why do we feel hungry while fasting?
low blood glucose lvls
glucose
- keeps body functions operational
- preferred source of energy for brain
how does the body store glucose?
- glycogen
- released in btwn meals
- stored in muscles + liver
- liver glycogen is converted back into glucose when circulating glucose lvls r low
which hormone mediates glucose-glycogen balance
insulin in pancreas
glucose-glycogen steps/process after eating
- spike in blood sugar upon eating
- pancreas secretes insulin
- cells uptake glucose for immediate use
- excess glucose stored as glycogen OR adipose - blood sugar decreases after a while
- liver breaks down glycogen into glucose
- when glycogen in liver decreases, signal sent to brain - hungry again, eat again
neuropeptide Y (NPY)
- stimulates appetite
- in hypothalamus
- similar impacts on feeding behaviour in fish, reptiles, and mammals
where does brain get satiety signals from?
- stretch receptors in stomach which send signal to brain via vagus nerve
- digestive hormones secreted by gastrointestinal tract
- the liver
if we take a dog that is eating and inject glucose into a vein tht connects to the liver, wht happens? what happens if the glucose is injected in a vein that doesn’t connect with the liver?
- liver: stop eating
- other vein: keep eating
CCK
- hormone produced by small intestine
- when food moves form stomach to guts
- signals to stop eating in the short-term
what happens when CCK is injected in rats?
- feel satiated sooner
- shorter avg meal durations
- HOWEVER, rats on CCK ate more meals per day than the control
- thus, daily food intake was the same for both
adipose tissue
long term energy storage
why is fat/adipose the ideal form of long-term energy storage
- fat has twice the energy density than carbs like glycogen have
- stores more energy for the long-term
how many kcal in a gram of adipose vs glycogen?
- adipose: 1g = 9kcal
- glycogen: 1g = 4kcal
is adipose tissue an organ? how?
- endocrine organ
- bc it releases leptin
leptin
- act on receptors in the hypothalamus to reduce appetite
- food consumption decreases
which gene controls leptin prod’n?
OB gene
OB gene knockout mice
- leptin prod’n stops
- appetite increases
- fat storage increases = obesity
- reversed w/ regular leptin administration
what happens when leptin is administered to an obese animal with a normal leptin system? wht does this mean?
- no weight loss occurs
- when high enough leptin is reached, animals become leptin resistant
leptin resistance
beyond a certain level, the impact on leptin on appetite is reduced
primary adaptive function of leptin
- served as indicator of low energy stores
- not a signal to directly reduce food intake
- low leptin = more foraging and less physical activity
what does leptin do to NPY?
inhibits NPY
order of hormones in eating cycle
- NPY triggers food-seeking when glycogen reserves deplete
- if leptin is secreted from fatty tissue, need for food is not urgent
- eventually, drive to eat wins - meal is eaten and blood glucose levels rise
- CCK released to trigger short-term satiety
what happens when NPY is injected directly into brains of satiated rats who already ate
- increased intake of sucrose
- rats work harder for cue associated with sucrose
- increased consumption of saccharide (same taste, no calories)
- rats preferentially choose diet of carbohydrates over protein/fat
- rats w/ higher baseline preference for carbohydrates showed a greater preference for carbs following injection
what specifically does NPY action promote the intake of?
carbohydrates
