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
well-fed versus fasting animals: have HIGH BLOOD CONCENTRATIONS of...
well-fed: a) glucose b) amino acids c) insulin d) leptin fasting: a) glucagon b) glucocorticoids
26
well-fed versus fasting animals: HIGH STORES of...
well-fed: a) body fat in adipose tissues b) glycogen in liver fasting: a) free fatty acids
27
well-fed versus fasting animals: which have high LIPOGENIC (FAT-SYNTHESIZING) ENZYMES?
well-fed animals fasting animals have high: a) lipolytic enzymes b) ketone bodies c) circulating ghrelin
28
well-fed versus fasting animals: other hormones/neuropeptides they're high in
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)
29
orexigenic hormone/compound
an appetite stimulant a) increases appetite b) may induce hyperphagia
30
hyperphagia
medical term for an extreme, insatiable hunger
31
anorexigenic hormone/compound
reduces appetite results in lower food consumption
32
examples of orexigenic molecules
NPY MCH orexin noradrenaline
33
examples of anorexigenic molecules
alpha-MSH CRH TRH CART ocytocin serotonin
34
2 phases of energy utilization and storage after a meal
1. postprandial phase 2. postabsorptive phase
35
posprandial phase
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
36
postabsorptive phase
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
37
when do the posprandial and postabsorptive phases occur?
postprandial: a) immediately after food ingestion postabsorptive: a) insulin secretion has to have risen, while glucagon secretion has fallen
38
basic overview of well-fed state
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
39
basic overview of fasting state
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
40
what powers the brain in the well-fed versus fasting states?
well fed = glucose fasting = liberated glucose and ketone bodies
41
5 points on insulin
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
42
what does the liver do to glucose?
converts it into glycogen some of this glycogen = stored in liver, some in muscle
43
what does liver do to amino acids?
converts them into ketone bodies
44
what is insulin needed for in peripheral cells?
for glucose oxidation and lipogenesis these processes result in storage of fat in adipose tissue
45
hormones other than insulin that are involved in metabolism during the well-fed state
epinephrine, norepinephrine, glucocorticoids, thyroid hormones, growth hormone, somatomedin, glucagon
46
two phases of insulin release
1. cephalic phase 2. gastrointestinal phase
47
cephalic phase of insulin release
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
48
gastrointestinal phase of insulin release
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
49
metabolism during the fasting state: 5 points
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
50
what are formed after fasting, and they can be used by what?
ketones can be used by brain when glucose is scarce
51
fasting state: most common mechanism for raising blood sugar levels without eating
glucagon release gluconeogenesis sympathetic stimulation of fat breakdown
52
during fasting state, cells in periphery switch from...
metabolizing glucose for ATP production to metabolizing free fatty acids mobilized from lipids stored in adipose tissue
53
metabolic system is designed to provide sufficient...
levels of energy to the brain
54
glycogenolysis, lipolysis and gluconeogenesis are all part of...
part of fasting state
55
glycogenolysis
breakdown of stored glycogen in the liver or muscles to provide a steady supply of glucose for energy
56
lipolysis
breakdown of adipose tissue into free fatty acids
57
gluconeogenesis
production of glucose from amino acids process that occurs in liver in response to mild fasting
58
where does gluconeogenesis occur?
in the liver in response to mild fasting
59
deranged energy metabolism can lead to...
type 1 and type 2 diabetes
60
insulin dependent versus resistant: type 1 and type 2 diabetes
type 1 diabetes: insulin-dependent - less insulin production type 2 diabetes: insulin-resistant - insulin is produced, but doesn't bind to enough glucose
61
control of food intake: 3 forces
1. homeostatic needs 2. hedonic intake 3. executive function: decision making and impulse control
62
obesity isn't only the result of overeating...
studies have observed more than 32 candidate obesity GENES most of which are expressed in the brain
63
control of food intake: sensory system
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
goal of sensory system in control of food intake
to maintain constant supply of metabolic fuels for intracellular oxidation
65
GI hormones serve as what?
satiety signals that converge on the dorsal hindbrain
66
what brain areas control food intake and blood glucose levels?
hypothalamus ARC hindbrain
67
what produces leptin?
adipose cells leptin circulates in concentrations that are proportional to total amount of body fat
68
leptin levels when stored fat is being used for energy...
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
leptin is a _______ signal. why?
starvation because when stored fat is being used for energy, blood levels of leptin fall faster than the levels of fat being metabolised
70
lots of leptin in circulation means lots of _______ in body...
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
leptin: connection between body fat and feeding behaviour
communication between adipose tissue and brain
72
leptin is the protein encoded by what?
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
leptin regulates body mass by...
acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure
74
4 broad effects of leptin
1. regulation of energy homeostasis 2. regulation of neuroendocrine function 3. regulation of metabolism 4. regulation of immune function
75
there's an association between insulin release and...
meal termination hunger ensures when insulin levels drop at the end of the post-absorptive phase
76
are there insulin receptors in the brain?
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
ghrelin induces...
food intake and body mass
78
systemic injections of ghrelin stimulated...
food intake increased body mass (in rats)
79
blood concentrations in ghrelin peak around...
time of MEAL ONSET
80
ghrelin is produced by what
the gut
81
ghrelin expression in brain
ghrelin expression occurs in neurons adjacent to the third ventricle these neurons send axons onto hypothalamic circuits
82
ghrelin stimulates activity of ____ neurons in the ____ ______
NPY arcuate nuclei mimicked effects of NPY in the PVN
83
ghrelin works in opposition to...
leptin has opposite effects on hypothalamic neurons that produce the anorectic neuromodulators and oxigenic peptides
84
circulating concentrations of ghrelin and ______ are inversely correlated
leptin
85
lateral hypothalamic syndrome
anorexia caused by lesions of the LATERAL HYPOTHALAMUS
86
brain circuits associated with: homeostatic feeding, hedonic feeding and learning/memory related feeding
1. homeostatic feeding: HYPOTHALAMIC circuits 2. hedonic feeding/motivational feeding/meal anticipation behaviour: MESOLIMBIC circuits 3. learning/memory feeding behaviour: HIPPOCAMPAL CIRCUITS
87
ventromedial hypothalamic syndrome
obesity cased by lesions of ventromedial hypothalamus
88
lesions of lateral versus ventromedial hypothalamus
lateral: anorexia ventromedial: obesity
89
bilateral lesions of lateral hypothalamus interfere with what in addition to feeding?
all motivated behaviours
90
hypothalamus general regulatory functions
homeostatic regulation of: energy food intake thirst temperature sleep circadian rhythm
91
arcuate nuclei of the hypothalamus contain two...
opposing sets of neuronal circuitry
92
two opposing sets of neuronal circuitry in the hypothalamus
1. feeding stimulatory circuit 2. feeding inhibitory circuit
93
both circuits of the arcuate nuclei send signals...
primarily to the PVN and to other nuclei of the hypothalamus and therefore modulate feeding behaviour
94
feeding stimulatory and feeding inhibitory circuits are modulated by...
peripheral hormonal signals that cross the blood-brain barrier like leptin, insulin, ghrelin
95
feeding stimulatory circuit
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
reduction in blood levels of leptin is detected by neurons where? what do they do in response?
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
feeding inhibitory circuit
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
elevated leptin levels is detected by neurons where? and what happens in response?
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
NPY and AgRP do what? CART and POMC do what?
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
central anabolic effectors: 5 peptides that promote food intake
1. neuropeptide Y 2. agouti-related protein 3. melanin-concentrating hormone (MCH) 4. pancreatic polypeptide 5. orexin
101
neuropeptide Y (NPY)
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
NPY interacts with receptors in ______ to cause what?
PVN hyperphagia
103
LHA
NPY neurons terminate on neurons that secrete other peptides critical for body mass regulation: orexin and melanin-concentrating hormone (MCH)
104
agouti-related protein (AgRP)
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
melanin-concentrating hormone (MCH)
cell bodies of neurons that secrete MCH are located in the LHA (lateral hypothalamus)
106
injections of MCH into lateral ventricles/various brain regions evoke...
feeding behaviour
107
pancreatic polypeptide (PP)
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
orexin
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
orexin A does what to food intake?
increases it possibly by inhibiting sleep
110
central catabolic effectors: peptides that inhibit food intake
1. melanocortin 2. cocaine- and amphetamine-regulated transcript (CART)
111
melanocortins - proopiomelanocortin (POMC)
proopiomelanocortin (POMC) is the pituitary precursor endocrine products: 1. melanocortins: alpha-MSH, beta-MSH, adrenocorticotropic hormone 2. opioids
112
leptin and insulin ____ POMC gene expression in the arcuate nuclei
increase
113
stimulation of POMC-producing neurons does what?
causes them to secrete alpha-MSH which in turn stimulates MC4 receptors
114
POMC activation increases conversion of...
white adipose tissue to brown adipose tissue which is involved in thermogenesis increasing brown fat compared to white adipose tissue increases energy expenditure
115
what does increasing brown fat compared to white adipose tissue do?
increases energy expenditure POMC activation promotes this conversion
116
5 points: CART
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
leptin and insulin stimulate what kind of pathway?
catabolic (POMC/CART) and repress an anabolic pathway
118
the anabolic and catabolic pathways mediated by leptin and insulin begin and project where?
BEGIN in arcuate nuclei PROJECT to PVN and LHA
119
alpha-MSH
alpha-melanocyte-stimulating hormone located in arcuate nucleus anorectic peptide inhibits feeding behaviour
120
CART
cocaine- and amphetamine-regulated transcript located in arcuate nucleus anorectic peptide inhibits feeding behaviour
121
NPY
neuropeptide Y located in arcuate nucleus orexigenic peptide stimulates feeding behaviour
122
AgRP peptide
Agouti-related peptide located in arcuate nucleus orexigenic peptide stimulates feeding behaviour
123
MCH
melanin-concentrating hormone located in lateral hypothalamic area (LHA) orexigenic peptide stimulates feeding behaviour
124
orexin
located in lateral hypothalamic area (LHA) orexigenic peptide stimulates feeding behaviour
125
7 protein hormones that STOP food intake
cholecystokinin (CKK) bombesin amylin corticotropin-releasing hormone glucagon-like peptide 1 adiponectin peptide tyrosine-tyrosine (PYY)
126
cholecystokinin (CKK)
primary hormonal factor that provokes satiety gastrointestinal peptide hormone that's released during feeding to aid with digestion
127
CKK pathway
1. released during a meal 2. binds to CKK-A receptors on the vagus nerve 3. hypothalamus 4. stop feeding behaviour
128
influence of gonadal steroid hormones on body mass
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
role of serotonin in motivation
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
stress and eating behaviour: comfort food in lab
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
comfort food intake is most associated with what kind of stress?
acute
132
stress induced obesity and the emotional nervous system
during stressful periods (like exams)... a) gravitate towards comfort foods b) less gravitation towards healthy foods
133
early life stress and eating behaviour
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
in cases of early life adversity, what things affect eating behaviour?
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
mind over milkshakes
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
mind over milkshakes study suggests what?
effect of food consumption on ghrelin may be psychologically mediated mindset meaningfully affects physiological responses to food
137
ozempic
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
GLP-1
the hormone mimicked by Ozempic reduces food intake and body mass gut hormone