Hunger and feeding Flashcards
What controls our hunger and tells us to stop eating when we have had enough?
Brain receptors Liver Stomach and intestines Small intestine Fatty tissue External cues
3 main fates of nutrients
Supply energy e.g. for muscle contraction, body T, active transport, DNA replication etc.
Provide building blocks e.g. for complex molecules such as muscle proteins, cell membranes, DNA, hormones, enzymes etc
Stored for the future - glucogen in muscle and liver, triglyceride in adipose tissue
(evolutionary advantage vs obesity epidemic)
Main dietary constituents
Proteins Fats Carbohydrates Minerals Vitamins Water -failure to meet minimum nutritional requirement threatens physical fitness and general health
Proteins
Essential for growth and repair of body tissues and cells, especially muscle
Fats
An energy source and valuable source of fat soluble vitamins, brain and cell wall construction
Carbohydrates
Our bodies’ main source of energy essential for brain metabolism
Minerals
Inorganic elements necessary to normal body processes
Vitamins
Play an important part in many chemical processes in the body
Water
Essential to our normal body function
60% of human body made up of water
Essential dietary constituents
No single food can supply all our anabolic needs
Essential fatty acids cannot be synthesised and must be obtained from diet
Amino acids - 22 required for protein synthesis (9 can only be obtained from diet)
Essential fatty acids exmaples
Linoleic acid
Linolenic acid
Arachidonic acid
Amino acids
We can synthesise 11 of the amino acids from carbohydrate precursors
9 essential amino acids can only be obtained from diet
Essential amino acids
Any Help in Learning These Little Molecules Proves Truly Valuable
(Arginine), histidine, isoleucine, leucine, tryptophan, lysine, methionine, phenylalanine, threonine, valine
Daily calorific intake
57% carbs (4kcal/g)
30% fats (9kcal/g)
13% protein (4kcal/g)
Liver
Glucose –> glycogen
Glycogen –(glucogon)–> glucosee
Liver monitors blood glucose and as it begins to drop, it converts stored glycogen into usable glucose
Brain receptors
Hypothalamic cells sensitive to dropping blood glucose - ‘glucoreceptors’
Stomach
Stretch receptors in wall of stomach - say when approaching being full
Chemoreceptors sensitive to small amounts of food dissolved in fluid in stomach - send signals to brain saying ‘filling up’
Duodenum
Small intestine
Hormone cholecystokinin - CCK released from mucousal cell layer of duodenum
-says ‘stop eating’
Fat cells compared to glycogen
- Fat is longer term energy store
- Slower to use (cf glycogen)
- More energy per unit mass than glycogen
Fat cells and leptin
Not just an inert store
Adipose tissue (‘brown fat’) releases leptin into bloodstream
Hypothalamic receptors detect leptin which may be message ‘plenty of fat in storage - dont eat anymore’
Unsure of its role in humans - no miracle cure for obesity yet
Dual centres for feeding
Hypothalamus contains ‘on’ and ‘off’ switch for feeding
On = lateral region of hypothalamus
Off = ventromedial region of hypothalamus
Evidence from ‘lesioning’ experiments
Dual centre hypothesis
Theory has fallen out of favour over last few decades - far too simplistic
Neuropeptide Y - potent stimulator of appetite - but actions are outside hypothalamus
Thus hypothalamus can’t be ‘centre’ of appetite control
Viscious circle - insulin
Ventromedial lesions to hypothalamus - damage to parasympathetic system
Animal eats more and gets fatter and fatter –> thus more insulin secreted –> blood glucose falls so animal eats more –> food converted into adipose tissue rather than glucose - animal stays hungry –> animal eats more…etc.
Average person calorie excess
15/day
adds up to 5475 calories per year = 1.56 pounds
What explains loss of appetite after a meal?
Could be nerve signals from gut to brain
Or hormone, secreted by gut, that reaches brain via blood stream
-Ghrelin (>food intake) - peptide made by stomach cells in stomach wall
-PYY (
Ghrelin
Hormone of hunger
Levels are high when one is fasting and fall after eating
When volunteers were given ghrelin, they ate more than on days when they received a placebo
PYY(3-36)
Produced by cells in small and large intestines
Potent inhibitor of appetite
Selectively inhibits appetite - stimulating neurones by binding to receptors called NPY Y2.PYY
Thus hormone of satiety - makes you feel satisfied with amount you’ve eaten so you stop
Effects last for 24hr (don’t want breakfast after big meal night before)
more you eat, bigger rise in PYY
Slowly digested food (fat and high fibre foods) give bigger rise
Obesity theory PYY
Reduced sensitivity to PYY?
Refined carb diet reducing rise in PYY levels after a meal?
Since PYY and ghrelin are hormones they have no side effects - synthetic forms being produced and clinically assessed
