Metabolism Review

Question 1

4 metabolic states

Answer 1

fed: 2-4 hr postprandial
fasted: overnight w/o food
starved: long period of fasting
hypercatabolic: not related to food consumption–ie trauma, sepsis, etc

Question 2

Glucagon control

Answer 2

inhibited by insulin

indirectly regulated by BG

insulin is directly responsive to BG

Question 3

Insulin receptor type

Answer 3

TK receptor

Question 4

Glucagon after high-protein meal

Answer 4

promotes gluconeogenesis in liver

Question 5

In fed state, metabolism of:

brain

RBC

white adipose

sk. muscle

cardiac muscle

intestinal epithelial cell

colonocytes

Answer 5

brain: glucose ox

RBC: glucose → lactose fermentation

white adipose: glucose → glycerol-3-P

sk muscle: glucose → CO₂, FA beta-ox, glycogenogenesis, protein synthesis

cardiac muscle: FA beta-ox, oxidation of Glc and Lac

intestinal epithelial cells: Glu, Gln, Asp → alpha-KG

colonocytes: ox of FA produced by gut bacteria

Question 6

Glucagon release

receptor-level response

Answer 6

adenylate cyclase activation

cAMP production

PKA activation (protein kinase A)

substrates are phosphorylated

change in overal metabolic state of cell

Question 7

In fed state, metabolism of:

liver

sk muscle

cardiac muscle

gut epithelial cells

white adipose

Answer 7

fed state metbolism:

liver: first glycogenolysis, then gluconeogenesis from aa freed from sk muscle protein, lactate, and glycerol.

→ powered by FADH₂ and NADH from FA beta-ox

→ acetyl-CoA from FA beta-ox used for ketone synthesis

sk muscle: proteolysis of branched chain aa, export to liver of Ala and Gln

cardiac muscle: FA beta-ox, does not use ketones

gut epithlial cells: Gln

white adipose: lipolysis

→ FA and glycerol into blood

→ formation of ketone bodies from FA

Question 8

Starvation metabolism changes:

cardiac muscle

sk muscle

liver

brain

RBC

Answer 8

cardaic muscle: FA beta-ox

sk muscle: proteolysis decreases to preserve mass

liver: gluconeogenesis decreases due to less aa, ketone formation from acetyl-CoA from FA beta-ox increases
brain: ketone body utilization

RBC: use Glc still

Question 9

Defining characterisitc of hypercatabolic metabolism

Answer 9

sustained muscle and organ protein breakdown

⇒ rapid mobilization of fuel

Question 10

Regulation of hypercatabolic metabolism

Answer 10

CNS regulation

Question 11

Hormones involved in hypercatabolic metabolism

Answer 11

epi: activates hormone-sensitive lipase in Ebb phase
cortisol: muscle proteolysis
glucagon: increase gluconeogenesis and glycogenolysis

Question 12

2 phases of hypercatabolic metabolism

Answer 12

Ebb: with epi

flow: when epi wears off, cortisol and glucagon remain high

Question 13

Nitrogen blaance in patients recovering from hypercatabolic state

Answer 13

important to maintain positive nitrogen balance

Question 14

N balance formula

Answer 14

N balance = N intake - (urinary urea N +2)

3 for PRN peds

4 for PO peds

Question 15

Total urinary N formula

Answer 15

total urinary N = total urea N/0.85

Question 16

Creatinine

Answer 16

breakdown product of creatine

renal excretion

Question 17

Creatine

Answer 17

renal and hepatic synthesis

used as high energy intermediate in sk and cardiac muscle and brain

Question 18

Cr-height index

Answer 18

measures nutritional status

Question 19

Starvation vs Hypercatabolism

fuel source

Answer 19

starvation: fat (FA and ketones)
hypercatabolism: protein → aa → glucose in liver

Question 20

Hormones in starvation

Answer 20

increased glucagon

decreased insulin

Question 21

Hormones in hypercatabolism

Answer 21

increase in:

cytokines

glucagon: gluconeogenesis
insulin: clotting factors
cortisol: main regulator of protein metabolism