7 - HOMEOSTASIS & ENERGY & EATING Flashcards
1
Q
information:
the fact that cells need specific conditions to survive and function suggests that multicellular organisms evolved from single cells, living and moving in a salt water environment
A
-
2
Q
cells in a multicellular organism…
A
- cannot move to a suitable environment (they are stationary - except red blood cells and microglia) so cannot escape environmental changes
- cut off from ‘natural’ environment as on the inside of the body
- cells must work together and cooperate to create and maintain a suitable environment (suitable for all cell types, some might have different requirements - all needs need to be met)
3
Q
optimum
A
cells require a stable environment
- survive only small deviations from ‘working conditions’
- large deviations = disrupted cell function and can lead to cell death (eg too hot)
4
Q
internally generated environmental conditions that cause constant change
A
- nutrients being used up
- waste products accumulating (due to metabolism etc)
- growth and reproduction
5
Q
externally generated environmental conditions that cause constant change
A
- temperature, humidity etc
- light and dark
- availability of nutrients (changes seasonally etc)
6
Q
what is homeostasis?
A
actively keeping an organisms (multi or single celled) internal states within a critical range - to allow cells to survive
7
Q
what are homeostatic systems?
A
- negative feedback loops
- oscillating behaviour around the set point (optimum)
- eg like a temperature control (central heating)
- eg 1c above and below = critical range
- buffer around the set point
- never actually on set point
- when too hot, turns off, when too cold, turns on etc
8
Q
statement:
thirst is a part of homeostatic fluid control
A
-
9
Q
eating is a homeostatic process
why do we need to eat?
nutrition (4 types)
A
- nutrition builds and maintains the body
- essential amino acids
- essential fatty acids
- minerals
- vitamins
10
Q
essential amino acids
A
- 9 cannot be synthesised by the human body (need to get from diet)
- 20 amino acids in total
- they are the building blocks of proteins (need them to be produced by the human body)
11
Q
essential fatty acids
A
- building blocks of fat (eg cell membranes and myelin sheath of neurons)
12
Q
minerals
A
- elements like iron, sodium, calcium
- parts of all body structures
- eg iron in red blood cells, calcium in bones etc
13
Q
vitamins
A
- no common chemical structure
- organic nutrients needed in small amounts
- eg chemical partners for enzymes etc
14
Q
what is used for energy generation?
3 things
A
- carbohydrates
- fats
- proteins (to a lesser extent)
15
Q
short term control of eating (nutrient and energy regulation)
A
- when to start a meal
- when to end a meal
16
Q
long term control of eating (nutrient and energy regulation)
A
- food not constantly available
- evolution of mechanisms to store energy
- release stored energy
- anticipate the need for energy and nutrient
17
Q
how short term and long term control of eating interact (nutrient and energy regulation)
A
- meal size and frequency determines long term body weight
- start meals frequently and don’t end for long time = increase body weight
- start meals infrequently and end meals early = decrease body weight
18
Q
short term eating control
how are meal sizes and frequency controlled?
A
- usually start eating before we feel hungry
- usually stop eating before the brain can receive satiety signals
- control of eating is related to ‘feeling hungry’ but that’s not the whole story
- homeostatic factors and non homeostatic factors involved
19
Q
homeostatic factors involved in short term eating controls
A
- biochemical signals indicating state of energy stores (corresponds to what you keep in a critical range)
- systems or structures to detect and interpret these signals
20
Q
non-homeostatic factors involved in short term eating control
A
- learning: adapting the system to its specific environment
- mood as a non-adaptive factor
21
Q
why do we eat?
A
to build up energy
energy is needed by all chemical processes to make the body survive
22
Q
energy generation model
A
1 - eat fats, carbohydrates and proteins
2 - digest
3 - fatty acids, glucose and amino acids in blood stream
4 - further breakdown
5 - acetyl-CoA
6 - mitochondria of cells = citric acid cycle
7 - mitochondria of cells = oxidative phosphorylation
8 - ATP
23
Q
ATP
A
- ATP = natures universal rechargeable battery!
- found in every cell
- ATP stores energy
- it has 3 phosphate groups which are linked together by compressed spring like structure
- if one phosphate group is removed = energy released
- store energy by adding phosphate group
- we produce our own weight in ATP each day
24
Q
what is available energy used for?
A
- mainly used in basal metabolism (letting cells do what they need to do - eg keeping heart beating, and neurons firing etc)
- next largest consumption is active behaviour
- next is digestion (breaking molecules down)
- then finally the remainder is added as a reserve for storing
- 20% of intake goes to the brain but it’s only 2% of our body mass
25
basal metabolism adjusting to caloric intake
less intake = less spending so reduced basal metabolism
- but return to normal intake and reserves build up before basal metabolism increases
- because organisms live in uncertain conditions - so need to replenish reserves
- also means dieting can be reversed in a few days lol
- if intake is reduced then reserves are used, so reducing the basal metabolism means active behaviour still have the energy required to go and get food
- could reduced basal metabolism increase life expectancy? (shown in mice and primates)
- but would mean having a constantly reduced caloric intake, not fluctuating like diets
26
what can excess energy be converted into in the short term?
liver and muscles cells store glucose as glycogen
glycogen = chains of glucose linked around a protein
27
what can excess energy be stored as in the long term?
fat cells store fat
fat = 3x palmatic acid (O) and 1x glycerol (H) form bonds
- and form water
- which breaks off to leave a fatty acid
28
information:
stored energy must be converted into usable energy (cells cannot utilise glycogen or fat)
- neurons = almost exclusively utilise glucose (don’t need insulin help)
- all other body cells (except red blood cells - only glucose) = utilise glucose (with help of insulin) and fatty acids
-
29
which protein hormones (produced by the pancreas) convert energy?
(2)
1 - insulin = converts glucose into glycogen
2 - glucagon = converts glycogen back into glucose
30
statement:
glycogen and fat can be transformed into each other
-
31
what does insulin do?
| 2
- make direct use of some glucose provided by a meal
| - store some glucose (in the form of glycogen)
32
the multiple systems involved in insulin release
| 3
3 INDEPENDENT SYSTEMS
1 - cephalic phase = before a meal
- signals from the brain to the pancreas to release insulin in preparation
2 - digestive phase = during a meal
- signals from gut hormones to tell pancreas to keep insulin coming
3 - absorptive phase = after a meal
- signals from the liver
33
how do we know about the phases involved in insulin release?
- disrupt the signal pathway and see what happens
- eg could stop signals reaching the pancreas = find insulin is still released at other times = can then find out where signals for each phase comes from
34
are blood levels of insulin a crucial signal for eating control?
not quite!
hypothesis:
- insulin levels low = start meal
- insulin level high = end meal
experimental evidence:
- low blood insulin levels = animal keeps saying
- inject insulin = higher insulin levels (medium ish), animals eat less
problem
- injecting more insulin (high but safe level) = animal eats more!
possible explanation:
- high insulin levels convert all glucose to glycogen
- now glucose level low
- signals hunger
- would need to measure glucose instead of insulin levels
35
are the blood levels of glucose crucial for eating control?
hypothesis:
- glucose levels low = start a meal
- glucose levels high = end a meal
experimental evidence
- low blood glucose levels = animal keeps eating
- inject glucose = higher glucose levels (medium) = animal eats less
supporting evidence = glucose receptors in the hypothalamus (VMH - ventromedial nucleus) - monitors blood glucose levels and can monitor it
problems:
- glucose levels don’t vary much during the day (body controls it carefully to keep it constant)
- diabetics = highly increased glucose levels, but often feel constant hunger - don’t have enough insulin so not enough glucose is taken away and stored / so higher glucose would mean reduced appetite according to hypothesis - but not the case
- injecting glucose into VMH does NOT make animals eat less
36
is the utilisation of glucose crucial for signalling eating control?
hypothesis:
- start meal when glucose levels in liver (storage organ) are low
- end meal with liver gets lots of glucose
experimental evidence:
- functional anatomy = liver sends signals to the brain via VAGUS NERVE (autonomic ns)
- interfering with this signal by either cutting vagus nerve (signal not transmitted) or providing the liver (but not the rest of the body) with glucose (liver fails to signal low blood glucose levels)
- both reduce eating in hungry unfed animals
conclusion:
- when the liver does not signal low glucose levels (or brain does not receive signal) = animals does not act(feel? - cannot know in animals) hungry
problem:
- reduced eating after cutting vagus nerve is only temporary
- will return to normal eating behaviour even though nerve isn’t back
37
other possible hunger/satiety signals
- blood levels of free fatty acids
- blood levels of CKK (a hormone released by the intestines in the presence of fat)
- gut distension (size)
- all showing basically the same problems with signals as described before
- conclusion = probably no single signal under all conditions necessary and sufficient for controlling meal size and frequency
- several signals integrates and utilised in varying combinations
- most likely site for this is hypothalamus
38
hypothalamus inputs
limbic system
- smell and taste
- emotion and stress
blood
- hormones (eg steroids)
- non-hormonal chemicals (eg glucose and toxins - responds directly to toxins in the blood)
retinae
- light / dark
brainstem nuclei
- skin temperature
- visceral information (eg gut distension)
39
hypothalamus outputs
limbic system
- emotion and stress
- learning and memory
blood
- hormones
pituitary gland
- control of endocrine system
brainstem nuclei
- heart rate, sweating, digestion etc
40
what are the two centres in the hypothalamus for eating control?
dual centre hypothesis
1 - VMH (ventromedial hypothalamus)
stimulation = reduced eating
lesion = overeating
- satiety centre?
2 - LH (lateral hypothalamus)
stimulation = overeating
lesion = aphagia (no eating)
- hunger centre?
ALL MUST BE TOGETHER TO SUPPORT THE MODEL - can’t have only one in support
41
evidence against dual centre hypothesis of the hypothalamus
*week 7 pg 5 for diagram*
DEFENDING PATHOLOGICAL BODY WEIGHT = EVIDENCE AGAINST
- VMH lesioned rats (won’t feel satiety, so should always feel hungry) less likely to eat bitter food (more picky) than normal controls
- VMH lesioned = gain weight after lesion
- if given no food, body weight decreases and then they eat more to go back to new pathological normal level
- if force fed then they voluntarily diet to lose body weight back to new pathological normal
- similar to normal rat, just with the different pathological normal
- the plateau at the beginning of the model doesn’t fit well with it (that VMH is the only satiety centre) but it doesn’t directly contradict it
- lesioned rats defend their new (pathological) body weight just as well as normal rats
- rats reach new set point
- no change in control centre
- LH lesioned = eat less so decreases body weight to new pathological normal (assume it doesn’t get hungry)
- given no food= voluntarily eat more after to bring body weight back to new pathological normal
42
conclusion about eating behaviour structures
- not one single system or structure
- eating (probably) regulated by hierarchic network
1 (lowest) peripheral structures (liver, intestines) (peripheral to nervous system, not to body)
2 brain stem centres
3 hypothalamic nuclei (LH and VMH)
4 ‘higher’ brain areas (particularly limbic system)
43
why have multiple systems to control eating behaviour?
- to ensure redundancy
- if one component no longer operates properly, other components can partially compensate
- system is relatively failsafe
- makes sense from evolutionary perspective = survival strategy - need backups
44
what type of amino acid is phenylalanine?
essential
- other non essentials are made by adding groups onto it
45
what would happen if levels of blood sugar were drastically lowered?
- amnesia
- speech impairment
- uncoordinated movements
- unconsciousness
- because neurons need glucose!
