GI 3 Flashcards
Lectures GI 7- GI 8
hunger center
lateral hypothalamus
satiety center
ventromedial hypothalamus
long term regulation of feeding behaviour (2 theories)
- glucostatic: glucose metab in the hypothalamus regulates food intake
- lipostatic: signals from body’s fat stores regulate food intake
what’s leptin
protein found in rats, gene encode for the protein that tells brain fat reserves are normal
where is leptin released from
adipocytes and regulates body mass by directly acting on neurons of hypothalamus that decrease appetite and increase energy expenditure
responses to elevated leptin
act on articulate nucleus:
1. inhibit lateral feeding center
2. activate paraventricular nucleus
i. humoral/hormone response:
- high TSH, ACTH from pituitary (increased metab rate)
ii. visceromotor response:
- increase symp output = increase body temo
responses to decrease leptin
- reduced activation of a-MSH and CART neurons
- reduce active of PVN (low TSH and ACTH)
- low metab rate
- activate parasymp - activate NPY and AgRP containing neurons
- stim feed center
- inhibit PVN more
short term regulation of feeding behaviours
- balance between satiety signals that are generates during digestion and orexigenic signals (GI to CNS) generated during fasting
Ghrelin, gastric distension, CCK, insulin
what does Ghrelin do
- released by cells in stomach in response to emptying
- stim NPY/AgRP neurons in articulate
- ghrelin injection will stim food intake
- mice lacking NPY/AgRP neurons won’t respond to ghrelin
gastric distension and CCK regulating satiety
- distension sensed by mechanosensory neuron, info sent to NTS/medulla, has connections to PVN and ARC
- CCK released by I cell in response to fats and aa entering small int
- inhibit meal frequency and size
- both act on NTS to stim feeling of satiety
insulin and blood glucose levels for regulating satiety
- during cephalic and gastric phase increase insulin causes drop in blood glucose driving hunger through activation of NPY/AgRP
- int phase increase blood glucose and insulin increase act as satiety signal by activating aMSH/CART in articulate nucleus
marijuana and appetite
- prescribed to stim appetite in pts w chronic disease w no appetite (cancer, AIDs)
- enhanced sense of smell in mice
- indirect activation of NPY/AgRP neurons in ARC
- CB1 receptors in LH
energy output breakdown stats and types
heat 50%
- unregulated
- thermoregualtion
work 50%
1. transport across membranes
2. mechanical work-moving
3. chemical work
- synthesis for growth and maintenance
- energy storage: high- energy P bonds ATP, phosphocreatine, chemical bonds glycogen or fat
6 factors effecting overall basal metab rate (BMR)
- age and sex: male 1kcal/hr/kg, females 0.9kcal
- amount of lean muscle mass- decrease w age
- activity level-metab rate aboce BMR
- diet, diet induced thermogenesis: energetic cost of food digestion and storage differs between food components
- hormones: thyroid hormones considered MOST IMPORTANT determinant of BMR, influence oxygen consumption and heat production of most tissues in body
- genetics
3 categories of metab
- extract energy from nutr
- use energy for work
- store energy for later
fed state skeletal muscle
takes up glucose for energy use and stores glucose as glycogen (70% of body storage)
aa taken up for natural protein turnover
fed state liver
covert glucose to glycogen (24% body stores)
convert glucose to fa (transport to adipocytes)
aa used for synthesis and convert to keto acids (energy or fa synth)
fed state adipocytes
- take up dietary triglycerides from chylomicrons
- excess glucose taken up and converted to triglycerides
- stores triglycerides synth in liver
fed state is what type of metab
anabolism (build)
fasted state is what type of metab
catabolism (breakdown)
most cells utilize __ to spare __ for CNS
FA, glucose
fasted skeletal muscle
convert glycogen to G6P (glycogenolysis) for its own use
forms pyruvate and lactate
fasted liver
- glycogen converted to glucose and transported through body (glycogenolysis)
- produce new glucose from pyruvate, lactate, glycerol, aa (gluconeogenesis)
- convert fa to ketone bodies for energy usage
fasted adipocytes
lipolysis occurs, fa and glycerol enter bloodstream to be used as energy in most cells
