters
c) neuromodulators

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17
Q

prandial state

A

after consuming a meal

  1. blood is full of NUTRIENTS
  2. energy is stored in 2 forms:
    a) GLYCOGEN
    b) TRIGLYCERIDES
  3. glycogen reserves: liver and skeletal muscles
  4. triglyceride reserves: adipose (fat) tissues
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18
Q

what kinds of nutrients are absorbed from a meal?

A
  1. glucose
  2. fatty acids
  3. triglycerides
  4. glycogen
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19
Q

anabolism

A

occurs after eating a meal

during the prandial state

process by which proteins are formed from amino acids

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20
Q

post-absorptive state

A

fasting condition

  1. glycogen and triglycerides are BROKEN to be used as fuel

catabolism

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21
Q

catabolism

A

during post-absorptive state

glycogen and triglycerides are broken down (catabolized) into smaller molecules that can be used as fuel by the cells of the body

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22
Q

the feeding system is in proper balance when…

A

energy reserves are replenished at the SAME AVERAGE RATE that they are expended

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23
Q

when does obesity occur?

A

simplified answer:

if intake and storage of energy consistently exceeds the usage

then amount of body fat increases

eventually results in obesity

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24
Q

when does starvation occur?

A

simplified answer:

if intake of energy consistently fails to meet body’s demands

loss of fat tissue occurs

eventually results in starvation

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25
Q

well-fed versus fasting animals: have HIGH BLOOD CONCENTRATIONS of…

A

well-fed:
a) glucose
b) amino acids
c) insulin
d) leptin

fasting:
a) glucagon
b) glucocorticoids

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26
Q

well-fed versus fasting animals: HIGH STORES of…

A

well-fed:
a) body fat in adipose tissues
b) glycogen in liver

fasting:
a) free fatty acids

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27
Q

well-fed versus fasting animals: which have high LIPOGENIC (FAT-SYNTHESIZING) ENZYMES?

A

well-fed animals

fasting animals have high:
a) lipolytic enzymes
b) ketone bodies
c) circulating ghrelin

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28
Q

well-fed versus fasting animals: other hormones/neuropeptides they’re high in

A

well-fed:
a) CCK
b) alpha-MSH
c) CART

fasting:
a) NPY
b) MCH
c) orexin
d) corticotropin-releasing factor
e) catecholamines (NE and EP)

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29
Q

orexigenic hormone/compound

A

an appetite stimulant

a) increases appetite

b) may induce hyperphagia

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30
Q

hyperphagia

A

medical term for an extreme, insatiable hunger

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31
Q

anorexigenic hormone/compound

A

reduces appetite

results in lower food consumption

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32
Q

examples of orexigenic molecules

A

NPY

MCH

orexin

noradrenaline

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33
Q

examples of anorexigenic molecules

A

alpha-MSH

CRH

TRH

CART

ocytocin

serotonin

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34
Q

2 phases of energy utilization and storage after a meal

A
  1. postprandial phase
  2. postabsorptive phase
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35
Q

posprandial phase

A

first phase of energy utilization/storage after a meal

a) the fed state

b) embodies the digestion and absorption of nutrients

c) 6-12 hours

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36
Q

postabsorptive phase

A

second phase of energy utilization/storage after a meal

a) once the nutrients are digested, absorbed and utilized

b) they’re stored in designated tissues

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37
Q

when do the posprandial and postabsorptive phases occur?

A

postprandial:
a) immediately after food ingestion

postabsorptive:
a) insulin secretion has to have risen, while glucagon secretion has fallen

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38
Q

basic overview of well-fed state

A
  1. good is broken down into glucose, free fatty acids, amino acids. glucose powers brain and muscles
  2. insulin is released from pancreas to facilitate the transport of glucose
  3. excess glucose is converted to glycogen and stored in liver and muscles
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39
Q

basic overview of fasting state

A
  1. glucagon is released from pancreas
  2. glycogenolysis breaks down stored glycogen in liver
  3. lipolysis in adipose tissue releases free fatty acids and glycerol
  4. liberated glucose and ketone bodies power the brain
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40
Q

what powers the brain in the well-fed versus fasting states?

A

well fed = glucose

fasting = liberated glucose and ketone bodies

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41
Q

5 points on insulin

A
  1. liver: conversion of glucose to glycogen
  2. glycogen is stored in liver and muscle
  3. insulin facilitates transport of glucose into muscle and fat cells
    - and transport of amino acids into muscle cells
  4. liver: amino acids are converted into ketone bodies
  5. in peripheral cells: insulin is needed for glucose oxidation and lipogenesis, processes that result in storage of fat in adipose tissue
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42
Q

what does the liver do to glucose?

A

converts it into glycogen

some of this glycogen = stored in liver, some in muscle

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43
Q

what does liver do to amino acids?

A

converts them into ketone bodies

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44
Q

what is insulin needed for in peripheral cells?

A

for glucose oxidation and lipogenesis

these processes result in storage of fat in adipose tissue

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45
Q

hormones other than insulin that are involved in metabolism during the well-fed state

A

epinephrine, norepinephrine, glucocorticoids, thyroid hormones, growth hormone, somatomedin, glucagon

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46
Q

two phases of insulin release

A
  1. cephalic phase
  2. gastrointestinal phase
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47
Q

cephalic phase of insulin release

A

release of insulin from pancreatic cells occurs as result of SENSORY STIMULI associated with FOOD INTAKE

even before nutrients are present

ie. arrive at home and smell your fav dinner - even before your first bite, body starts to release insulin

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48
Q

gastrointestinal phase of insulin release

A

primary storage of excess nutrients taken in during meal occurs in this phase

when insulin is released in response to absorption of nutrients from gut

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49
Q

metabolism during the fasting state: 5 points

A
  1. energy reserves are mobilized from storage to meet energy needs
  2. metabolic system is designed to provide sufficient levels of energy to brain
  3. after fasting, ketones are formed, and these can also be used by brain when glucose is scarce
  4. glucagon release, gluconeogenesis, and sympathetic stimulation of fat breakdown are the most common mechanisms for raising blood sugar levels without eating
  5. during fasting state, cells in periphery switch from metabolizing glucose for ATP production to metabolising free fatty acids mobilized from the lipids stored in adipose tissue
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50
Q

what are formed after fasting, and they can be used by what?

A

ketones

can be used by brain when glucose is scarce

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51
Q

fasting state: most common mechanism for raising blood sugar levels without eating

A

glucagon release

gluconeogenesis

sympathetic stimulation of fat breakdown

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52
Q

during fasting state, cells in periphery switch from…

A

metabolizing glucose for ATP production

to metabolizing free fatty acids mobilized from lipids stored in adipose tissue

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53
Q

metabolic system is designed to provide sufficient…

A

levels of energy to the brain

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54
Q

glycogenolysis, lipolysis and gluconeogenesis are all part of…

A

part of fasting state

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55
Q

glycogenolysis

A

breakdown of stored glycogen in the liver or muscles

to provide a steady supply of glucose for energy

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56
Q

lipolysis

A

breakdown of adipose tissue into free fatty acids

57
Q

gluconeogenesis

A

production of glucose from amino acids

process that occurs in liver in response to mild fasting

58
Q

where does gluconeogenesis occur?

A

in the liver

in response to mild fasting

59
Q

deranged energy metabolism can lead to…

A

type 1 and type 2 diabetes

60
Q

insulin dependent versus resistant: type 1 and type 2 diabetes

A

type 1 diabetes: insulin-dependent
- less insulin production

type 2 diabetes: insulin-resistant
- insulin is produced, but doesn’t bind to enough glucose

61
Q

control of food intake: 3 forces

A
  1. homeostatic needs
  2. hedonic intake
  3. executive function: decision making and impulse control
62
Q

obesity isn’t only the result of overeating…

A

studies have observed more than 32 candidate obesity GENES

most of which are expressed in the brain

63
Q

control of food intake: sensory system

A

there’s a sensory system that monitors:

a) metabolic fuel oxidation and changes food intake

b) energy expenditure and body fat storage and breakdown

in goal of maintaining constant supply of metabolic fuels for intracellular oxidation

64
Q

goal of sensory system in control of food intake

A

to maintain constant supply of metabolic fuels for intracellular oxidation

65
Q

GI hormones serve as what?

A

satiety signals that converge on the dorsal hindbrain

66
Q

what brain areas control food intake and blood glucose levels?

A

hypothalamus

ARC

hindbrain

67
Q

what produces leptin?

A

adipose cells

leptin circulates in concentrations that are proportional to total amount of body fat

68
Q

leptin levels when stored fat is being used for energy…

A

blood levels of leptin FALL FASTER than the levels of fat being metabolized

this reduction in circulating. leptin suggests that this hormone is a “starvation” signal

69
Q

leptin is a _______ signal. why?

A

starvation

because when stored fat is being used for energy, blood levels of leptin fall faster than the levels of fat being metabolised

70
Q

lots of leptin in circulation means lots of _______ in body…

A

nutrients

leptin levels tell brain how many nutrients are in the body

ie. leptin is high - brain is like ok lots of nutrients atm - decreases food intake

71
Q

leptin: connection between body fat and feeding behaviour

A

communication between adipose tissue and brain

72
Q

leptin is the protein encoded by what?

A

the ob gene

if you knockout the ob gene in mice, they become obese

and when these knockouts are treated with leptin, they lose weight

73
Q

leptin regulates body mass by…

A

acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure

74
Q

4 broad effects of leptin

A
  1. regulation of energy homeostasis
  2. regulation of neuroendocrine function
  3. regulation of metabolism
  4. regulation of immune function
75
Q

there’s an association between insulin release and…

A

meal termination

hunger ensures when insulin levels drop at the end of the post-absorptive phase

76
Q

are there insulin receptors in the brain?

A

yes

mostly in the ARCUATE NUCLEI

the brain doesn’t require insulin for glucose to enter cells

insulin receptors here are MONITORS of metabolic fuels

77
Q

ghrelin induces…

A

food intake and body mass

78
Q

systemic injections of ghrelin stimulated…

A

food intake

increased body mass

(in rats)

79
Q

blood concentrations in ghrelin peak around…

A

time of MEAL ONSET

80
Q

ghrelin is produced by what

A

the gut

81
Q

ghrelin expression in brain

A

ghrelin expression occurs in neurons adjacent to the third ventricle

these neurons send axons onto hypothalamic circuits

82
Q

ghrelin stimulates activity of ____ neurons in the ____ ______

A

NPY

arcuate nuclei

mimicked effects of NPY in the PVN

83
Q

ghrelin works in opposition to…

A

leptin

has opposite effects on hypothalamic neurons that produce the anorectic neuromodulators and oxigenic peptides

84
Q

circulating concentrations of ghrelin and ______ are inversely correlated

A

leptin

85
Q

lateral hypothalamic syndrome

A

anorexia

caused by lesions of the LATERAL HYPOTHALAMUS

86
Q

brain circuits associated with: homeostatic feeding, hedonic feeding and learning/memory related feeding

A
  1. homeostatic feeding: HYPOTHALAMIC circuits
  2. hedonic feeding/motivational feeding/meal anticipation behaviour:
    MESOLIMBIC circuits
  3. learning/memory feeding behaviour:
    HIPPOCAMPAL CIRCUITS
87
Q

ventromedial hypothalamic syndrome

A

obesity

cased by lesions of ventromedial hypothalamus

88
Q

lesions of lateral versus ventromedial hypothalamus

A

lateral: anorexia

ventromedial: obesity

89
Q

bilateral lesions of lateral hypothalamus interfere with what in addition to feeding?

A

all motivated behaviours

90
Q

hypothalamus general regulatory functions

A

homeostatic regulation of:
energy
food intake
thirst
temperature
sleep
circadian rhythm

91
Q

arcuate nuclei of the hypothalamus contain two…

A

opposing sets of neuronal circuitry

92
Q

two opposing sets of neuronal circuitry in the hypothalamus

A
  1. feeding stimulatory circuit
  2. feeding inhibitory circuit
93
Q

both circuits of the arcuate nuclei send signals…

A

primarily to the PVN and to other nuclei of the hypothalamus

and therefore modulate feeding behaviour

94
Q

feeding stimulatory and feeding inhibitory circuits are modulated by…

A

peripheral hormonal signals that cross the blood-brain barrier

like leptin, insulin, ghrelin

95
Q

feeding stimulatory circuit

A

in the underfed state, leptin and insulin are low

NPY and AgRP stimulate food intake

reduction in blood levels of leptin = detected by neurons in arcuate nucleus that contain NPY and AgRP

96
Q

reduction in blood levels of leptin is detected by neurons where? what do they do in response?

A

neurons in thee ARCUATE NUCLEUS

  1. these neurons contain NPY and AgRP
  2. these neurons inhibit neurons in the paraventricular nuclei that control release of TSH and ACTH from pituitary
  3. also activate neurons in lateral hypothalamus that stimulate feeding behaviour
97
Q

feeding inhibitory circuit

A

in fed state, have high levels of leptin and insulin

in response to rise in blood levels of leptin, neurons in ARCUATE NUCLEUS that contain alpha-MSH and CART are activated

alpha-MSH/CART and POMC neurons decrease food intake

98
Q

elevated leptin levels is detected by neurons where? and what happens in response?

A

detected by neurons in the ARCUATE NUCLEUS

these neurons contain peptides alpha-MSH and CART

these neurons project to lower brain stem and spinal cord, PVN and lateral hypothalamus

each of these connections contributes to coordinated responses to increased leptin levels

99
Q

NPY and AgRP do what? CART and POMC do what?

A

NPY and AgRP:
- stimulate food intake

(when leptin/insulin levels are low)

CART and POMC:
- inhibit food intake

(when leptin/insulin levels are high)

100
Q

central anabolic effectors: 5 peptides that promote food intake

A
  1. neuropeptide Y
  2. agouti-related protein
  3. melanin-concentrating hormone (MCH)
  4. pancreatic polypeptide
  5. orexin
101
Q

neuropeptide Y (NPY)

A

potent activator of food intake

orexigenic peptide:

a) increases motivation to eat

b) decreases amount of food consumed passively

c) increases food-seeking and hoarding behaviours

102
Q

NPY interacts with receptors in ______ to cause what?

A

PVN

hyperphagia

103
Q

LHA

A

NPY neurons terminate on neurons that secrete other peptides critical for body mass regulation:

orexin and melanin-concentrating hormone (MCH)

104
Q

agouti-related protein (AgRP)

A

stimulates eating

very small amounts infused into ventricles of brain stimulate food intake for up to 6 days

low circulating levels of leptin and insulin activate NPY/AgRP neurons in arcuate nuclei

105
Q

melanin-concentrating hormone (MCH)

A

cell bodies of neurons that secrete MCH are located in the LHA (lateral hypothalamus)

106
Q

injections of MCH into lateral ventricles/various brain regions evoke…

A

feeding behaviour

107
Q

pancreatic polypeptide (PP)

A

PP may serve as a satiety signal

food consumption elevates PP in circulation for up to 6 hours after the meal

suggests that PP may serve to regulate intervals between meals

108
Q

orexin

A

produced by neurons whose cell bodies are located in the LHA

2 versions of orexin: A and B

orexin A increases food intake, possibly by inhibiting sleep

109
Q

orexin A does what to food intake?

A

increases it

possibly by inhibiting sleep

110
Q

central catabolic effectors: peptides that inhibit food intake

A
  1. melanocortin
  2. cocaine- and amphetamine-regulated transcript (CART)
111
Q

melanocortins - proopiomelanocortin (POMC)

A

proopiomelanocortin (POMC) is the pituitary precursor endocrine products:

  1. melanocortins: alpha-MSH, beta-MSH, adrenocorticotropic hormone
  2. opioids
112
Q

leptin and insulin ____ POMC gene expression in the arcuate nuclei

A

increase

113
Q

stimulation of POMC-producing neurons does what?

A

causes them to secrete alpha-MSH

which in turn stimulates MC4 receptors

114
Q

POMC activation increases conversion of…

A

white adipose tissue to brown adipose tissue

which is involved in thermogenesis

increasing brown fat compared to white adipose tissue increases energy expenditure

115
Q

what does increasing brown fat compared to white adipose tissue do?

A

increases energy expenditure

POMC activation promotes this conversion

116
Q

5 points: CART

A
  1. neurons in the arcuate nuclei secrete POMC in the PVN and LHA and CART
  2. elevated circulating levels of leptin and insulin activate the POMC/CART neurons in the arcuate nuclei
  3. activation of CART-secreting neurons increases metabolic rate
  4. CART has a net catabolic effect on metabolism
  5. secretion of these peptides activates the melanocortin receptors in the PVN: decreases food intake
117
Q

leptin and insulin stimulate what kind of pathway?

A

catabolic (POMC/CART)

and repress an anabolic pathway

118
Q

the anabolic and catabolic pathways mediated by leptin and insulin begin and project where?

A

BEGIN in arcuate nuclei

PROJECT to PVN and LHA

119
Q

alpha-MSH

A

alpha-melanocyte-stimulating hormone

located in arcuate nucleus

anorectic peptide

inhibits feeding behaviour

120
Q

CART

A

cocaine- and amphetamine-regulated transcript

located in arcuate nucleus

anorectic peptide

inhibits feeding behaviour

121
Q

NPY

A

neuropeptide Y

located in arcuate nucleus

orexigenic peptide

stimulates feeding behaviour

122
Q

AgRP peptide

A

Agouti-related peptide

located in arcuate nucleus

orexigenic peptide

stimulates feeding behaviour

123
Q

MCH

A

melanin-concentrating hormone

located in lateral hypothalamic area (LHA)

orexigenic peptide

stimulates feeding behaviour

124
Q

orexin

A

located in lateral hypothalamic area (LHA)

orexigenic peptide

stimulates feeding behaviour

125
Q

7 protein hormones that STOP food intake

A

cholecystokinin (CKK)

bombesin

amylin

corticotropin-releasing hormone

glucagon-like peptide 1

adiponectin

peptide tyrosine-tyrosine (PYY)

126
Q

cholecystokinin (CKK)

A

primary hormonal factor that provokes satiety

gastrointestinal peptide hormone that’s released during feeding to aid with digestion

127
Q

CKK pathway

A
  1. released during a meal
  2. binds to CKK-A receptors on the vagus nerve
  3. hypothalamus
  4. stop feeding behaviour
128
Q

influence of gonadal steroid hormones on body mass

A

gonadal steroid hormone influence FEEDING BEHAVIOUR and subsequent body mass

  1. ESTROGENS have CATABOLIC effects: increasing energy expenditure, thermogenesis, lipolysis, body fat loss
  2. ANDROGENS have ANABOLIC effects
129
Q

role of serotonin in motivation

A

homeostatic circuitry:

  1. contributes to INTEGRATION OF METABOLIC SIGNALS about body’s energy status
  2. facilitates ability to SUPPRESS FOOD INTAKE when homeostatic needs have been met

hedonic circuitry:

  1. serotonergic signalling may REDUCE REWARD RELATED, motivational food consumption
130
Q

stress and eating behaviour: comfort food in lab

A

in controlled lab circumstances

acute physical/emotional distress induce increased intake of ‘comfort’ foods in humans and animals

even when not hungry/have no homeostatic need for calories

131
Q

comfort food intake is most associated with what kind of stress?

A

acute

132
Q

stress induced obesity and the emotional nervous system

A

during stressful periods (like exams)…

a) gravitate towards comfort foods

b) less gravitation towards healthy foods

133
Q

early life stress and eating behaviour

A

early life stress heightens REACTIVITY to stress

leads to alterations in HOMEOSTATIC and HEDONIC MECHANISMS

changes in cognition, stress response, mental health disorders

all of these things tie into eating behaviour

134
Q

in cases of early life adversity, what things affect eating behaviour?

A
  1. altered homeostatic mechanisms
    (impaired glucose/insulin sensitivity, altered brain-gut axis, changes in basal metabolic activity, changes in leptin signalling)
  2. altered hedonic mechanisms
    (changes motivations to eat palatable food, reward system dysfunction, impaired reward evaluation, changes in dopaminergic/opioid/endocannbinoid systems)
  3. cognition
    (memory, attention, impulsivity problems)
  4. stress response
    (HPA dysfunction)
  5. mental health disorders
    (anxiety, depression)
135
Q

mind over milkshakes

A

mindsets, not just nutrients, determine ghrelin response

over the course of a day, participants were given two doses of the same milkshake

except they were presented differently: one was “indulgent” and “comfort”-coded and the other was “healthy” (with “no added sugar and low calorie etc)

even though the milkshakes were identical, differences in perceived healthiness mapped on to GHRELIN EXPRESSION

ghrelin levels were way higher for the “indulgent” shake

136
Q

mind over milkshakes study suggests what?

A

effect of food consumption on ghrelin may be psychologically mediated

mindset meaningfully affects physiological responses to food

137
Q

ozempic

A

designed for diabetics

helps weight loss and lowers blood sugar spikes

through hormonal action - it mimics GLP-1

GLP-1 tells us when we’re full and slows gastric emptying of stomach (helps with blood sugar spikes and feeling of fullness)

also has receptors in the brain which suppress hunger signals

but then it was marketed for weight loss - now harder for diabetics to get this treatment

trivialized as an easy weight loss solution

138
Q

GLP-1

A

the hormone mimicked by Ozempic

reduces food intake and body mass

gut hormone

Psyc 342 (10 decks)

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