Metabolic Reactions; Endocrine and Neural Control of Metabolism

insulin

the reactions during the absorptive state result from the actions of what hormone

amino acids to proteins (protein synthesis)

glycerol-3-phosphate, fatty acids to triglycerides (lipogenesis)

glucose to glycogen (glycogenesis)

what are the reactions that occur during the absorptive state (amino acids, fatty acids, glucose)

insulin

the reactions during the absorptive state result from the actions of what hormone

amino acids to proteins (protein synthesis)

glycerol-3-phosphate, fatty acids to triglycerides (lipogenesis)

glucose to glycogen (glycogenesis)

what are the reactions that occur during the absorptive state (amino acids, fatty acids, glucose)

GLUCOSE, glucose to CO2, H2O, energy

what is the prime source of energy during the absorptive state? How is this source converted into energy?

stored in the liver as glycogen and triglycerides

what happens to excess glucose during the absorptive state

decreased insulin

the reactions during the post-absorptive state result from the actions of what hormone

proteins to amino acids (proteolysis)

triglycerides to glycerol and fatty acids (lipolysis)

glycogen to glucose (glycogenolysis)

what are the reactions that occur during the post-absorptive state (amino acids, fatty acids, glucose)

fatty acids and ketones

converted by most cells into energy (glucose sparing for NS)

what is the prime source of energy during the post-absorptive state? How is this source converted into energy?

Gluconeogenesis

the formation of new glucose from pyruvate, lactate, glycerol, and amino acids

occurs in the liver and kidney

Islets of Langerhans

endocrine portion of the pancreas

insulin

beta cells of pancreas secrete

function of insulin

anabolism/ net storage, stimulates the absorptive rxns, inhibits the post absorptive rxns

glucagon

alpha cells of pancreas secrete

function of glucagon

catabolism/ mobilization of fuel sources

stimulates post-absorptive state reactions
inhibits absorptive state reactions

peptide, on plasma membrane, coupled to secondary messenger cascades

what chemical class are insulin and glucagon? where are their receptors? what are their receptors coupled to?

high blood glucose

what conditions is insulin secreted

increase plasma glucose

increase insulin secretion from beta islet cells

increase plasma insulin

1. increase glucose uptake by adipocytes and muscles
2. cessation of glucose output; net glucose uptake in the liver

restoration of plasma glucose to normal (negative feedback onto the beta islet cells)

explain what happens when there is an increase in plasma glucose during the absorptive phase

FALSE

true or false: insulin release is regulated by the pituitary

1. insulin binds to the insulin receptor on the surface of muscle and fat cells

2. signal transduction causes vesicles containing GLUT-4 to fuse with the cell membrane

3. GLUT 4s on the surface of the cell allow for the facilitated diffusion of glucose into the cells

4. GLUT 4s are recycled by endosomes

(**remember: membrane turnover, so not permanent placement of the transporters--> increase in Tm is transient)

how does the binding of insulin to its receptor lead to the uptake of blood glucose

GLUT-4

transporter of glucose into the cells

amino acids

in addition to glucose, insulin also increase the # of transporters for

FALSE, uses insulin independent Glut-2 transporter

(the brain doesn't need insulin for glucose transport)

true or false: the brain utilizes GLUT-4 for transport of glucose into cells

glucose transporters go to the membrane without insulin stimulation

(this is why exercise can help improve conditions for Type II diabetics)

explain what happens to glucose transporters during exercise

1. plasma glucose levels (+)
2. plasma amino acid levels (+)
3. incretins (e.g. GIP) (+)
4. sympathetic activity (-)
5. parasympathetic activity (+)

what are the inputs to pancreatic islet beta cells that affect insulin secretion

1. increase in plasma glucose
2. increase in plasma amino acids
3. incretins (GIP)
4. decrease in sympathetic activity
5. increase in parasympathetic activity (via Ach to M-AchR)

what are the inputs that increase insulin secretion

glucagon from islet alpha cells

what hormone is released in response to low plasma glucose

decrease in plasma glucose (during post-absorptive phase)

increase glucagon secretion

increase plasma glucagon

in liver:
1. increase glycogenolysis
2. increase gluconeogenesis
3. increase ketone synthesis

increase plasma glucose
increase plasma ketones

explain how glucagon is released from alpha cells

1. glycogenolysis
2. gluconeogenesis
3. lipolysis

effects of epinephrine on the mobilization of glucose

1. gluconeogenesis
2. lipolysis
3. inhibition of glucose uptake by muscle cells and adipose tissue cells

effects if cortisol on the mobilization of glucose

1. gluconeogenesis
2. lipolysis
3. inhibition of glucose uptake by muscle cells and adipose tissue cells

effects of growth hormone on the mobilization of glucose

ensures fuel substrates are always available to burn

why is it important to have multiple hormones that can cause gluconeogenesis

INSULIN ONLY

what hormones protect against excess plasma glucose

they’re permissive for stimulation of gluconeogenesis and lipolysis in the postabsorptive state

effects of baseline levels of cortisol on organic metabolism

1. increase protein catabolism
2. increased gluconeogenesis
3. decreased glucose uptake by muscle cells and adipose tissue cells
4. increased triglyceride breakdown

effects of increase stress on organic metabolism