NUTR 600 - Carbs
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Who uses majority of glucose? How much (g)?
Brain - 160 g
How many days can the average man live w/o food?
Theoretically: 62-63 days
Actuality: 45 days bc heart muscle will break down.
How long can glycogen stores supply glucose to peripheral tissues during resting state? During exercise?
How many hrs after a meal is gluconeogenesis activated?
When does GNG reach full rate?
GNG is activated 4-6 hrs after a meal (if resting)
GNG reaches full rate after glycogen stores are depleted
Main enzymes in glycogenesis? (2)
What else is needed in glycogenesis? (2)
Enzymes: glycogen synthase + branching enzyme
UDP-glucose & glycogenin (or residual glycogen).
Explain glycogenesis mechanism
- 1. Glucose --> G6P --> G1P --> UDP-Glucose
- 2. Glycogen synthase makes 1,4 bonds
- 3. Branching enzyme chops off 6-8 glucoses and tacks it back on with a 1,6 bond.
Which organs can release free glucose into the blood? which one in particular CAN'T?
Can: liver, kidney, intestines
Depends on availability of glucose-6-phosphatase
What is the point of regulating glycogen metabolism? (2)
To maintain homeostasis. Also, these processes req energy, so you don't want to waste energy and resources.
When do you want to increase glycogen degradation? Why?
During fasting, to keep serum glucose levels up for glucose-dependent organs, such as the brain, erythryocytes, etc.
Do we care if glycogen degradation is fast or slow? Under which conditions?
- In muscle, we want fast glycogen degradation to provide quick bursts of energy during exercise. Thus, would want a non-glucagon dependent way to breakdown glycogen.
- (role of AMP: activates glycogen phosphorylase w/o phosphorylation). Phosphorylation is covalent modificatoin (seconds to minutes)
In liver, we want slow glycogen degradation to efficiently use stores in times of fasting. Hormone regulation is much slower.
When do we want to increase glycogen synthesis? Do we care if it's fast or slow? What hormones will be present?
During fed state - when there's an abundance of nutrients.
Yes, we would want it to be slower to ensure that all tissues get sufficient glucose uptake.
Insulin, but glucagon to a smaller extent
What is the role of calcium in the muscle? Name 3 steps in its mechanism of action.
Can activate glycogenolysis w/o glucagon.
- 1. During muscle contraction, calcium is released from SR.
- 2. Ca binds to calmodulin subunit of phosphorylase kinase activating it w/o phosphorylation.
- 3. Phosphorylase kinase can then activate glycogen phosphorylase causing glycogenolysis.
What enzymes are involved in glycogen degradation? (3) Which additional enzymes/compounds are involved in glycogen degradation regulation? (4)
Glycogen degradation: (1) glycogen phosphorylase (2) glucosyl transferase (3) debranching enzyme
Glycogen degrad regulation: (1) Adenylyl cyclase (2) cAMP (3) protein kinase A (4) glycogen phosphorylase kinase
What is the role of AMP in muscle?
In extreme conditions of anoxia & depletion of ATP, AMP activates glycogen phosphorylase w/o it being activated!
1 step in front of Ca2+.
Compare the mechanisms of Ca2+ and AMP in muscle? 2 differences
AMP can directly activate glyc p'lase, whereas Ca2+ must work through glyc p'lase kinase --> glyc p'lase.
So AMP is faster and AMP is used under more dire conditions!
- 1. Ca2+ released from SR during muscle contractions
- 2. Ca2+ binds to calmodulin subunit of glyc phosphorylase kinase activating it.
- 3. Glyc phosphorylase kinase p'lates glyc p'lase, activating glycogenolysis.
AMP: In extreme cases of anoxia & deprivation of ATP, AMP can activate glycogen p'lase w/o phosphorylation.
In glycogen metabolism, who is responsible for p'lating and who is responsible for dep'lating?
Insulin - dephosphorylation via protein phosphatase 1
Glucagon - phosphorylation due to cAMP-dep kinases.
How does insulin affect glycogen metabolism? (2)
- 1. Insulin activates protein phosphatase 1, which dephosphorylates glycogen phosphorylase a--> b (deactivating it) and dephosphorylates glyc synthase b--> a (activating).
- 2. Insulin also activates a phosphodiesterase that degrades cAMP, oppositng the effects of glucagon/epinephrine.
Important to remember! Opposing hormones must turn off each opposing step, not just one of them!
Under what allosteric conditions is glycogenesis stimulated? Glycogenolysis?
What is important about having allosteric regulation on top of hormonal regulation? Which one is stronger?
Glycogenesis: stimulated with high substrate availability and energy levels
Glycogenolysis: stimulated with low energy levels & low glucose.
Allosteric regulation allows rapid response to needs of cell and can override the effects of hormone-mediated covalent regulation.
How does cAMP-directed pathway activate glycogen degradation?
How does it inhibit glycogen synthesis?
- 1. cAMP activates PKA
- 2. PKA activates glycogen p'lase kinase
- 3. glycogen p'lase kinase activates glycogen p'lase
1. Glycogen synthase's inactive form is phospohrylated - a product of KINASE (glucagon) activity.
How are all glycogenolysis enzymes stopped?
- 1. Insulin activates PP1, which dephosphorylates glyc p'lase and glyc p'lase kinase --> inactive.
- 2. Insulin activates phosphodiesterase which degrades cAMP, decreasing PKA activity.
How is glycogen metabolism regulated allosterically by G6P?
1. G6P - activates glycogen synthase in muscle & liver & inhibits glycogen phosphorylase.
Free glucose in liver can INHIBIT glycogen phosphorylase
How does calcium affect glycogen metabolism?
1. Activates glycogen phosphorylase kinase in muscle and liver & activates PKC which deactivates glycogen synthase.
What four things allosterically regulate glycogen metabolism?
- 1. G6P (free glucose) activate glycogen synthase & inhibits glycogen p'lase
- 2. Ca2+ activates glycogen p'lase kinase and deactivates inhibits glycogen synthase via PKC!!!
- 3. AMP - activates glyc p'lase
- 4. ATP - inhibits glyc p'lase
Name 3 facts about T1D (what is it? what happens to insulin production? future treatment?)
- 1. Chronic autoimmune disease that begins years before clinical presentation
- 2. Progressive decline in insulin production
- 3. Future treatment: preserve pancreatic b-cell function to maintain residual insulin production.
What % of b-cells are destroyed until clinical presentation of T1D?
What is T2D associated with? (4)
Obesity, old age, rare genetic defects, and gestational diabetes
How does gestational diabetes affect (1) child and (2) mom?
- 1. Increased risk for large baby with low blood sugar (but can't give insulin bc its fat!)
- 2. Mom's chances of developing T2D increase --> 35-60% within next ten years.
What is a "normal" glucose range?
How can HbA1C measure glucose levels?
What does it give you a measure of?
When can't this work?
HbA1C = amount of Hb attached to glucose --> gives you measure of glucose serum levels over 3 month span (lifespan of RBC).
HbA1C cannot be used to measure glucose levels when lifespan of RBC is shortened, bc it will give you falsely lower results.
Can HbA1C be used in pregnancy? severe bleeding? blood transfusion? anemia? kidney/liver disease?
Name complications of diabetes (8)
- 1. Heart disease/stroke
- 2. Kidney disease
- 3. Eye complications (blood vessel disease--> blindness)
- 4. Diabetes, oral health, hygiene --> gum disease.
- 5. Foot complications: nerve damage --> injury/infection --> gangrene --> amputation
- 6. Skin infections
- 7. Diabetic neuropathy and nerve damage
- 8. Gastroparesis - nerve damage --> slower stomach emptying)
Summary of cellular respiration:
In rxn form
C6H12O6 + 6O2 + 6H2O --> 12 H2O + 6CO2.
- Breakdown of glucose to two pyruvates
- Oxidation of 2 pyruvates into carbon dioxide and water.
1. Which is regulated by insulin?
2. Present on muscle cells, adipocytes, and cardiomyocytes?
3. Present on b-cells?
4. Present on hepatocytes?
- 1. GLUT 4 is regulated by insulin.
- 2. GLUT 4
- 3. GLUT 2
- 4. GLUT 2
What are the three regulated enzymes of glycolysis?
Hexo/glucokinase, PFK-1, pyruvate kinase
What is the most important factor in determining hormonal regulation of key enzymes in glycolysis?
Diet: high carb diet vs fasting, etc
Gene transcription affects which three enzymes in glycolysis?
What increases/inhibits synthesis?
glucokinase, pfk-1 and pyruvate kinase in the liver
High CHO diet increases synthesis and fasting inhibits synthesis.
How does glucose --> G6P differ in liver (4) vs. most tissues?
Liver has glucokinase: high Km, high Vmax, indirectly inhibited by F6P and indirectly activated by glucose.
Glucokinase properties allow liver to remove high amounts of glucose from boody after meal to prevent hyperglycemia.
Most tissues have hexokinase: low Km, low Vmax, feedback inhibition by G6P (allosteric reg = fastest), so can respond faster.
What does it do? Act by 3; deact by 23.
- PFK-1F6P--> F1,6BP
- Activated by AMP, F2,6BP (PFK2); deactivated by ATP & citrate
Explain how PFK2 works in glucose metabolism
1. Fed (5)
2. Fasting (3)
- 1. High insulin:glucagon decreases cAMP and reduces PKA levels
- 2. Reduced PKA levels favor dephosphorylation of PFK2 (PFK2 is active)
- 3. PFK2 activates synthesis of F2,6BP
- 4. F2,6BP allosterically activates PFK-1.
- 5. Glycolysis increases
- 1. High glucagon:insulin --> high levels of cAMP --> high levels of PKA
- 2. High levels of PKA favor phosphorylated form of enzyme: F2,6BPtase
- 3. Decreased levels of F2,6BP decreases inhibition of FBP-1, leading to increased gluconeogenesis.
How does F2,6BP affect glucose metabolism?
High levels: Activate PFK-1 and inhibit FBP-1 --> glycolysis.
Low levels: decrease inhibition of FBP-1 --> GNG
How is pyruvate kinase regulated? What does it do?
Activated by F1,6BP (feedforward regulation)
Inhibited by glucagon in fasting conditions.
Where is GLUT 1 found? GLUT 3? GLUT 4? GLUT 2?
In RBCs and blood brain barrier, low in muscle
- GLUT 3 - neurons
- GLUT 4 - fat, heart muscle, skeletal muscle.
- GLUT 2 - liver/kidney/pancreatic b cells
What can pyruvate be converted to? (4) Under what conditionS?
- 1. Lactate (under anaerobic conditions)
- 2. OAA (GNG)
- 3. Acetyl CoA (FA synthesis)
- 4. Alanine (reversible) via ALT (alanine amino transferase) - protein synthesis.
Is pyruvate a central molecule? How about acetyl CoA?
BOTH ARE CENTRAL MOLECULES!
Do you see a lot of pyruvate --> lactate in cancer cells?
Where does this take place?
# of enzymes? # of coenzymes? Name vitamins.
pyruvate--> acetyl CoA (2 Acetyl CoA + 2 NADH); mitochondrial matrix
3 enzymes; 5 coenzymes.
- 1. thiamine pyrophosphate (thiamine)
- 2. CoA - pantothenic acid
- 3. NAD+ - niacin
- 4. FAD - riboflavin
- 5. lipoic acid.
How does carbs enter TCA cycle? How about proteins?
Carbs --> monosaccharides ---glycolysis --> pyruvate --> Acetyl CoA
Proteins --> AA --> acetyl CoA (or can go straight to pyruvate or TCA)
TAGS: FFAs -->(Ketone bondies) -->Acetyl CoA --> TCA
What is the product of TCA cycle?
Coenzymes & ATP
3 NADH, 1 FADH2 --> potential for 11 ATP from ETC
1 GTP --> 1 ATP
Total: 12 ATP from one acetyl CoA (24 from one glucose)
How is PDH regulated?
Activated by insulin --> PDH phosphatase
Inhibited by high levels of Acetyl CoA; NADH:NAD+, ATP:ADP, PDH kinase(glucagon)
Why do we want PDH to be inactive during fasting?
Bc we want energy to come from FA oxidation so we can conserve glucose for energy in cells that ONLY use glucose.
What if someone has a def of PDH?
Lethargy, muscle weakness, cognitive deficiencies due to lack of ability to use glucose efficiently. Effects are extremely great in organs that depend on glucose for energy.
What are the regulated enzymes in TCA cycle? What activates/inhibits them?
- 1. Citrate synthase: X by ATP, NADH, succinyl CoA, long chain fatty acyl CoA
- 2. Isocitrate dehydrogenase: X by ATP, NADH, act by ADP
- 3. A-ketoglutarate dehydrogenase: X by ATP, GTP, NADH, and succinyl CoA
Can you make gluconeogenesis from acetyl CoA?
Why does lack of oxygen stop TCA cycle?
Bc coenzymes (NADH/FADH2) are used up by ETC cycle which requires O2 to run. W/ no O2, reduced enzymes build up, inhibiting regulatory enzymes.
Which steps in TCA create NADH? FADH2? GTP?
1. NADH: isocitrate --> a-ketoglutarate; a-ketoglutarate --> succinyl CoA; malate--> OAA
2. FADH2: Succinate --> fumarate
3. GTP" succinyl CoA --> succinate.
What physiological conditions will inhibit the TCA cycle?
What does distribution of glucokinase and hexokinase in body's tissues tell us about speeds?
Glucokinase --> high Vmax/high Kmax --> can process high amounts of glucose quickly. But low affinity, so requires high amount of glucose to begin processing
Hexokinase --> low Vmax/low Kmax --> can process low amounts of glucose slowly --> slower process
Makes sense bc liver needs to be able to uptake glucose quickly relative to tissues and only when there's an abundance, but tissues need to be able to take up glucose even in low amounts.
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