Content 9/15 to 9/19

Question 1

T/F - Elevated lipid levels and negative factors derived from fat cells can enhance transcription of the insulin gene in beta cells?

Answer 1

FALSE

Question 2

What factors are associated with the short-term (acute) effects of a rise in plasma FFAs?

Answer 2

Enhanced release of insulin by Beta cells

Higher mitochondrial FFA oxidation and production of ATP

Question 3

T/F - At the very beginning of the development of insulin resistance the levels of glucose and insulin in the blood rise simultaneously?

Answer 3

FALSE

Question 4

Sulfonylureas can be used to treat Type 2 Diabetes by increasing insulin secretion and reducing hyperglycemia through doing the job of ____ by binding to and closing ____

Answer 4

They act as ATP to bind to and close K+ Channels

Question 5

Long-term elevations in what factors can contribute to the loss of Beta cells?

Answer 5

Leptin
Glucose
Inflammatory cytokines
FFAs

Question 6

Which of the following are false based upon alpha cell regulation during the development of type 2 diabetes?

• SNS overactivity will affect Ach receptors on the alpha cell increasing glucagon release
• As in the beta cell, the condition of oxidative stress will increase the apoptotic activity of caspases in the Alpha cells
• SNS overactivity can enhance glucagon release from the alpha cell even when blood glucose levels are elevated
• Glucagon release by alpha cells may increase as insulin decreases due to a removal of inhibition

Answer 6

SNS overactivity will affect Ach receptors on the alpha cell increasing glucagon release
As in the beta cell, the condition of oxidative stress will increase the apoptotic activity of caspases in the alpha cell

Question 7

T/F - The initial part of the phase of beta cell failure coincides with the transition from a state of impaired glucose tolerance to overt type 2 diabetes?

Answer 7

TRUE

Question 8

T/F - Following the consumption of a meal containing carbohydrates, circulating insulin levels increase and circulating glucagon levels normally are suppressed?

Answer 8

TRUE

Question 9

Which of the following statements about glucagon signaling in the hepatocyte is FALSE?

• The glucagon receptor is a GPCR that associates with Gs
• PKA will directly phosphorylate and activate phosphorylase
• PKA will directly phosphorylate and activate phosphorylase kinase
• Glucagon action in the cell depends on an increase in cAMP levels

Answer 9

PKA will directly phsophorylate and activate phosphorylase is FALSE. . . all the others are true

Question 10

During exercise or fasting glucagon will mediate an increase in HGP. What factors aid this enhancement of HGP?

Answer 10

Increased G6Pase expression
Phosphorylation of phosphorylase kinase
An increase in cAMP levels

Question 11

T/F - GSK-3 and GS are inactive when phosphorylated. In sulin can activate Akt which will phosphorylate and inactivate GSK-3 allowing Gs to be in a dephosporylated more active form thereby promoting glycogen synthesis?

Answer 11

TRUE

Question 12

T/F - Glucagon stimulates both glycogenolysis and gluconeogenesis in the liver?

Answer 12

TRUE

Question 13

Altered transcription of the enzymes PEPCK and G6Pase is a major mechanism for the regulatoin of gluconeogenesis in hepatocytes. Which of the following are involved in the SUPPRESSION of PEPCK and G6Pase transcription by insulin?

• Signaling initiated by activation of the insulin receptor by insulin binding
• Signaling involving tyrosine phosphorylation or IRS-1 by the insulin receptor
• Suppression of gene transcription directly by activation of the p38 kinase
• Suppression of gene transcription directly by activation of MAPK
• Inhibition of GSK-3-dependent gene transcription by AKT-mediated phosphorylation of GSK-3

Answer 13

Signaling initiated by activation of the insulin receptor by insulin binding
Signaling involving tyrosine phosphorylation or IRS-1 by the insulin receptor
Suppression of gene transcription directly by activation of the p38 kinase
Inhibition of GSK-3-dependent gene transcription by AKT-mediated phosphorylation of GSK-3

Question 14

When activated by insuiln PP1 will decrease the activity of ____ and increase the activity of ____?

Answer 14

Phosphorylase and glycogen synthase

Question 15

T/F - Glucose transport into/out of the hepatocyte via GLUT-2 is not regluated by insulin signaling in the hepatocyte?

Answer 15

TRUE

Question 16

T/F - Insulin-mediated effects on HGP occur more quickly than glucagon-mediated effects b/c insulin can modulate glycogenolysis while glucagon can only modulate gluconeogenesis?

Answer 16

FALSE

Question 17

T/F - GSK-3 can disrupt insulin action in cells by phosphorylating IRS-1 on tyrosine residues or by phosphorylating and inhibiting glycogen synthesis?

Answer 17

FALSE

Question 18

T/F - The insulin-dependent inhibition of an inhibitory process in a metabolic pathway is the same as a stimulatory effect of insulin in this metabolic pathway?

Answer 18

TRUE

Question 19

During the course of the development of the Metabolic Syndrome and Type 2 Diabetes when does GP normally start to become elevated?

Answer 19

Elevated HGP beings to develop once beta cells failure starts

Question 20

T/F - In type 2 diabetic subjects suppressing glucagon secretion by a pharmacological intervention results in a greater glucose excursion in response to a carbohydrate feeding?

Answer 20

FALSE

Question 21

In type 2 diabetic patients the lesser rise of insulin following a carbohydrate containing meal (compared to non-diabetics) can contribute to the lack of suppression of glucagon levels?

Answer 21

TRUE

Question 22

T/F - Decreased tyrosing phosphorylation of IR and IRS-1 in the hepatocyte will result in a decreased rate of HGP?

Answer 22

FALSE

Question 23

Excess serine phosphorylation of IR and IRS in hepatocytes causes insulin resistance. Which of the following are associated with this serine phosphorylation of IR and IRS?

• Decreased insulin-dependent tyrosine phosphorylatoin of IR and IRS
• Reduced suppression of glycogenolysis by insulin
• Enhanced suppression of gluconeogensis by insulin
• Decreased activation of glycogen synthesis by insulin
• Decreased HGP

Answer 23

Decreased insulin-dependent tyrosine phosphorylatoin of IR and IRS
Reduced suppression of glycogenolysis by insulin
Decreased activation of glycogen synthesis by insulin

Question 24

T/F - Inappropriate elevations in HGP in the Metabolic Syndrome can lead to the transition from IGT to overt type 2 diabetes?

Answer 24

TRUE

Question 25

While the glucagon:insulin ratio is enhanced in later stages of the Metabolic Syndrome it underestimates the elevation of HGP b/c it doesn’t take into account insulin resistance?

Answer 25

TRUE