Metabolism 1 and 2 : Metabolism overview, carbohydrate metabolism Flashcards

1
Q

What are the fates of acetyl CoA

A

Fatty acid synthesis and sterols
Citric acid cycle
Ketone bodies

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1
Q

Preferred fuels of liver

A

glucose, fatty acid oxidation, amino acids

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2
Q

Preferred fuels of adipose tissue

A

Fatty acids

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3
Q

Preferred fuels of skeletal muscle

A

At rest - beta oxidation (FA)

During exercise - glucose

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4
Q

Preferred fuels of heart muscle

A

Beta oxidation

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5
Q

Preferred fuels of brain

A

Glucose always, but in starvation it’ll use ketone bodies

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6
Q

Major carbohydrates and fuels in which they are found

A
Amylose (starch) 
Sucrose (table sugar, desert)
Lactose (milk products) 
Fructose (fruit and honey)
gluocse (fruit, honey)
Maltose (barley)
trehalose (mushroom)
cellulose (plant walls)
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7
Q

What will happen if a person who is lactose intolerant eats milk?

A

This person is deficient in lactase - this is going to make lactase go through tract an led to osmotic diarrhea and co2 production from bacteria metabolising the lactose.

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8
Q

Carbohydrate metabolism pathways active in red blood cells

A

Glycolysis only - no mitochondria

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9
Q

Carbohydrate metabolism processes in brain

A

Glycolysis, TCA, ETC

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10
Q

Carbohydrate processes available to heart and skeletal muscle

A

Glycolysis, TCA, ETC, Glycogenolysis

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11
Q

Adipocytes

A

Conversion of glucose to fats

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12
Q

Hepatocytes

A

glycolysis, TCA, ETC, glycogenolysis, gluconeogenesis, pentose phosphate pathway

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13
Q

Glut2

A

Insulin independent transporter (liver)
High capacity, low affinity (almost never saturated)
Bidirectional

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14
Q

glut 4

A

insulin dependent transporter (low capacity, high affinity) - heart, skeletal muscle, adipocytes - not active in fasting states

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15
Q

SGLT1

A

will transport glucose or galactose with using sodium as a secondary active transport assistant

16
Q

3 irreversible enzymes of glycolysis

A

hexokinase/glucokinase
phosphofructokinase 1
pyruvate kinase

17
Q

Tissue localization: Hexokinase vs glucokinase

A

Hexokinase - everywhere

glucokinase - liver and pancreas technically

18
Q

kinetic characteristics of hexokinase / glucokinase

A

Hexokinase - Low Km for glucose (constantly saturated)

Glucokinsae - High Km for glucose (rarely saturated)

19
Q

Regulation of hexokinase / glucokinase

A

Hexokinase - constitutively active, constant amount, but allosterically regulated by its product, G6P
Glucokinase- shuttled between nucleus and cytosol for activity, F6P will suttle to nucleus and glucose brings to cytosol - this one is also inducible and will be induced by insulin to be synthesized

20
Q

allosteric regulators of glucokinase and hexokinase

A

Hexokinase - allostericlally inhibited by glucose 6 phosphate

Glucokinase - allosterically activated by glucose, inactivated by fructose 6 phosphate

21
Q

Allosteric regulation of phosphofuctokinase 1

A

Activators: F-2,6-BP, AMP, ADP (low energy, high glucose/ active PFK2)
Inhibitors: Citrate, ATP (high energy, glycolysis and TCA are going on)

22
Q

Allosteric regulation of pyruvate kinase

A

Positive: F-1,6-BP (upstream)

Negative ATP, alanine

23
Q

Covalent regulation of pyruvate kinase

A

Insulin –> dephosphorylated –> more active

Glucagon/ epinephrine –> phosphorylated –> less active

24
Hepatic PFK2 is phosphorylated in the ___ domain when glucagon and epinephrine are around, meaning __________.
Kinase | It going to have phosphatase activity going (you will not have F-2,6 BP and glycolysis is inhibited)
25
Muscle PFK2 is going to be phosphorylated in -____ domain in presence of epinephrine? Meaning _____ about its activity
phosphatase | You get a lot of F-2,6-BP, glycolysis is going to be active
26
What pancreatic hormone inhibits hepatic glycolysis
Glucagon
27
How does glucagon affect hepatic glycolysis?
Inhibit enzymes (PFK1 via PFK2 being put in "phosphatase mode", pyruvate kinase), and also decrease enzyme synthesis (glucokinase, PFK1, pyruvate kinase)
28
How does epinephrine inhibit hepatic glycolysis but promote muscle glycolysis
differential pFK2 covalent modifications Hepatic --> kinase phosphorylation (inactivates kinase) muscle --> phosphatase phosphorylation (inactivates phosphatase)
29
When will lactate --> pyruvate and acetyl coA
When there is extensive NAD - also in tissues with LDH that favors the lactate --> pyruvate conversion (like heart, instead of skeletal muscle which would prefer pyruvate --> lactate)
30
heart LDH isozyme
LDH4 (favors making pyruvate)
31
Skeletal muscle LDH isozyme
LDH5 M4 (favors lactate)
32
negative regulators of PDH
NADH, Acetyl CoA
33
Positive regulators of PDh
CoASH, NAD+, ADP, pyruvate, magnesium, calcium
34
Is PDH active or inactive when phosphorylated
Inactive
35
Vitamin cofactors that participate in reactions catalyzed by pdh
riboflavin, niacin, thiamine
36
Arsenic poisoning does what to pdh activity
fucks it up
37
Genetic deficiency in fructose aldolase
Intracellular trapping of F1P is result --> decline in inorganic phosphate and inability to make ATP --> absolutely must avoid fructose
38
galactokinase or galactose 1 phosphate uridyl transferase deficiencies, what food should people avoid
avoid lactose at all costs galactokinase deficiency -- you get diarrhea, can't utilize galactose galactose 1 uridyl transferase deficiency is bad , you trap sugar phosphates and die