1/21
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
how is energy balance achieved
settling point - focused on environment and behaviour, system without active feedback control of food intake and energy expenditure
to help explain why overweight and obesity are more than problems of metabolism, humans are more related to the patterns of diet and PA that people settle into habits based on the interaction of genetics and environment
passively adapts and this and the set point can exist at the same time

how is this balance achieved
set point - feedback control system to regulate a particular variable to match a specified target
says the body has an integral control mechanism which is the set point that regulates metabolism to maintain a certain level of body fat
there can be an active compensation to weight loss or gain
more tighlty controlled and faster when it comes to going back to steady state

what are the variables related to body fat that may be regulated
body weight
body fatness
body temp.
energy intake
energy expenditure
energy balance

what are some reasons we eat or spend energy
to maintain homeostasis
long term vs short term (more related to gut function and how much we can store)
pleasantness of food (hedonics)
emergency circuits - hypoglycemia, stress, inflamation
cognitive control
-doesnt function in isolation and can be overwhelmed by other needs

what are 3 ways we measure appetite
Hunger
• sensations that promote food consumption and is multidimensional with metabolic, sensory, and cognitive facets
Satiation
• following initiation of a meal, eating proceeds, hunger subsides while satiation, the sensations that govern meal size and duration become increasingly dominant, feelings of satiation will contribute to cessation of eating and begin a period of abstinence from eating - intermediate stage
Satiety
• sensations that determine the intermeal period of fasting are termed satiety
orexigenic vs anorexigenic
Orexigenic
• Having a stimulating effect on the appetite.
Anorexigenic or anorectic
• Causing loss of appetite.
agonist vs antagonist
Agonist
• chemical that can combine with a receptor on a cell to produce a physiologic reaction typical of a naturally occurring substance.
Antagonist
• chemical substance that interferes with the physiological action of another, especially by combining with and blocking its nerve receptor.
what are ways we can measure appetite
brain imaging
biomarkers
food intake
questionnaires
all 4 have limitations
most common is visual analogue scales (VAS)

what are some peripheral signals with energy balance regulation
leptin, insulin, glucagon, ghrelin, PYY, CCK, GLP-1, GIP
KNOW: What they are, Where they are secreted, When they are secreted, How does they affect EE or EI
what is leptin, what does it do, and where is it secreated
protein secreated from adipose tissue
concentration is porportional to fat mass
leads to decrease in food intake (anorexigenic, increase in EE) and weight loss
tracks food intake and fasting, most obese ppl are leptin resistant not deficient
what happens if you treat obesity with leptin
it depends
Ob/Ob rats = leptin deficient
Db/Db rate = leptin receptor deficient
many obese ppl treated with leptin didnt show major/consistent weight loss, a lot of variability, they have leptin but their brain isnt responding to it
but it can potentially help with weight loss maintenance
what is insulin, where is it secreated, and what does it do
peptide hormone secreated by beta cells of pancreas
increases in response to glucose load porportional to fat mass
insulin crosses blood brain barrier (BBB) and reduces appetite or increases EE
less effective in obese or type 2 diabetes
if you have too much it can cause hyperglycemia and low blood sugar which is an emergency circuit
what is glucagon, where is it secreated, and what does it do
• Peptide hormone secreted by the α-cells of the pancreas
• Main role as counter-regulatory hormone (protect against hypoglycemia) but also secreted during meals.
• Glucagon crosses blood brain barrier (BBB) and reduces appetite or increase EE.
• Increases free fatty acid deliver to liver, but in some conditions can contribute to fatty liver disease.
secreated with higher protein meals which counteracts the release of insulin
what are the GI tract peptides
ghrelin
peptide YY - PYY
glucagon-like-peptide1 - GLP-1
gastric inhibitory polypeptide - GIP
cholecystokinin - CCK
what is ghrelin
• Peptide synthesized predominantly in stomach specifically from fundus
• Stimulates growth hormone (GH) and helps prevent muscle breakdown, levels rise with fasting and fall with feeding
• Increases food intake (orexigenic), stimulates hunger
what is peptide YY
• Secreted from small and large bowel (member of neuropeptide Y family; NPY)
• Released after feeding and leads to reduced food intake
lower in obesity
what is glucagon like peptide 1
originally approved for type 2 diabetes and now approved for weightloss
hormone in body, in ozempic its GLP-1 RA (receptor agonist) which stays in the body longer
• Co-secreted with PYY in response to nutrients in the gut
• Inhibits feeding
• “incretin” = increase in the amount of insulin released when glucose levels are normal or particularly when they are elevated
• Enhances insulin secretion, suppresses glucagon after a meal

what is gastric inhibitory polypeptide
• Now also known as glucose-dependent insulinotropic polypeptide (GIP)
• Weak inhibitor of gastric acid secretion, secreated earlier in intestine
• GIP & GLP-1 belongs to a class of molecules known as incretins (stimulate
insulin release on oral food intake)
• Secreted by K cells (duodenum and the jejunum)
• Mechanisms of weight loss not large on its own, but seems to enhance effects of GLP-1
• Interesting to note that, unlike GLP-1 receptor, GIP receptor is expressed in fat cells

what is cholecystokinin
• Petptide hormone that inhibits feeding. May have CNS effect and slowing of gastric emptying
• Secreted from I cells in the duodenum
• May synergize leptin’s action
more short term effect and can decrease meal size but there is a compensatory increase in meal frequency
what does the hedonic food intake regulation include input from
Endocannabinoid and Opioid Systems
Dopamine and Serotonin
there are multiple pathways in the CNS that effect energy balance

what happens when you increase PA
theres a decrease in our NEAT to try and maintain a balance
what is a summary of energy regulation
Many peripheral & central signals affect EE/EI
EE/EI for homeostatic & non homeostatic reasons
In human it seems that
Homeostatic systems “kick in” to prevent weight loss
Hedonic (pleasure) may have more of a to favor weight gain