GI 8 Flashcards
Aside from social and cultural factors what does short term regulation of feeding behaviour depend on
How long it has been since the last meal and how much we consumed at that time
After meal
Decreased orexigenic (food seeking behaviour)
Increased satiety after meal
In hours following meal
Decreased satiety
Increase orexigenic
What acts on long term regulation of feeding behaviour
Ghrelin, gastric distension, CCK, insulin/glucose
When and where ghrelin released
By cells in stomach in response to emptying (less distension)
What does ghrelin stimulate
NPY/AGRP containing neurons in arcuate to increase feeding behaviour
What will ghrelin injection stimulate
Food intake
Mice lacking NPY/AgRP neurons
Will not respond to ghrelin
What is gastric distension sensed by
Mechanosensory neurons
Where is gastric distension info sent to
NTS which has connections to PVN and ARC
What is CCK released by
I cells
What is CCK released in response to
Fat and amino acids entering small int
CCK does what
Inhibits meal frequency and size
What do both gastric distension and CCK act on
NTS to stimulate the feeling of satiety
During cephalic and gastric phase increased insulin
Causes a drop in blood glucose driving hunger through activation of NPY/AgRP neurons
During intestinal phase the increased blood glucose and increased insulin acts as
Satiety signal through activation of aMSH/CART neurons in arcuate nucleus
Why did marijuana cause munchies in mice
Enhanced sense of smell
Why marijuana causes munchies in humans
Indirect activation of NPY/AgRP neurons in ARC
- CB1 receptors in LH
Energy output
Heat 50%
Work 50%.
How is energy input measured
Bomb calorimeter
How is bomb calorimeter used
Heat released from burned food is measured
Heat needed to raise temp of 1L of water by 1C
One kilocalorie
Why is bomb calorimeter a slight over estimation
Do not completely digest and absorb most foods
Energy output=
Work+heat
Two ways of measuring energy output
Direct calorimetry (most accurate)
Indirect calorimetry
What does direct calorimetry measure
Amount of heat person produces
What does indirect calorimetry measure
O2 consumption or CO2 production
An individuals lowest metabolic rate
Measured as resting metabolic rate (RMR)
Basal metabolic rate
Amount of energy just to be alive
6 factors affecting overall metabolic rate
- Age and sex
- Amount of lean muscle mass
- Activity level- metabolic activity above BMR
- Diet, diet induced thermogenesis
- Hormones
- Genetics
Age and sex
Male 1kcal/hour per Kg of body mass, females 0.9 kcal/hour/kg
Diet induced thermogenesis
Energetic cost of food digestion and storage differs between food components (ie. diet high in protein)
Hormones
Thyroid hormones considered biggest determinant of BMR, influence O2 consumption and heat production of most tissues in body
Metabolism
Sum of all chemical reactions in body
3 categories of metabolism
- Extract energy from nutrients
- Use energy for work (transport, mechanical, synthesis)
- Store excess energy for later use
Energy metabolism during fed state
Mainly anabolic
Taking small molecules and converting to larger storage molecules
Where is glucose stored
As glycogen in liver and muscle
Converted to triglycerides for liver and adipose
Where is fattty acids stored
Liver and adipose tissue as triglycerides
Where are amino acids stored
Liver as fatty acids
Muscle ad other cells as protein
How many carbs, proteins and fats can be stored
Finite amount carbs and proteins
Unlimited to store fats so all excess converted to fatty acids
Skeletal muscle storage fed state
Glucose for energy usage and stores glucose as glycogen (70%)
AA’s taken up for natural protein turnover
Liver fed state
Converts glucose to glycogen (24%)
Convert glucose to fatty acids (to adiposcytes)
AAs used for synthesis and converted to keto acids
Adipocytes fed state
Dietary triglycerides from chylomicrons
Excess glucose taken and converted to triglycerides
Store triglycerides synthesized in liver
Glycogen stores can sustain activity for
Quiet activity for only a few hours
Proteins can sustain activity for
Potentially long periods but decreased protein levels eventually compromise cellular function
Fats can sustain activity for
Approximately 2 months
During fasted state between meals what occurs
Catabolism to utilize stored energy
What is maintaining glucose levels important for
Nervous system functioning
- most cells utilizes FAs to spare glucose for CNS
Skeletal muscle fasted state
- can convert glycogen to glucose-6-P (glycogenolysis) for own use
- forms pyruvate and lactate to make more glucose
liver in fasted state
- glycogen converted to glucose (glycogenolysis) and transported throughout body
- produced new glucose from pyruvate, lactate, glycerol and certain AA’s
- converts FA to ketone bodies for energy
Adipocytes during fasted state
Lipolysis occurs
Fatty acids and glycerol enter bloodstream to be used as energy in most cells
Hormones are primarily dependent on
Blood glucose concentration
Review of fed state
- glucose primarily used by cells
- glycogenesis (liver and muscle)
- lipogenesis
- AA uptake and protein synthesis (muscle)
Fasted state review
- FAs used by most cells for energy
- glycogenolysis (liver and muscle)
- lipolysis
- gluconeogenesis
- ketogenesis
- protein degradation
Hormone during fed state
Insulin
Hormone during fasted state
Glucagon
What drive anabolism (fed state)
Insulin
What increases insulin secretion
Increased plasma glucose, plasma AAs, plasma GLP-1, parasympathetic activity
What secretes insulin
Beta cells
During increase insulin what happens in most tissues
Increased glucose uptake
Increased AA uptake
Increased protein synthesis
Decreased protein breakdown
What does increased insulin cause in adipose tissue
Increase fatty acid and triglyceride synthesis
Decreased lipolysis
Increased insulin affects on liver and muscle
Increase glycogen synthesis
Decreased glycogenolysis
Increased insulin affect on liver
Increased fatty acid and triglyceride synthesis
Decreased gluconeogenesis
How do beta cells get activated by increased in glucose to drive insulin secretion
Increase ATP production in response to elevated glucose results in blockage of some ATP-K leak channels
K leakage drops and cell retains K and cell depolarizes causing Ca to enter cell and trigger exocytosis of insulin
How does glucose enter beta cells
Facilitated diffusion
What is the insulin receptor
Tyrosine kinase receptor
The tyrosine kinase receptor causes
Insertion of glucose transporter (glut 4 usually internalized)
Increase or decrease metabolic enzyme activity
What regulates fasted state
Glucagon
What does glucagon promote
Catabolism
What is fasted state stimulated by
Decreased plasma glucose
Sympathetic activity
What cells have G protein coupled receptors for glucagon
Alpha cells in pancreas
What does catabolism cause
Adenylate cyclase pathways
Changes in enzymatic activity
What does increased glucagon do to liver
Increase glycogenolysis, gluconeogenesis, ketone sysnthesis, protein breakdown
Decrease glycogen synthesis, protein sysnthesis
What does increased glucagon cause in adipose tissue
Increase lipolysis
Decrease triglyceride synthesis
