Hunger Flashcards
(151 cards)
1
Q
How is eating shut off?
A
Through a satiety system - we feel full.
2
Q
What is metabolism?
A
How we extract energy
3
Q
What is the Fasting phase of metabolism?
What is the main component the pancreas secretes during the fasting phase when we still need glucose in our bodies?
How is it converted into glucose?
A
Fasting Phase – how can we feed our cells when our gut is empty?
The pancreas secretes Glucogen, which transforms Glycogen into Glucose.
4
Q
What is Absorptive Phase of metabolism?
A
Absorptive Phase – what happens to the food we eat?
Carbohydrates
Proteins
Fats
5
Q
How do we keep ourselves going when we don’t have food in our gut? *Short-term reservoir
A
1) Short-term reservoir - Located in muscles and Liver - is stocked with Glycogen
> Glycogen, is the insoluble form of Glucose molecule that cannot diffuse through membranes.
> Glycogen is made from Glucose by Insulin.
> Insulin takes free-floating glucose and turns it into glycogen and stores into the reservoir.
6
Q
What converts glycogen into glucose?
Which phase does this occur?
Why would we need to convert it?
A
Glucogen
During fasting phase
We convert it when we need to use it as energy
7
Q
Glycogen is made from Glucose by __________.
A
Insulin
8
Q
What phase is glucagon active in?
Where is glucagon secreted from?
When is it secreted?
Why is glucagon secreted?
A
Glucagon is active during the fasting phase.
Pancreas
> secreted when detectors signals low glucose levels in blood.
> It’s secreted to allow glycogen to be converted into glucose (usable form)
9
Q
Why is pancreatic cancer usually deadly?
A
With the loss of pancreas, you cannot power yourself.
10
Q
During fasting phase, what is our body cells powered by?
What is our brain powered by?
A
Triglycerides, in our long-term reservoir (Adipose tissue)
Glucose
11
Q
What are triglycerides?
What happens as triglycerides are released?
A
3 fatty acid chains, connected through Glycerol.
When we release triglycerides from Adipose tissue, it gets pulled apart into the fatty acid chains, and glycerol is then converted into glucose. Then this glucose feeds our brain.
12
Q
During fasting phase, where does glucose come from?
A
Both short-term and long-term reservoirs.
13
Q
Why does the brain get all the glucose?
Why would there be a problem getting glucose into the body during the fasting phase?
A
1) Glucose is translated into ATP faster than fatty acid or carbohydrate chains.
2) During fasting phase, cells can’t utilize the glucose in blood because glucose only transports through glucose transporters.
The problem is that glucose transporters in the brain (astrocytes) don’t need a key to open them, but the glucose transporters in the body need the key, insulin, to enter the brain; this is why the brain can get glucose.
> During the fasting phase, insulin levels are low, relative to glucogon levels.
14
Q
What’s the breakdown of how our brain and body gets “fed”?
A
Brain - During the fasting phase the pancreas secretes GLUCAGON which converts stored glycerol into glucose
Body - Also, triglycerides from adipose tissue can be broken down into glucose and fatty acids
15
Q
When is short-term storage used?
A
When blood glucose levels get really low.
16
Q
Explain the steps of digestion during absorptive.
A
We digest - starts with mouth with enzymes in saliva. Goes to stomach.
Partially digested food is released through the duodenum (connection between the stomach and the small intestine) into the small intestine.
Nutrients are absorbed from the small intestine.
Indigestible material is formed into feces in the large intestine.
17
Q
Where is short term reservoir located?
What does the storage contain?
What is the synthesization and convertion process to and from glucose?
A
Located in liver and muscles
Contains glycogen (a complex, insoluble carbohydrate)
Glycogen is synthesized from glucose by insulin
Glycogen is converted back into glucose by glucagon
18
Q
What are the function of small intestines?
A
Small intestines – part of the immune system ; bacteria is blocked from absorption, toxins eliminated;
Macronutrients and vitamin absorbed here in different parts, so taking surgery to take this part out = specific vitamin deficiency
Colon – pulls out water
19
Q
Why is fiber important?
What’s the difference bw simple and complex carbohydrates?
A
Since it’s insoluble, it functions as a GI cleanser.
Increases peristalsis, which keeps food moving along.
Since complex carbohydrates have more fiber, there is more slow sustained release of macronutrients and blood sugar into bloodstream.
Simple carbs release blood sugar too quickly, resulting in spikes (makes sense when we talk about insulin and diabetes).
20
Q
What is carbohydrates broken into?
What happens once it’s broken into _______.
*Insulin
A
Carbohydrates are broken down into glucose - once it hits blood stream, the increase in blood glucose levels trigger the pancreas to release insulin.
Insulin opens up the glucose transporter cells in our body cells so it can pull the glucose, also converts glucose into glycogen to be stored in liver and muscles.
Also transports glucose into adipose tissue where it’s converted into glycerol, then into triglycerides.
21
Q
During absorptive phase levels of ___________ is much higher than levels of ___________.
A
Levels of insulin is much higher than levels of glucagon.
22
Q
Describe Type 1 and Type 2 Diabetes
A
Type 1 diabetes:
Cells that produce insulin in pancreas is degenerating.
Type 2 diabetes:
Fully functional cells stop producing insulin. Deuces (2) felicia.
Insulin dysregulation, but mechanism is different.
23
Q
If you change your diet, which diabetes can you reverse?
A
Type 2 diabetes.
24
Q
Why are diabetics always so thirsty?
Start with talking about Glucose transporters…
A
Diabetics obviously have insulin dyregulation.
Glucose must have a transporter (insulin) in the body to move around, because it is water soluble. Therefore, now there is increased tonicity in the blood.
Since diabetics cannot produce insulin, hormones signal to start pulling water from interstitial fluids, which makes you thirsty. The cells are saying, “you’re dying, we need more water”.
25
What's insulin's end goal?
What happens when we increase tonicity of the blood?
Insulin is not important for glucose, but really important for cardiac function, as it regulates the circulatory system.
Insulin's end goal is to maintain TONICITY of blood. By pulling in water from the Interstitial fluid (2nd biggest compartment) to balance the tonicity of the blood, we stress the heart out.
-When we increase food, we increase tonicity of blood, and every time we increase tonicity in blood, we pull water in to balance the tonicity, thereby, increasing stress on heart and arteries
>Important for blood pressure and energy partitioning (regulates which reservoirs it goes to)
26
Long-term Reservoir
- Adipose tissue
- Contains triglycerides (a soluble carbohydrate combination of fatty acids and glycerol)
- Fatty acids are used by body cells
- Glycerol is converted to glucose by liver to feed brain
27
Is glycerol a short-term reservoir or long-term reservoir?
What is the conversion process?
LT reservoir
-Glycerol is converted to glucose by liver to feed brain
28
How come the brain gets all the glucose?
Because glucose transporters in the brain does not need insulin, or the key, to open.
29
In body cells, how do glucose transporters work?
In the body cells, glucose transporters only work when it is bound to insulin.
30
During the absorptive phase the pancreas secretes ________.
It opens glucose transporters in cells
It converts excess glucose into which of the following, for storage?:
a. Glucogon
b. Glycogen
c. Glycerol
d. Glue
During the absorptive phase, the pancreas secretes insulin.
It converts excess glucose into glycogen for storage.
31
Which diabetes cannot be reversed?
Type 1 - cells literally have degenerated.
32
Type 2 diabetes is usually diagnosed when?
What leads to insulin resistance?
Type 2 diabetes is usually diagnosed in middle aged adults.
Obesity leads to insulin resistance.
33
What percentage of type 1 diabetes is diagnosed in USA?
5-10%
34
Which diabetes is usually diagnosed in children or young adults?
Type 1. Destruction of insulin producing cells.
35
What is the def. of diabetes mellitus?
Failure to move glucose out of blood supply due to insulin dysfunction.
36
What are the internal cues of eating?
+Peristalsis - really the small intestines are empty, not stomach)
+Glucose availability
+Quantities of stored fats (low long-term reservoir)
37
What are the external cues of eating?
+Food availability: We eat more, when there's food around us. The more food that is present, the more we eat (buffets).
+Smell - salivation preps our digestion system
+Conditioning -
Time of day: if I usually eat 11 am, looking at the clock at 11 am will make me hungry.
People: More people, more hunger... possibly competition?
38
Why does obesity problems continue? In other words, why is obesity so hard to fight?
Most treatments focus on internal cues rather than external cues. Calories in = Calories out... but it's not always right.
39
How are internal hunger signals detected?
There are 2 internal detectors: Brain detectors and Liver detectors.
1) The brain hunger detectors are in the brain side of the BBB, monitors glucose availability only. The receptors are located in the nucleus of the solitary tract (NST), and info about glucose levels is communicated to the Hypothalamus.
2) The liver detectors are in the blood side of the BBB, monitors availability of both glucose AND fatty acids. It primarily regulates release of insulin when glucose levels in bloodstream drop.
Communicates the nutrient availability (glucose and fatty acids) to the Nucleus of the Solitary Tract and the brain via. Vagus nerve.
40
What drives craving?
Why is it so hard to not give into these cravings?
*bacteria
Bacteria in our small intestines. They crave certain macronutrients and produce neuropeptides and hormones.
Bacteria have receptors for Neurotransmitters like Serotonin and Dopamine.
They also induce production of Serotonin and Dopamine in brain. If they are NOT getting what they want, they start to release TOXINS and which signals the brain of a deficit of a food that the bratty bacteria wants.
We are just puppets to their self-serving ways.
41
What are the main brain structures involved in hunger?
Where are they all very close to?
- Lateral hypothalamus
- Ventromedial hypothalamus
- Arcuate nucleus
- Paraventricular nucleus
All close to the 3rd ventricle
42
A lab rat got legioned in the Lateral Hypothalamus, what happens to this rat?
They starve to death, even with appetizing food, because they do not initiate eating.
They can be force-fed and will eat.
43
Electrical stimulation of the LH produces what?
Overeating behavior - non-stop until food is gone
44
Hunger signals coming from the liver and brain project to what?
The arcuate nucleus
45
In response to the hunger signals, the Arcuate Nucleus releases what?
The arcuate nucleus neurons release NPY and AGRP.
NPY induces ravenous eating and increases Insulin release.
The AGRP also induces eating. A tiny amount infused into the 3rd ventricle made rats eat for 6 days!
46
What does the NPY/AGRP neurons stimulate?
LH MCH/orexin neurons.
| Also increases eating behavior
47
AGrP is an _________ at receptors located in the Lateral Hypothalamus, called ______ receptors.
To decrease eating behavior, one idea would be to create a drug that is an ___________ at the MC4 receptors to block the effects of _____.
When stimulated, MC4 receptors produce what type of potential?
Stimulation of MC4 receptors decrease activity of _________________ neurons.
AGrP is an ANTAGONIST to receptors located in the Lateral Hypothalamus, also called MC4 receptors.
To decrease eating, create a drug that is an AGONIST to stimulate the MC4 receptors (αMSH), or just block the effects of AGrP.
When stimulated, MC4 receptors produce IPSPS- they decrease the activity of the NPY and AgRP neurons.
48
What type of cells secrete Leptin?
Once full, Leptin signals to the arcuate nucleus to _______ it.
What happens when there are low levels of Leptin?
Fat cells from the long-term storage, when full, secrete Leptin.
Leptin signals to the Arcuate nucleus to INHIBIT IT... no more food necessary.
When Leptin drops, the Arcuate Nucleus releases NPY and AgRP... and get increased eating.
49
Once Leptin drops and the Arcuate Nucleus releases NPY and AgRP, what does it communicate with?
What is being suppressed?
The NPY and AGrP communicates with LH and the paraventricular nucleus.
Pituitary hormones TSH and ACTH are suppressed.
50
What type of cells secrete Leptin?
Which cells are inhibited by Leptin?
What does it mean if Leptin levels drop?
Fat cells secrete Leptin.
Cells in the Arcuate Nucleus of the Hypothalamus is inhibited by Leptin.
This when fat stores are low, Leptin drops.
When Leptin drops, the Arcuate Nucleus releases NPY and AgRP.
The NPY and AGrP communicates with LH and the paraventricular nucleus. Then TSH and ACTH are suppressed.
51
What does the Nucleus of the solitary tract know?
How much glucose and fatty acids are available.
52
In response to knowing the glucose and fatty acid levels, the Nucleus of the Solitary Tract sends information to where?
What are the 2 things the Nucleus of the Solitary Tract regulates?
Arcuate nucleus
Lateral Hypothalamus
Paraventricular nucleus
1) To regulate how much we are going to eat and
2) whether or not we are in the Fasting or Absorptive phase.
>It influences the hormone release from the Pancreas, either Glucagon dominant or Insulin dominant.
53
How good are we estimating our blood glucose levels? What does this have to do with anything?
Terrible - our internal cues are not good at telling us how hungry we really are.
54
What are most of the protein amino acids used for?
Most of them are first converted into fats in LT storage and hang out in form of Triglycerides.
55
Insulin helps to convert free-floating glucose into ______________, to be stored in the liver and _______.
Insulin helps to convert free-floating glucose into glycogen, which is then stored into the liver and muscles.
56
Which macronutrient do we extract energy from?
Carbohydrates - Glucose!
57
Which levels are higher in the absorptive phase? Glucogon or Insulin?
Why?
Insulin - because once glucose hits the bloodstream, the pancreas signals the insulin. The insulin has many jobs. It's the key to opening the door to the glucose-transporter cells in the body, so that it can now pull Glucose from the bloodstream.
Insulin also helps to convert free-floating Glucose into Glycogen, so that it can be stored in the liver and muscles.
Insulin also shunts glucose into the adipose tissues, which converts it into Glycerol, and converted into Triglycerides.
Glucogen is used when Glucose is gone ;), or during the fasting phase.
58
During the absorptive phase, what converts triglycerides?
Insulin takes Glucose and shunts it into the Adipose Tissue, which then converts it into Glycerol, which turns into Triglycerides in this long-term storage.
59
What happens with insulin-producing cells before type 2 diabetes?
The cells are fully functional, but they STOP producing insulin. It starts when they stop listening to the signal - so the insulin producing cells start to OVER-PRODUCE because they think the cells are deaf... but the cells keep ignoring the signals, so finally, they just shut down business and stop producing all together.
A change of diet can get those cells to produce insulin again.
60
What are macronutrients oxidized by?
Can be oxidized by AceythlCoA and prep cycle to be converted into ATP.
61
What happens with insulin-producing cells before type 2 diabetes?
The cells are fully functional, but they STOP producing insulin. They stop listening to the signal - so they start to OVER-PRODUCE because they think the cells are deaf... but the cells keep ignoring the signals, so finally, they just shut down business and stop producing all together.
62
Insulin is trying to prevent us from getting _________ ________.
Heart attacks.
63
Why are diabetics so tired?
What does the body cells depend on? (answer first)
Why does insulin prevent fatty acids from feeding body cells?
You cannot get glucose into the body cells, so you're tired all the time.
The body cells depend on fatty acids, EXCEPT that the insulin keeps the fatty acids locked away, because when you break down triglycerides, you get both the fatty acids AND glucose... and insulin is like, oh hell no bitch, you already got too much glucose- we are not taking shit out of storage for you.
64
Why are unmedicated diabetics so skinny?
Because their body starts to leach all of the triglycerides in a desperate attempt to feed themselves.
65
What is insulin important for?
+Blood pressure regulation (tonicity maintenance to prevent heart attacks)
+Energy partitioning: Insulin determines where the energy stores go into and out of cells, brain, short-term, or long-term reservoir.
66
High levels of Glucagon signals what?
The fasting phase - signals that we haven't eaten in a while. Tells us to eat!
67
When Glucose is low, what is high?
Glucagon!
68
What are the effects of antibiotics on the gut?
It kills all bacteria, good and bad... so it gives us tummy troubles and poor nutrient absorption.
69
Why is it important to have a varied diet?
Omnivores have a more diverse population of bacteria, and makes it harder for 1 type of bacteria to grow larger and take-over.
70
How can fecal transplants change the way rats will eat?
By changing the way rats want to eat by manipulating the contents of their gut with fecal transplants.
71
What are the 2 phases of metabolism?
Fasting and absorptive phase.
72
What does Glucagon do for us in the fasting phase?
It has to transform Glycogen back into Glucose.
73
Where do most macronutrients end up? Does it stay there forever?
Long-term storage, in our fat.
It doesn't stay there forever... we are constantly pulling energy from this storage.
74
If we most of the stuff we eat end up in LT storage, how come most ppl don't get fat?
It is an "energy wallet" so we can constantly pull from it.
75
Most likely thing to kill a diabetic first is:
Heart attacks and strokes
76
Where does both the brain and liver hunger signals converge?
Nucleus of the Solitary Tract
77
When you cut out sugar, what happens? What happens when you give in?
Initially, the cravings are INTENSE. And VERY satisfying if you give in due to huge bursts of Serotonin and Dopamine.
If you cut out sugar, the intensity of craving dies down - mirroring the dying down of the bacteria.
78
The Lateral Hypothalamus functions mostly as...
An initiator of eating behavior.
79
Where does the Arcuate Nucleus receive signals from?
Where doe the Arcuate Nucleus send signals to?
What type of hormone does the Stomach produce?
The Arcuate Nucleus produces which 2 hormones?
The Arcuate Nucleus receives information about glucose and fatty acid availability from the Nucleus of the Solitary Tract.
The Arcuate Nucleus then passes signals to the Lateral Hypothalamus, to send signals to other areas of the brain, mainly in Medulla and Hypothalamus to reduce metabolic rate and induce eating.
The stomach itself secretes GRELIN. The amount of Grelin secreted is larger when I'm hungrier.
*Grelin, When the stomach's Growling.
The Arcuate Nucleus produces the NPY and the AGrP.
NPY - Signals to pancreas to produce insulin
AGrP - Increases eating behavior
80
If AGrP is infused into the LH or the ventricular system, what happens to the rat?
It eats more at every opportunity for almost a week.
81
What would a drug that acts as an AGONIST on MC4 cells do?
Why would be want a drug that does this?
AGONIST stimulates MC4 receptors that produces IPSPs - which increases inhibition.
This would work for increasing inhibition of eating behavior.
82
The Lateral Hypothalamus has 2 chemicals, what are they?
What happens when those cells are stimulated?
What is suppressed?
The Lateral Hypothalamus has 2 chemicals: NCH and Orexin.
When these cells are stimulated, they increase eating behavior, decrease metabolic rate, and suppresses release of thyroid-stimulating hormone (TSH) and adreno-corticotropic hormone (ACTH).
Important because TSH tells Thyroid to start spending energy instead of conserving, like the MCH and Orexin.
Then the ACTH tells Adrenal glands to produce Cortisol which increases metabolic rate through stimulation of the sympathetic NS. It also increases release of energy stores from both short-term and long-term reservoir - This is opposite of what we want because we are trying to FILL the reservoirs, not SPEND it all away.
83
Who are liberals and Republicans?
TSH (thyroid-stimulating hormones)
MCH
Orexin
MCH and Orexin are Republicans, don't want to spend anything and keep it all for themselves...
TSH are liberals, want to spend it all!
84
If we suppress MCH and Orexin, will we eat more or less?
If we suppress MCH and Orexin, we would get less eating.
85
If there was a drug that INCREASED Leptin, what would this do?
Suppress eating - Leptin inhibits the Arcuate Nucleus, which in turns communicates with food inducing behavior neurons NPY and AGrP.
86
What will determine whether I eat half a sandwich or a whole sandwich plus a bag of chips, and then a cookie RIGHT NOW?!
Grelin from my stomach secretions, and all the information from the NST (tracking my glucose and fatty acid levels) has a great impact on the amount of food you eat at a given meal RIGHT NOW.
87
How is leptin different from Grelin?
*How much I eat...
Leptin has a greater impact on nutrient consumptions. Higher leptin levels will cause me to eat less, lower leptin levels make me eat more food, more frequently.
88
If I created a drug to help people lose weight, what is better:
a. Blocking Grelin
b. Mimicking Leptin
Mimicking Leptin - It's a long-term signal and will have more influence on overall pattern of eating.
89
Why is it better to eat 5 small meals a day vs. 2 large meals?
+Keeps blood sugar leveled, which means our Insulin is leveled, and since it's a Satiety signal... the higher insulin levels are, the fuller we feel.
+Also affects Grelin levels - The longer it's been since I've had a meal, the stronger the Grelin signals are. Waiting 5 hours to eat will make me overconsume.
90
Describe the different satiety signals in the Short-term reservoir and the Long-term reservoir.
Short-term satiety signals are related to Glycogen levels and fulfilling immediate cell needs.
Long-term satiety signals are based on general level of how filled my long-term storage (adipose tissues) are. This influences eating patterns over longer periods of time.
91
If we are trying to help ppl lose weight, do we want to go after short-term satiety signals or long-term satiety signals?
Long-term satiety signals since it influences eating pattern over longer periods of time.
92
Define satiety mechanisms.
It is a brain mechanism that causes cessation of thirst or hunger, produced by adequate supplies of water or nutrients.
93
How do we figure out we're full?
*detectors
+Receptors in mouth detect EFFORT (why ppl say chewing gum helps to curb hunger)
+Detectors in esophagus
+Stretch receptors in the stomach (why ppl drink water before eating meal and provokes satiety signal to signal that you're full).
94
Why are we satiated when we eat foods high in fat?
When we eat foods high in fat, the duodenum releases CCK - a powerful satiety signal.
95
What is the function of the CCK?
Is it a hunger signal or satiety?
+It is a satiety signal, and therefore promotes insulin production
+Causes release of bile from ball gladder (to break down fats)
96
Which 1 initiates eating?
CCK agonist
CCK antagonist
Why?
CCK antagonist initiates eating - because it is an antagonist to a satiety signal (which tells us we are full). So if we are blocking something that tells us we are full, we are going to keep eating.
97
What happened to the rat when it's Ventral Medial Hypothalamus (VMH) was legioned?
Legions of the VMH = Very much hungry for delicious foods.
The rats overconsumed but are PICKY to just delicious foods.
98
What's the diff. between a rat that's been stimulated in the LH vs. the VMH?
Lh stimulations cause rats to eat ANYTHING - like plastic and wood.
VMH stimulations cause rats to eat FOOD, delicious foods. It's just less extreme than stimulations to the LH.
99
What pathways are you disrupting when lesioning the VMH?
Disrupt the pathways between the Nucleus of the Solitary tract and the Paraventricular Nucleus...
100
What happens when there's a disruption between the pathways of the Nucleus of the Solitary tract and the Paraventricular Nucleus...
Excess insulin production - shows signs of Type 2 diabetes.
101
What are the "lets have lunch" chemicals?
What are the "no thanks I'm full" chemicals?
Let's have lunch = NPY and AGrP
No thanks, I'm full = αMSH and CART (cocaine - amphetamine related transcription)
102
High leptin levels stimulate the release of what?
What does it suppress?
Stimulates the αMSH and CART - which inhibits the neurons in LH and PVN
It suppresses the NPY and AGrP to stimulate neurons in LH and PVN
103
Which of the following stimulates the release of TSH and ACTH by the pituitary gland, raising metabolic rates?
a. NPY
b. CART
c. (αMSH
d. AgRP
αMSH and CART
104
αMSH is an Agonist for what receptor?
| What would this do?
αMSH is an AGONIST for the MC4 receptors - will inhibit eating.
105
What is the satiety signal coming from the small intestine that inhibits NPY and AGrP (let's have lunch neurons)?
The PYY hormone - Pretty Yum Yum
106
What does the Paraventricular nucleus do when it is inhibited?
* Insulin
* Metabolism
When inhibited, the paraventricular nucleus (PVN) increase insulin production to get rid of all the stuff hanging out in blood... and increase metabolism.
107
Concerning the difference between the mechanisms of hunger and satiety, which Nervous system is activated in each mechanism?
Hunger mechanism = parasympathetic, we are in an anabolic state- body stores nutrients and energy.
Satiety mechanism = sympathetic, we are in a catabolic state - body expends nutrients and energy.
108
Concerning the difference between the mechanisms of hunger and satiety: TSH and ACTH from the pituitary gland is suppressed or activated?
Hunger mechanism = TSH and ACTH is suppressed - lowered metabolic activity
Satiety mechanism = TSH and ACTH is activated, higher metabolism activity.
109
Consider the difference between the mechanisms of hunger and satiety- how is MC4 receptors in the Hypothalamus involved?
Hunger mechanism = AgRP blocks MC4 receptors in the LH - stimulating eating behavior.
Satiety mechanism = αMSH stimulates MC4 receptors in LH - suppressing eating behavior.
110
The percentage of obese Americans jumped from ___% in 1991 to ____% in 2001.
What percentage is obese and overweight now?>
The percentage of obese Americans jumped from 12% in 1991 to 21% in 2001.
According to Trevitt, about 30% are obese and 2/3rds are overweight.
111
How many Americans are diagnosed with anorexia or bulimia?
Just 1-3%
112
The BMI is what type of ratio?
Height to weight.
113
According to the BMI, body fat of more than ___% for women and ___% for men is obese.
Body fat of more than 32% for women and 25% for men is considered obese.
114
What part of the brain shrinkage is linked to obesity?
Temporal lobe
115
Why is glycogen stored in muscles?
We are pulling it for short bursts of energy.
116
Dr. Trevitt went to the gym early morning on an EMPTY stomach and decides to start doing bench presses.
What type of energy source is she running on?
Why is this bad?
She is running on fatty acids (from long-term storage).
Her muscles give out because she ran out of glycogen (there was nothing in her muscles!)
117
Where does the Nucleus of the Solitary Tract live all by its lonely self?
In the medulla
118
What happens when you legion the LH?
Starve to death
119
When MC4 receptors are stimulated, it inhibits eating in the LH, so what does this mean about AgRP?
AgRP blocks the MC4 receptors (IPSP receptors) - increasing the activity in LH.
120
What happened to the rat when it's Ventral Medial Hypothalamus (VMH) was legioned?
What happens when the VMH is stimulated?
When the VMH is legioned, the rats eat...
If VMH is stimulated, the rats starve..
121
What is the opposite hunger signal from Grelin?
What does this signal inhibit?
PYY - whereas Grelin tells us we're hungry (hunger signal), PYY tells us we're full (satiety signal)!
PYY inhibits the NPY/AgRP signals
122
When we talk about satiety cues between short term vs. long term, between PYY and Leptin, which is short term and long term signal?
PYY is short term signal, tells us we have food RIGHT NOW.
Leptin, long term. Tells us we have plenty of energy resources.
123
What are some environmental reasons why people are obese?
Learned behavior - plate cleaners ignore their internal cues (CCK, insulin, leptin)
Overnourishment - decreases anti-eating effects of Leptin
Toxins - pesticides make you fat
124
Adenovirus-36- antibodies found in obese ppl, suggests what?
That ppl who are exposed to these anti-bodies can change gene transcription (epigenetics)
125
Which one of the trans fats are found in vegetable oil:
Omega 3
Omega 6
Omega 6 - bad for you
126
Why was it easier to be skinny in the 70's than now - even though we ate the exact same calories; etc?
Maybe due to the different types of pesticides and toxins that we find in our food NOW.
127
Besides helping us to avoid heart attacks, what else does insulin do in terms of fat storage?
Insulin makes us really fat - fat cells are less resistant to insulin and participates in lipidogenesis, helping to make even more fat cells.
128
What are the important functions of insulin on the following macronutrients:
Carbohydrates
Protein
Fat (LPL, Triglycerdies, HPL, estrogen)
+Carbohydrates
- Promotes entrance of glucose into cells
- Converts glucose to glycogen for short-term reservoir
+Protein
-Increases protein storage in muscles (amino acids for protein synthesis)
+Fat
-Activates enzyme lipoprotein lipase (LPL) which increases entry of fatty acids into cells = increasing ingredients for Triglycerides
>Triglycerides are synthesized INSIDE the fat cells… so to access the glucose and fatty acids, it gets broken down and released into the blood stream…. That is done by the HPL.
+However, Insulin Suppresses activity of hormone-sensitive lipase (HPL) - suppresses the break down of triglycerides in fat cells.
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What happens when insulin suppresses HPL (hormone-sensitive lipase)?
Which hormone is it sensitive to?
It suppresses the break down of triglycerides in fat cells.
>Sensitive to estrogen… which is why females have variations of adipose tissue… packs away fat during ovulation!
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Why would someone with insulin dysregulation suffer from fatty liver disease?
Due to increased conversion of glucose into fatty acids in liver, there is an increased formation of triglycerides in liver.
Some accumulates at liver (i.e., fatty liver disease) – alcoholics…
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What is Sucrose made of? What is it?
50% glucose
50% fructose
It's table sugar
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What is HFCS made of?
55% fructose
45% glucose
More fructose...
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How is fructose and glucose different?
* Insulin
* Metabolized where?
+Fructose doesn't stimulate insulin production as much as glucose - so there's less satiety, so you're less satisfied.
+Fructose promotes insulin resistance.
+Fructose is metabolized in the liver, into Triglycerides. Build-up of triglycerides = fatty liver disease.
+Fructose inhibits ENOS, which is necessary in producing Nitric Oxide - helps to dilate blood vessels to open up the arteries for tonicity- Can lead to cardiac issues.
+Fructose increases AGEs -increases inflammation, oxidative stress, and accelerate aging.
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What are the genes that are specific to obese people?
Obesity (ob) gene on chromosome 4 (one form, while none obese ppl have alleles)
- Diabetes (db) gene on chromosome 6 (one form, while none obese ppl have alleles)
- Uncoupling protein (UcP)
- Mutations in the MC4R gene (one form, while none obese ppl have alleles) – 6% of obese population
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What happened when the Ob (obese) mouse was connected to normal weight mouse?
The Ob (obese) mouse lost weight and became normal weight - nothing happened to normal weight mouse.
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What happened when the Db (diabetic) mouse was connected to normal weight mouse?
The normal weight mouse became underweight - nothing happened to Db mouse.
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What happened when the Ob (obese) mouse was connected to Db (diabetic) weight mouse?
The Ob (obese) mouse loses weight - nothing happened to Db mouse.
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What does it indicate when Obese (ob) mouses were losing weight when connected to Diabetic mouses (db)?
The Ob mouse doesn't produce Leptin - It's a leptin problem, but it is sensitive to leptin. So getting a signal from the Db or normal mouse made it regulate it's storage levels; etc.
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What did the franken-rat experiments indicate about Db (diabetic) mouses?
The Db mouse produces lots of Leptin, but is NOT responsive to it. The Db genes seem to affect Leptin RECEPTORS.
We know this bc when a normal weight mouse was connected to the Db mouse, it lost weight.
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Basal Metabolic Rates (BMR) accounts for ___% of energy expenditure in an avg. sedentary person.
BMR accounts for 75% of energy expenditure in an avg. sedentary person.
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What determines whether I eat a plate of steak and green beans vs. a plate of donuts.
Depends on how long it's been since I've eaten, my glucose and fatty acid levels; etc.
I will eat the donut as long as they're available.
Foods that signal high resources in form of glucose or fat (sweet fatty things), are way more appealing to us.
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Is it easier to predict whether a group of participants will eat a plate of desserts or carrots?
Easier to predict carrots - candy and desserts are eaten by ppl regardless of other factors like their hunger level. As long as it's there, they will eat it.
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Calories in and calories out is not always:
a) Independent
b) Dependent
Is not always Independent, when we alter 1, the other 1 alters as well.
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What is the heritability estimate for weight?
50-90%
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What's wrong with the ob/ob mouse?
He doesn't make leptin, even if he's sensitive to it.
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What's wrong with the db/db mouse?
He makes tons of leptin, but isn't sensitive to it.
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Why is exercise the best treatment for obesity?
* Metabolism
* Muscles
* Cortisol
We burn more calories (especially from ST energy), and even after we stop, our metabolism remains high - THEN we pull from the LT storage.
Muscles also use up tons of energy and also consume fatty acids like triglycerides.
Initial high levels of cortisol due to activation of Symp. NS, - this good bc we're pulling the Glycogen out of ST storage. After we exercise though, there is a decline of cortisol. Low Cortisol levels will help us not store fat.
Boosts serotonin levels - satiety signal. We feel more satiated towards food.
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What are the similarities between obesity and Addiction?
They both have reduced D2 receptors in the prefrontal cortex. Lack of inhibition = impulse control.
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What percentage of body weight is anorexics, compared to normal weight ppl?
What percentage will die?
Symptoms?
Causes?
Treatments?
85% of normal weight
10% will die
Symptoms: Obsessed with food, ceased periods, soft downy hair (Lanugo), increased exercise, distorted body image of just themselves.
Causes: Culturally driven? Genetic? Basal ganglia disruptions (OCD)
Treatments: Serotonin antagonists to reduce feelings of satiety - to induce eating.
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Bulimia:
Causes?
Treatments?
Causes: Anxiety coping mechanism?
Treatments: Some success with 5-HT agonist like fluxetine (Prozac) OR anti-anxiety/depressants like SSRI
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What type of disorder is anorexia? How about bulimia?
Anorexia is a weight disorder, while bulimia is an eating disorder.
