lecture 9: fuel regulation and energy balance

Question 1

glucose fatty acid cycle

Answer 1

increased breakdown of endogenous TAG to promote the use of lipid fuels and block the use of glucose
regulate relative usage between glucose and FAs

Question 2

biochemical mechanisms by which FAs use supressed glucose use and vice versa

Answer 2

1) B-oxidation products (NADH, acetyl CoA) inhibit pyruvate dehydrogenase complex, which prevents glucose oxidation

2) glucose metabolism causes high levels of malonyl-CoA, inhibiting FA transfer into mitochondria

3) metabolism of glucose by adipose tissue results in G3P production and increases TAG storage

Question 3

short term regulatory mechanisms

Answer 3

involve changes in activity of an enzyme without changes in enzyme concentration

Question 4

long term regulatory mechanisms

Answer 4

change in enzyme concentrations without changes in kinetic properties

Question 5

what does AMPK regulate? what does it lead to?

Answer 5

regulates both catabolic and anabolic pathways, lead to an increase in catabolic activity

Question 6

Why must our bodies have the capacity to store energy?

Answer 6

Food intake is not continuous so the body must store energy for later use, mainly in the form of glycogen and TAG.

Question 7

What are the primary factors resulting in the activation of AMPK?

Answer 7

ADP and ATP converted to AMP > increased AMP > AMPK is phosphorylated
AMP binds to AMPK allosteric site, making AMPK a better substrate for phosphorylation

decreased glucose and oxygen, increase energy demand activate AMPK

Question 8

mTORC1 regulation

Answer 8

activated by insulin, IGF, AAs
inhibited by lack of fuel, low oxygen, AMPK
ensures that protein synthesis is only upregulated when body has plenty of substrates/fuel

Question 9

afferent signals

Answer 9

circulating nutrients, hormones, nerve inputs, provide info

Question 10

glucostatic theory

Answer 10

plasma/tissue concentrations of glucose or rate of utilization serves as feedback signal to brain for food intake

Question 11

ghrelin

Answer 11

peptide hormone produced in the GI tract, stimulates food intake
increased levels during food deprivation or before spontaneous food intake

lower levels in obese individuals

Question 12

CCK

Answer 12

released in response to certain AAs and FAs
initiation of satiety > signals brain to terminate meal

Question 13

Peptide YY

Answer 13

rise after meal initiation, long-term effect to determine timing of next meal and meal size

Question 14

GLP1

Answer 14

released in proportion to caloric intake
reduce appetite, increase energy expenditure

Question 15

insulin

Answer 15

satiety and adiposity signal - basal levels reflect obesity
mediate anorexigenic response

Question 15

pancreatic polypeptide (PP)

Answer 15

proportional to caloric intake, aids in reducing meal size

Question 16

leptin

Answer 16

adiposity signal, secreted by white adipocytes in proportion to body fat content, activates anorexigenic pathways, signal of energy sufficiency

spontaneous obesity results in individuals lacking a functional leptin gene

obese individuals have higher leptin levels, suggesting insensitivity

Question 17

What do the hormones insulin and leptin have in common?

Answer 17

Both adiposity signals, promote anorexigenic effects

Insulin: satiety (feelings of being full), decrease appetite

Leptin: energy sufficiency, secreted in proportion to body fat content