feeding and fasting

Question 1

insulin effect on blood glucose and fat metabolism

Answer 1

Decreases blood glucose and inhibits lipolysis/ facilitates fatty acid synthesis

Question 2

glucagon effect on blood glucose and fat metabolism

Answer 2

Increases blood glucose and facilitate fatty acid breakdown or ketogenesis

Question 3

catecholamines effect on blood glucose and fat metabolism

Answer 3

increases blood glucose and promotes lipolysis

Question 4

which energy source does muscle prefer?

Answer 4

fatty acids, but can use glucose

Question 5

role of insulin

Answer 5

to promote storage of excess glucose as glycogen in liver and muscle and as triglycerides in adipose tissue, promotes salt retention in kidney, promotes blood flow, growth promoter

Question 6

role of glucagon

Answer 6

Along with epinephrine, prevent fasting hypoglycemia and promote the liberation of an alternative fuel: free fatty acids

Question 7

what causes secretion of glucagon

Answer 7

increased amino acids and increased epinephrine. Regulated by low blood glucose and inhibited by high blood glucose and insulin.

Question 8

epinephrine effect on glucose and fat metabolism

Answer 8

Epinephrine stimulates glycogenolysis in muscle and the liver and the release of free fatty acids (lipolysis) by adipose tissue through the activation of hormone sensitive lipase

Question 9

Which two hormones act through G proteins

Answer 9

glucagon and epinephrine

Question 10

glucagon and epinphrine signaling

Answer 10

hormone activates adenylyl cyclase > increase cAMP >activates protein Kinase A > activation of glycogen phosphorylase and/or hormone sensitive lipase and inactivation of glycogen synthase and/or acetyl CoA carboxylase

Question 11

liver metabolism in fed state

Answer 11

Elevated insulin and nutrients delivered to liver. Glucose transformed into glucose-6-phosphate (glucokinase) then synthesized into glycogen (glycogen synthase). Also G-6-P > PEP > pyruvate > acetyl CoA (pyruvate dehydrogenase) > fatty acid synthesis (acetyl CoA carboxylase plus NADPH from pentose phosphate pathway) OR TCA cycle

Question 12

Muscle metabolism in fed state

Answer 12

High insulin:glucagon ration promotes: 1. glucose uptake (GLUT4) > glucose-6-phosphate (hexokinase) > glycogen formatin (glycogen synthase). 2. Amino acid uptake and protein synthesis. 3. uptake of fat is NOT favored

Question 13

Brain metabolism in fed state

Answer 13

glucose uptake > glucose-6-phosphate > pyruvate > TCA cycle

Question 14

What region of brain is insulin sensitive

Answer 14

region in hypothalamus- involved in food intake. Otherwise, the rest of the brain is insensitive to insulin

Question 15

compare hypoxia and hypoglycemia symptoms

Answer 15

They are the same! Confusion, motor weakness, visual disturbances, b/c brain relies on aerobic metabolism of glucose

Question 16

adipose metabolism in fed state

Answer 16

high insulin and low catecholamines promotes: 1. hormone sensitive lipase is not active so lipolysis is low. 2. glucose is taken up and can be converted to fatty acids then triglycerides via fatty acid synthesis or enter TCA cycle. 3. Uptake of dietary fat contained in chylomicrons facilitated by increased lipoprotein lipase and transformed into TGs.

Question 17

When is the fasting state time period

Answer 17

from 3-4 hours to 32-36 hours after a meal

Question 18

liver metabolism in fasting state

Answer 18

1. glycogen degradation- glucagon-induced activation of glycogen phosphorylase and inhibition of glycogen synthase. 2. gluconeogenesis- glucagon stimulates reduction in F2,6-BP concentration which removes inhibition of fructose-1,6-bisphosphatase (rate limiting) and reduces activation of phosphofructokinase 1. Also inactivation of pyruvate kinase via PKA prevents recycling of PEP. Glucose-6-phosphatase converts G-6-P to glucose to be released

Question 19

Muscle metabolism in fasting state

Answer 19

1. degradation of muscle protein into aa which are transported to liver for gluconeogenesis. 2. free fatty acids used as fuel source- skeletal muscle LPL increased and VLDL uptake increased. 3. glycogen degradation can be used as fuel for muscle for short periods of exertion. 4. glycogen > glycolysis > lactate >liver (Cori cycle)

Question 20

Brain metabolism in fasting state

Answer 20

Continues to use glucose as energy source

Question 21

When is the starvation state timeline and what is the bodies mechanism for fuel

Answer 21

Fasting for longer than 3-5 days. Fatty acids and ketone bodies used for fuel to maintain blood glucose at 60-65mg/dl and to spare muscle protein.

Question 22

Hormones during starvation state

Answer 22

Absence of insulin and high levels of counter regulatory hormones (glucagon, growth hormone, cortisol, catecholamines)

Question 23

liver metabolism in starvation state

Answer 23

1. gluconeogenesis decreases as aa supply decreases. 2. glycerol released by lipolysis > glycerol-3-P (glycerol kinase) > DHAP > glucose. 3. fatty acid oxidation used for providing energy for gluconeogenesis. 4. fatty acid > Acetyl CoA > ketone formation

Question 24

Muscle metabolism in starvation state

Answer 24

1. muscle protein degradation persists but decreases b/c demand for blood glucose is reduced. 2. free fatty acids, ketones and triglycerides used as energy sources in early starvation. 3. In late starvation, muscle relies on free fatty acids for energy, sparing ketones for brain

Question 25

Brain metabolism in starvation state

Answer 25

1. increasing ketone use spares blood glucose for use by RBCs which rely solely on glucose for energy. 2. Decreasing glucose use by the brain reduces the need for hepatic gluconeogenesis and thus indirectly spares muscle protein