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une ch 26

basic concepts in the regulation of fuel metabolism

QuestionAnswer
What is the effect of insulin on the following metabolic pathways? The storage of glucose in glycogen. Insulin increases the rate of the pathway for converting glucose to glycogen. (This is an example of anabolism.)
The mobilization of glucose from glycogen. Insulin inhibits glycogenolysis.(Insulin is an anabolic hormone. This is an example of catabolism.)
The synthesis of fatty acids from glucose in the liver. Insulin increases the rate of the pathway of fatty acid synthesis from glucose.
The synthesis of triacylglycerols in liver and adipose tissue. Insulin increases the rate of the pathway of the synthesis of triacylglycerols in liver and adipose tissue. (This is an example of anabolism.)
The mobilization of free fatty acids from adipose tissue (breakdown of TG & FA). Insulin inhibits the mobilization (breakdown) of free fatty acids from adipose tissue. (Insulin is an anabolic hormone. This is an example of catabolism.)
The synthesis of proteins in most tissues. Insulin increases the rate of protein synthesis in most tissues. (This is an example of anabolism.)
The mobilization of amino acids from proteins for gluconeogenesis. Insulin inhibits the mobilization (breakdown) of amino acids from proteins.
Would you expect this insulin effect after a high carbohydrate meal, after an overnight fast, during times of stress? High carb meal: Yes Overnight Fast: No Insulin low bc the glucose levels low. Stressful Times: No During stressful times, insulin is low because glucagon and epinephrine are high to raise blood glucose to cope with the stress.
What is the effect of glucagon upon the following metabolic pathways? The storage of glucose in glycogen. Glucagon inhibits the storage of glucose in glycogen.
The mobilization of glucose from glycogen. Glucagon increases the rate of glycogenolysis (mobilization of glucose FROM glycogen)
The synthesis of fatty acids from glucose in the liver. Glucagon inhibits the synthesis of fatty acids from glucose in the liver.
The synthesis of triacylglycerols in liver and adipose tissue. Glucagon inhibits the synthesis of triacylglycerols in liver and adipose tissue.
The mobilization of free fatty acids from adipose tissue. Glucagon increases the rate of lipolysis (mobilization of free fatty acids from lipids)
The mobilization of amino acids from proteins for gluconeogenesis. Glucagon increases the rate of amino acid mobilization from proteins for gluconeogenesis. However, in the skeletal muscle there is no effect because skeletal muscles lack glucagon receptors.
Would you expect this glucagon effect after a high carbohydrate meal, after an overnight fast, during times of stress? HC Meal:N(inc glucose= increase of Insulin->inhibits glucagon release.) ON Fast:Y(Both glucose n insulin levels drop after meal.allows glucagon release->cont thru overnight fast.) Stress:Y(Cortisol same effect as glucagon- inc catabolic reactions)
What is the effect of stress hormones as a group upon the following metabolic pathways? The storage of glucose in glycogen. No. It is inhibited except by cortisol which stimulates glycogen synthesis.
The mobilization of glucose from glycogen. Yes. It is activated/increased.
The synthesis of fatty acids from glucose in the liver. No. It is inhibited.
The synthesis of triacylglycerols in liver and adipose tissue. No. It is inhibited.
The mobilization of free fatty acids from adipose tissue. Yes. It is activated/increased.
The synthesis of proteins in most tissues. It is inhibited in most tissues. Some proteins must still be synthesized in order to maintain body functions. However, protein degradation happens at a much more rapid pace than synthesis.
The mobilization of amino acids from proteins for gluconeogenesis. Yes. It is activated/increased.
Cortisol stimulates both glycogen synthesis and gluconeogenesis.
What is the effect of the following upon insulin release and what is the hormone or metabolite directly affecting the B-cells?: (1) A high carbohydrate meal: Inc glucose/insulin=inhibit glucagon. Inc glucose= inc glycolysis n ATP. Inc ATP acting on Beta cells=inc insulin secretion.Blood carrying secreted insulin from Beta cells. insulin binds to alpha cells, where glucagon secretion is suppressed.
What is the effect of the following upon insulin release and what is the hormone or metabolite directly affecting the B-cells?: (2) A high protein meal: protein meals secrete less insulin compared to a carb meal. Insulin inc following a high protein diet that inc concentrations of AA Beta cells not inhibited by protein meals and inc glucagon caused by protein meal does not bind to Beta receptors.
What is the effect of the following upon insulin release and what is the hormone or metabolite directly affecting the B-cells?: Insulin inhibited due to increased epinephrine and norepinephrine, which bind to Beta cell receptors. Epinephrine and norepinephrine released during times of stress such as sickness, exercise and starvation.
how does glucose directly affect the beta cells? Glucose directly affects the B-cells. An increase in glucose causes an increase in ATP generated (from glycolysis, TCA cycle) which increases the amount of insulin secreted.
What is the effect of the following upon glucagon release and what is the hormone or metabolite directly affecting the a-cells? (1) A high carbohydrate meal: Insulin up, glucagon down. Glucose will rise in response to the high intake of carbohydrate. Once there is a rise in glucose, insulin hormone is triggered and released, causing a suppression of glucagon as a result.
What is the effect of the following upon glucagon release and what is the hormone or metabolite directly affecting the a-cells? (2) A high protein meal: AA up. Glucagon up. Glucagon made of AA,AA will form and trigger glucagon release. AA induce insulin secretion,just not as much as glucose. Glucagon will stimulate GNG from AA following a high protein, low carb (Atkins diet) meal.
What is the effect of the following upon glucagon release and what is the hormone or metabolite directly affecting the a-cells? (3) Starvation, trauma, or vigorous exercise: Inc epinephrine & cortisol leads to inc glucagon. (epi has a bigger effect because it inhibits insulin release). In cases of stress and trauma, insulin secretion is not matched to glucagon release and blood glucose present. (looksliketype2diabetes)
how does insulin affect the alpha cells? Insulin directly affects the a-cells. Increased insulin release causes an inhibition of glucagon release from a-cells.
To the extent that it is known, explain the series of events following an increase in insulin that results in more glucose transporters in muscle and adipose tissue cell membranes. insulin binds to alpha subunits->tyrosine kinase region of beta subunit autophosphorylates->beat subunit activated n binds IRS proteins-> binds PI3-kinase (has SH2)->becomes activated protein kinase B-> PKB puts GLUT-4 in membrane-> inc glucose uptake
Be able to list all the intermediates in the signal transduction of glucagon from the binding of the ligand to the activation of a protein by phosphorylation. Glucagon Binds --> Activates heterotrimeric G protein and releases--> GDP for GTP --> alpha subunit binds Adenylate Cyclase --> produces cAMP --> cAMP takes Protein Kinase A apart-> catalytic subunit phosphorylates phosphorylase kinase-> glycogen degraded
Created by: carolanimal
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