Metabolism/metabolism Quiz Flashcards
From GI tract, glucose enters the bloodstream and effects the muscle by: (absorptive)
Biggest atp producer from glucose and stored as glycogen (by glycogenesis)
From GI tract, glucose enters the bloodstream and effects the fat by: (absorptive)
Glucose is oxidized for atp or converted to triglycerides (lipogenesis)
From GI tract, glucose enters the bloodstream and effects the liver by: (absorptive)
Glucose stored as glycogen and converted into triglycerides
Triglycerides are not stored in the __ long term
Liver
Liver gets its ATP from ( absorptive state)
Amino acids
Primary site of triglycerides
Liver
From GI tract, glucose enters the bloodstream and effects the brain by: (absorptive)
Glucose oxidized for atp
From GI tract, amino acids enters the bloodstream and effects the muscle by: (absorptive)
Replace lost protein and build new protein in muscle to replenish what was lost in post absorptive state
From GI tract, amino acids enters the bloodstream and effects the liver by: (absorptive)
Amino acids are oxidized to atp or converted to triglycerides
From GI tract, amino acids enters the bloodstream and effects the fat and brain by: (absorptive)
AA Build new protein in the cell
Triglyceride is synthesized in the ___ and exported to ___ for long term storage
Liver, adipose tissue by VLDL
How does liver and adipose tissue make triglycerides from excess glucose?
In the liver and adipose tissue, Glucose is broken down into glycerol backBone (3 C) + fatty acids = triglyceride
How does liver and adipose tissue make triglycerides from excess amino acids?
- In liver cell, amino acids are deaminated
- NH3 (ammonia) which is toxic, converted to urea
- Amino acid converted to keto acid
- Keto acid is converted into atp for liver and to glucose to make triglyceride
Amino acids are converted into Keto acid before…
Oxidized for atp and converted to triglyceride
Once triglyceride enters GI tract and into bloodstream it….
- Liver produces VLDL (newly synthesized fats)
- VLDL is then stored in adipose tissue for long term
- Chylomicrons in blood come from fat absorption of dietary fats
- Fat of CM dissolves in blood
- CM is stored in adipose tissue for long term
Why do VLDLs and CM’s dissolve in the blood or are more soluble?
Their phospholipid is a mono layer (polar head faces water and hydrophobic faces fat)
In a regular cell, the inside and outside environment is mainly __ which is why it’s a bilayer
Water
Chylomicrons=
Come from:
Carry:
Taken up by/converted into:
Come from: SI
Carry: dietary fats
Converted into CM remnants that are taken up liver and remaining triglyceride is packaged into VLDL
Chylomicron remnants release…
Cholesterol and triglycerides
VLDLs:
Come from=
Contain/carry=
Transport=
Come from= synthesized by liver
Contain/ carry: triglycerides made from excess AA and glucose, triglyceride found in CM remnant
Transport= leave liver, into blood, and deposit triglyceride into adipose tissue for long term storage
VLDLs carry what two things
Newly synthesized triglyceride and dietary triglyceride
Explain how glycogenesis in liver prevents large spikes of plasma glucose after a meal:
Glucose is stored as Glycogen in liver and skeletal muscle
-removing excess glucose from plasma and storing it as glycogen helps lower plasma glucose in absorptive state
Very heavy to store
Glucose
Explain how lipogenesis in liver prevents large spikes of plasma glucose after a meal:
Triglyceride formed from glucose and excess amino acids; formation of triglycerides from excess glucose helps lower plasma glucose in absorptive state
Fat/triglycerides are what kind of energy storage? Heavy or lighter than glycogen? Easier or harder to access?
Large potential energy storage
Lightweight
Energy harder and slower to access
What stimulates insulin release (4 things)
- Increase in plasma glucose levels (insulin can then pull glucose out of blood plasma)
- Increased plasma AA
3 . Feedforward effects of incretins - Increased parasympathetics, decreased sympathetic activity
Explain the Feedforward effects of incretins (GI hormone) in releasing insulin…
Anticipatory (main stimulus not there yet), says that glucose plasma will rise
1. Incretins get released in blood and circulate to pancreas even if glucose in plasma looks normal
2. Senses what you’ve eaten and what levels are high
Prepare for elevated glucose levels in plasma
Intecrins
Functions of insulin
Increases glucose transport into muscle, liver, fat
Suppresses gluconeogenesis (production of glucose)
Inhibits lipolysis (fat release from adipocytes)
Why don’t we want lipolysis when glucose is high?
We don’t want the body to use fats to make energy (want body to use glucose and pull glucose out of plasma)
How does insulin increase glucose transport into muscle, liver, and fat?
Insulin binds receptor on cell surface—> inserts glucose transporters in membrane —> glucose exits blood
Glucose can’t pass into cells of muscle, and fat unless…
Insulin is present (besides the brain)
What are the problems with the absorptive state?
- Increase plasma glucose levels after meal
- Increase plasma fatty acids and amino acids
Why is too much glucose in plasma bad
Glucose is acidic and too mushy can acidify blood and damage Blood vessels
Why is increasing plasma fatty acids and AA bad
Can lead to atherosclerosis, proper fat storage required for healthy body, muscle needs amino acids to replace proteins lost in absorptive state, amino acids need for cell growth and repair
What is insulin’s effect on the liver tissue?
- Stimulates activation of hexokinase
- Changes shape or glucose and maintains high influx of glucose
- Phosphorylates glucose before entry into cell
- Activates Intracellular pathways to keep moving glucose into cell
Helps maintain the concentration gradient for glucose movement
Hexokinase
What are insulin’s effects on muscle and fat?
Binding of insulin on receptors on cell membrane inserts glucose transporters into plasma membrane
- allowing for glucose movement, down gradient into cell
Insulin is what kind of hormone
Protein
In muscle and fat, glucose transporters are stored….
In liver, glucose transporter are…
How are they different?
In muscle and fat, glucose transporters are stored Intracellularly and are only present when insulin is present
In liver, glucose transporters are in membrane all the time (no translocation)
Due to insulin deficiency, autoimmune disease that destroys B cells
Type 1
Due to development of insulin resistance, leads to long term effects of kidneys, BV, and nervous system
Type 2
Diabetes results in what level of glucose
Too high
Insulin comes from…
Pancreas, islet or langerhan (beta cells)
Beta cells secrete….
Insulin which lowers plasma glucose back to normal
Pancreas plays a role in…
Blood glucose regulation and releasing HCO3 and digestive enzymes
Glycogen is what kind of energy source
Rapid
Signal transduction pathway is NOT initiated and glucose transporters remain in intracellular vesicles–increase plasma glucose: in which form of diabetes
Both
What tests are used to diagnose diabetes?
Hemoglobin A1C and Glucose Tolerance Test
Blood test that measures the total amount of glucose bound to hemoglobin in bloodstream
Hemoglobin A1C
Marker of hemoglobin modification by glucose
Glycation in Hemoglobin A1C test
What indiciates diabetes in Hemoglobin A1C test?
increase glucose in blood, increase hemoglobin glycation
Insulin resistance is the greatest predictor of
type 2 diabetes
Fast overnight, ingest a large amount of glucose (75 g), watch how quickly your body is able to remove glucose from the bloodstream over time
Glucose tolerance test
In type 1 diabetes, if given ___ than their glucose levels can come back down
insulin injection
In type 2 diabetes, if given insulin injection…
not much change in high glucose levels
AGE formation how?
Glucose binds proteins
What happens when AGE binds a receptor (RAGE) for activation?
- Increase oxidative stress
- Increase inflammation
- Endothelial damage and increased permeability
- Reduction of NO–> limits vasodilation
When hyperglycemia occurs, what forms as a result?
AGE and H2O2 (oxidative stress)—These activate PKC
What is the role of PKC?
Activates vasoconstriction of blood vessels by communicating with smooth muscle
Common symptoms seen in the clinic for a patient with type 2 diabetes
BV damage (Increase BP), nerve damage (capillary damage that cuts off nutrient supply, amputation), eye damage (damage BV of retina), and kidney damage (damage of filtering system)
What is also increased when there is a low pH in the blood?
Ventilation
Absence of functioning insulin releases….
inhibition of lipolysis (body thinks its in post-absorptive state)–release fatty acids into plasma
When liver converts fatty acids into ___, which are acidic
Ketones
What else is impaired in diabetes that results in lactic acid production through _____
Mitochondria; increased anaerobic respiration (rely on glycolysis)
What from lactic acid moves into the blood to acidify blood in those with diabetes?
H+
Increases a patients sensitivity to insulin, allowing plasma glucose levels to fall : who gets this drug
Insulin sensitizers, type 2
Compounds capable of binding insulin receptors and mimicking the actions of insulin, causing plasma glucose levels to fall
insulin mimetics
Compounds that stimulate beta cells to secrete insulin, plasma glucose levels will fall in response to increased insulin production/release
insulin secretagogues
Prevents reabsorption of glucose which will then be excreted during urination, causing drop in plasma glucose levels
SGLT2 Inhibitors
Glucagon functions?
Stimulates glycogenolysis, gluconeogenesis, muscle break down, and fatty acid release from fat tissue
generates glucose from breaking down glycogen, released in the plasma and taken up by liver to brain: what pathway
Glycogenolysis
Generates new glucose from non-carb substrates. What is this process and what are the substances?
Gluconeogenesis; pyruvate, lactate, glycerol, and AA
Main source of energy for most tissues, besides brain, in post-absorptive state
Fatty acids
Majority of glucose produced comes from
AA in liver
What is glucose sparing
Instead of using glucose, liver uses AA & muscle/fat use fatty acids (brain uses glucose)
Glucagon activates release of
fat
When glucose arrives in the blood in post-absorptive state….
- Glucose goes straight to brain
- Fat tissues release fatty acids and glycerol into plasma (from triglyceride breakdown)
- Fatty acids travel to muscle and muscles glycogen storage are oxidized for ATP
- In muscle, lactate and pyruvate are made as a result of glucose oxidation, and muscle breakdown releases AA into plasma
- Lactate, pyruvate, and AA move into liver from blood
- Glycerol, fatty acids, AA, lactate, and pyruvate move into liver
- They are converted into glucose and ketone bodies
- Liver sends glucose to brain
In liver metabolism, how is glucose produced?
- Liver glycogen broken down
- AA from muscle deaminated and converted to glucose
- Lactate, pyruvate, and glycerol are converted to glucose
What are the gluconeogenic pathways in liver metabolism?
AA from muscle deaminated, lactate, pyruvate, and glycerol are converted
In liver metabolism, how are ketones produced
from fatty acids by beta oxidation
In liver metabolism, how is ATP produced
keto acids in the liver used to make ATP from AA
Why does the liver make ketone bodies and not ATP from fatty oxidation?
Liver contains low levels of oxaloacetate (needed for atp production) so Acetyl-CoA is converted into ketone bodies
Ketone bodies from liver enter the blood and go to the brain ONLY after
days of starvation/fasting
Where does glucagon come from?
alpha cells (not exocrine cells)
What stimulates glucagon release?
- decreased plasma glucose
- Increased plasma AA (same as insulin)
If you eat a high protein meal and no sugar, insulin is released but there’s no glucose present so glucose falls more. As a result, what is released to help prevent a further fall in glucose if no sugar in diet?
Glucagon
In a post-absorptive state in muscle and fat, in the absence of insulin—glucose transporters are….
removed from plasma membrane and sit in vesicles waiting for insulin stimulus
Adipose tissue, in post-absorptive state in muscle and fat, doesn’t have access to glucose unless…
insulin is present
In the liver in post-absorptive state, glucose transporters are….
always in plasma membrane
In the liver, in a post-absorptive state, glucose is produced by ___ and moves ____
pyruvate, glycerol, lactate, and AA; down concentration gradient through GLUT2 transporter
Glucose metabolism by hypothalamic centers regulate food intake
Glucostatic theory
What is the glucostatic theory pathway
decreased glucose–> suppress satiety —-> activate feeding center
Signal from body fat stores to the brain to modulate eating behavior so that the body maintains a particular weight
Lipostatic theory
What is the lipostatic theory pathway
Increased fat stores–> activates satiety—-> inhibits feeding center
Protein hormones produced by adipocytes that feeds back negatively on the brain, preventing increase in food intake
Leptin
Leptin was thought to curen ___. Was this true?
obseity; obese humans and mice exhibit elevated leptin because they are leptin resistant
Ketone bodies vs keto acids
Ketone bodies= from free fatty acids, doesn’t make glucose
Keto acids= from AA breakdown from muscle, used for glucose
In diabetes, even though glucose is high, what is still released
Fatty acids, because no insulin
Because insulin turns off lipolysis, what is released in diabetes
Fat
Insulin sensitizers cannot be given to…
Type 1 (give to type 2 because they are resistant)
Insulin secretagogues is given in what stage of diabetes
Early states while pancreas is still functioning
Where is the SGLT 2 located and what does it promote
Renal epithelium, apical side: wants to reabsorb glucose
If glucose concentrations are equal, and there is no gradient what is used to promote reabsorption
SLGT 2 (secondary transport), makes a gradient
On the basolateral side, how can glucose get back into the blood if SGLT2 is making a gradient
Facilitated diffusion
In diabetes, glucose is high in the plasma. This has what effect on filtration? What happens they to the glucose cotransporter?
Increases filtration (increases glucose in bowman’s capsule). Glucose cotransporter becomes too saturated and overwhelmed (excreted)
Gluconeogenesis in the liver occurs in what stage
Post absorptive
Which cannot be made into glucose by liver
Amino acids
Glycerol
Fatty acids
Fatty acids (only oxidized to make atp or converted into ketone bodies)
Dominant pathway for glucose production during post absorptive state
Amino acids
Lepton function
Acts on brain to decrease / inhibit food intake
Fatty acids cannot become
Glucose
Example of gluconeogenic pathway
Protein to amino acids to keto acids to glucose
