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Physiology > Metabolism > Flashcards

Metabolism Flashcards

1
Q

What is metabolism?

A

A series of chemical reactions in which the product of one reaction is the substrate for the next reaction.

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2
Q

Most important electron carriers

A

NAD+ and NADP+

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3
Q

Only organ which can synthesize glucose.

A

Liver (it can also store fat and glycogen)

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4
Q

Minimum fasting blood glucose which must be maintained for proper brain functioning.

A

60mg/100mL (120g/day)

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5
Q

Final product of glycolysis (aerobic vs anaerobic)

A

AEROBIC –> pyruvate

ANAEROBIC –> lactate

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6
Q

Glycogenolysis

A

Break down of glycogen to glucose-1-phosphate and glucose in liver/muscles

Stimulated by epi and glycogen

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7
Q

Glycogenesis

A

Formation of glycogen from glucose

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8
Q

SGLT1 vs. GLUT2 vs. GLUT4

A

ALL TRANSPORTERS

SGLT1: sodium glucose transporter. Transports one molecule of glucose or galactose along with two sodium ions.

GLUT2: Insulin independent low affinity. High capacity in liver. Also functions in intestines and kidneys.

GLUT4: Insulin dependent, higher affinity transporter in muscle, heart and adipocytes.

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9
Q

3 main steps of glycolysis

A

(1) Priming Stage: ATP investment to break down glucose (into glucose-6-phosphatate)
(2) Splitting stage: Fructose-1,6-bisphosphate is converted into 2 glyceraldehyde-3-phasphate molecules.
(3) Oxidoreduction-phosphorylation: ATP earnings (4), NADH creation (2) and pyruvate generation(phosphoenolpyruvate to pyruvate)

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10
Q

3 most important enzymes for glycolysis

A

(1) Hexokinase/glucokinase
(2) PFK-1
(3) Pyruvate kinase

Used only ONE WAY. For glycolysis and not gluconeogenesis

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11
Q

Hexokinase vs Glucokinase. Important differences, including, which has a higher Km and what does that mean?

A

Gluco is higher. It is not as easily saturated (not saturated at all at physiological levels of glucose)

HEXO: present in all cell types, inhibited by glucose 6-phosphate, non-inducible (constant)

GLUCO: present in liver and pancreas, inhibited by fructose 6-phosphate, inducible (insulin increases synthesis)

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12
Q

Relationship between PFK-1 and PFK-2

A

The activity of PFK-1 is regulated by the product of PFK-2, which is fructose-2,6-Biphosphate

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13
Q

Effect of glucagon/epi on PFK-2 and pyruvate kinase in the liver. How does this differ from the skeletal muscle?

A

LIVER: causes inhibition of PFK-2 (and thus PFK-1) and inhibition of pyruvate kinase

SKELETAL: opposite effect

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14
Q

Regulation of Pyruvate dehydrogenase (PDH)

A

◦not regulated by glucagon and epi

◦end products inhibit PDH by allosteric inhibition

◦end products cause the phosphorylation and inhibition of PDH (Acetyl CoA and NADH)

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15
Q

Lactate Dehydrogenase A Deficiency (LDHA)

A

Causes a limited level of NAD+ so these patients cannot maintain moderate levels of exercise due to inability to produce ATP needed for muscle contraction under anaerobic conditions

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16
Q

Net ATP of glycolysis

A

2 ATP

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17
Q

Galactosemia

A

Genetic disorder caused by a deficiency of certain enzymes (mainly galactose 1-phosphate uridyltransferase and lactose)

unmetabolized milk sugars build up.

LEADS TO:

Cataracts (cloudiness in the lens), Kidney damage, Liver damage, Jaundice, Brain damage.

TREATMENT: Remove galactose from diet

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18
Q

Hereditary Fructose Intolerance

A

Causes hypoglycemia, vomiting, jaundice and hepatic failure.

AVOID FOODS HIGH IN FRUCTOSE.

19
Q

Fates of Pyruvate and the enzymes responsible for each

A

4 Possible Fates

(1) Alanine (via transamination)
(2) Oxaloacetate (via pyruvate carboxylase)
(3) Lactate (via lactate dehydrogenase)
(4) Acetyl CoA (via pyruvate dehydrogenase)

20
Q

Insulin promotes the expression of the genes encoding for which glycolytic enzymes?

A
  • Glucokinase
  • PFK-1
  • Pyruvate Kinase
21
Q

Cori Cycle

A

Conversion of lactate to glucose. Lactate comes from muscle and RBC’s.

Requires additional ATP.

22
Q

Alanine Cycle

A

Conversion of alanine to glucose. Alanine comes from muscle, usually during severe exercise.

23
Q

Glucose 6-Phosphatase Function

A

Needed to convert glycogen into glucose for usage by the body.

24
Q

kcal/g conversions

A

carbohydrates: 4 kcal/g
proteins: 4 kcal/g
fat: 9 kcal/g

25
Q

Ultimate function of insulin

A

Clear the blood of glucose by any means

26
Q

Ultimate function of epi

A

Flood the blood with glucose by any means

27
Q

Ultimate function of glycogen

A

Flood the blood with glucose by any means

28
Q

NAD+ for glycolysis can be regenerated via…

A

(1) Lactate dehydrogenase
(2) Maltate-aspartate shuttle
(3) Glycerol-phosphate shuttle

29
Q

The most common form of PDH deficiency is caused by…? What is its inheritance pattern?

A

Mutations in the E1 alpha gene and is inherited in an X-linked manner.

30
Q

How many phosphates are generated from the CAC?

A

10

31
Q

AA conversion (gluconeogenesis)

A

Cori Cycle (RBC’s all the time, muscles anaerobically): lactate –> glucose

Alanine cycle (muscles): alanine –> glucose

32
Q

During an overnight fast, what serves as the major source of ATP?

A

Oxidation of fatty acids

33
Q

4 enzymes which are mandatory for glycolysis reversal (glucose formation)

A
  1. PEP Carboxykinase
  2. Pyruvate Carboxylase
  3. Fructose 1,6-biphosphate
  4. Glucose 6-phosphatase
34
Q

Major symptom of glucose 6-phosphatase deficiency

A

Fatty liver (enlarged)

35
Q

Effect of ethanol metabolism

A

Hypoglycemia

Ethanol metabolism increases NADH/NAD ratio. This decreases the formation of pyruvate/oxaloacetate from G3P.

Removes them from the pool for glucogenic mechanisms.

36
Q

Glucose 6-phosphate dehydrogenase deficiency

A

G6P Dehydrogenase is the key enzyme in the pentose phosphate pathway.

W/o this enzyme, there is very little formation of` NADPH, which leads to high levels of hydrogen peroxide and eventual cell lysis.

37
Q

Role of Carnitine. What blocks this?

A

These are needed to transport fatty acids into the mitochondrial matrix. Without these transporters, fatty acids can’t be used.

Malonyl CoA blocks these Carnitine transporters (CPT1), thereby inhibiting beta-oxidation of fatty acids.

38
Q

Why can’t the liver use the ketone bodies which it creates

A

No thiophorase (aka succinyl-CoA Transferase)

39
Q

Cofactor for Enzymes

A

Apo-CII: activates lipoprotein lipase (LPL)

Apo-A1: activates (LCAT)

40
Q

Ligand for Remnant Receptor function

A

Apo E

41
Q

Ligand and structural protein for LDL/VLDL receptor

A

Apo B-100 and B-100

42
Q

Ligand and structural protein for HDL

A

Apo A-1 and A-1

43
Q

Structural protein for chylomicrons

A

B-48

Physiology (12 decks)

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