Wk1 Review of Metabolism

Question 1

Glucagon response to high carb meal:

Answer 1

Decreased

-inhibited by insulin

Question 2

Insulin and glucagon response to high protein intake?

Answer 2

Less insulin

more glucagon (excess AAs are used for gluconeogenesis)

Question 3

Insulin triggered pathway leading to transcription:

Answer 3

MAP kinase

Question 4

Liver role after protein rich meal:

Answer 4

amino acids –> gluconeogenesis

Question 5

Brain metabolic response to feeding:

Answer 5

oxidizes glucose to CO2 for ATP via oxidative phosphorylation

Question 6

RBC metabolic response to feeding:

Answer 6

ferment glucose to pyruvate

exports lactate

Question 7

White adipose cells response to feeding:

Answer 7

ferment glucose to glycerol 3-phosphate (backbone for triacylglycerol synthesis)

Question 8

Skeletal muscle response to feeding:

Answer 8

glycolysis

fatty acid beta oxidation

glycogenogenesis (for its own use)

protein synthesis

Question 9

Cardiac muscle response to feeding:

Answer 9

fatty acid beta oxidation (60-80%)

oxidation of glucose and lactate (20-40%)

Question 10

Gut intestinal epithelial cells response to feeding:

Answer 10

convert glutamine, glutamate and aspartate from the DIET to a-ketoglutarate

Question 11

Colonocyte response to feeding:

Answer 11

use short chain fatty acids produced by gut bacteria

Question 12

Pancreas response to fasting:

Answer 12

release glucagon

Question 13

glucagon pathway to glycogenolysis and gluconeogenesis in fasting state:

Answer 13

G protein receptor –> cAMP –> protein kinase A

Question 14

Liver response to fasting:

Answer 14

glycogenolysis

gluconeogenesis

Question 15

substrates for hepatic gluconeogenesis in fasting:

Answer 15

carbon skeletons from AA (and after high protein meal with excess AAs in the blood)

lactate

glycerol

Question 16

Where does the ATP come from to power fasting hepatic gluconeogenesis?

Answer 16

FAD(2H), NADH

fatty acid beta oxidation

Question 17

substrate from fatty acid beta oxidation for ketone body synthesis:

Answer 17

acetyl CoA –> acetone

Question 18

Skeletal muscle response to fasting:

Answer 18

proteolysis –> branched chains used for fuel

Alanine/glutamine –> liver for gluconeogenesis

later can use ketone bodies for energy

Question 19

Cardiac muscle response to fasting:

Answer 19

fatty acid beta oxidation increases

glycolysis decreases

Question 20

Primary fuel for gut epithelial cells during fasting:

Answer 20

glutamine from the BLOOD

Question 21

White adipose tissue response to fasting:

Answer 21

lipolysis of triacylglycerol –> fatty acids (heart, liver fuel)

glycerol – > gluconeogenesis (liver)

Question 22

Adipose response to starvation:

Answer 22

lipolysis of triacylglycerol increases

Question 23

Liver response to starvation:

Answer 23

increased production of ketone bodies

decreased gluconeogenesis

Question 24

Skeletal muscle response to starvation:

Answer 24

ketone body utilization decreases

breakdown decreases (not sustainable)

Question 25

Brain response to starvation:

Answer 25

ketone body use increases

Question 26

Cardiac muscle response to starvation:

Answer 26

continues to use fatty acids

does not like ketone bodies

Question 27

What happens to urea cycle during starvation?

Answer 27

decreases – less nitrogen waste to deal with

Question 28

Hypercatabolism is characterized by:

Answer 28

Sustained muscle and organ protein breakdown

Question 29

Catecholamine role in hypercatabolism:

Answer 29

Ebb phase spike

epinephrine activates hormone sensitive lipase to mobilize FA from adipose

Question 30

Cortisol role in hypercatabolism:

Answer 30

rises in Ebb phase, remains elevated in Flow phase

activates muscle proteolysis

Question 31

Glucagon role in hypercatabolism:

Answer 31

Spikes in Ebb and slowly declines in flow

activates hepatic glycogenolysis and gluconeogenesis

Question 32

Insulin role in hypercatabolism:

Answer 32

increased

Question 33

Normal nitrogen balance equation:

Answer 33

intake - (urinary urea N - 2)

• 4 in normal Peds pts
• 3 in Peds pts receiving TPN