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
Q

Hepatic PFK2 is phosphorylated in the ___ domain when glucagon and epinephrine are around, meaning __________.

A

Kinase

It going to have phosphatase activity going (you will not have F-2,6 BP and glycolysis is inhibited)

25
Q

Muscle PFK2 is going to be phosphorylated in -____ domain in presence of epinephrine? Meaning _____ about its activity

A

phosphatase

You get a lot of F-2,6-BP, glycolysis is going to be active

26
Q

What pancreatic hormone inhibits hepatic glycolysis

A

Glucagon

27
Q

How does glucagon affect hepatic glycolysis?

A

Inhibit enzymes (PFK1 via PFK2 being put in “phosphatase mode”, pyruvate kinase), and also decrease enzyme synthesis (glucokinase, PFK1, pyruvate kinase)

28
Q

How does epinephrine inhibit hepatic glycolysis but promote muscle glycolysis

A

differential pFK2 covalent modifications
Hepatic –> kinase phosphorylation (inactivates kinase)
muscle –> phosphatase phosphorylation (inactivates phosphatase)

29
Q

When will lactate –> pyruvate and acetyl coA

A

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
Q

heart LDH isozyme

A

LDH4 (favors making pyruvate)

31
Q

Skeletal muscle LDH isozyme

A

LDH5 M4 (favors lactate)

32
Q

negative regulators of PDH

A

NADH, Acetyl CoA

33
Q

Positive regulators of PDh

A

CoASH, NAD+, ADP, pyruvate, magnesium, calcium

34
Q

Is PDH active or inactive when phosphorylated

A

Inactive

35
Q

Vitamin cofactors that participate in reactions catalyzed by pdh

A

riboflavin, niacin, thiamine

36
Q

Arsenic poisoning does what to pdh activity

A

fucks it up

37
Q

Genetic deficiency in fructose aldolase

A

Intracellular trapping of F1P is result –> decline in inorganic phosphate and inability to make ATP –> absolutely must avoid fructose

38
Q

galactokinase or galactose 1 phosphate uridyl transferase deficiencies, what food should people avoid

A

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