Chapter 19
What is the threshold for insulin release?
Approximately 80 mg of glucose/dL
How does insulin directly inhibit glucagon
As glucose levels increase in the blood, insulin is secreted into the blood by B-cells. The direction of blood flow in the islets of the pancreas carries insulin from the β-cells in the center of the islets to the peripheral α-cells, where it suppresses glucagon secretion.
T or F: Insulin binding to receptor activates PI-3K signaling pathway which leads to cell growth and gene expression
FALSE Activation of PI-3K signaling pathway leaders to synthesis of lipids, proteins, and glycogen It also leads to cell survival and proliferation
T or F: The amount of cAMP is unaffected by hormone binding and activity of adenylate cyclase
FALSE Amount of cAMP present at any time is a direct reflection of hormone binding and the activity of adenylate cyclase
T or F: Insulin is a major catabolic hormone
FALSE Anabolic
T of F: Only glucagon increases after a high protein meal
FALSE Both insulin and glucagon increase to some extent after a high-protein meal Amino acids also induce insulin secretion but not to the same extent that glucose does Insulin release stimulates amino acid uptake by tissues and enhances protein synthesis. However, because glucagon levels also increase in response to a protein meal, the critical factor is the insulin-to-glucagon ratio Sufficient glucagon is released that gluconeogenesis is enhanced (at the expense of protein synthesis) and the amino acids that are taken up by the tissues serve as a substrate for Gluconeogenesis.
T or F: Cortisol only has a genomic signal transduction pathway
FALSE Cortisol has both a genomic and no genomic signal transduction pathway
T or F: Epinephrine binds to receptors on plasma membrane or can diffuse across the plasma membrane and bind with cytosolic receptors
FALSE Epi can not cross plasma membrane. Only binds to receptors on plasma membrane
T or F: The release of Epinephrine, Norepinephrine, and Cortisol are similar to insulin and glucagon in that they are released in direct response to changing levels of fuels in the blood
FALSE Epinephrine, Norepinephrine, and Cortisol release is mediated by neuronal signals
T or F: Glucose enters Alpha-cells of pancreas through GLUT-2 to stimulate glucagon secretion
FALSE GLUT-1 GLUT-2 is on Beta-cells for insulin secretion
T or F: During insulin signal transduction, GSK3 phosphorylates glycogen synthase causing it to become active
FALSE GSK3 deactivates/phosphorylates glycogen synthase, therefore, PKB inactivating GSK-3 leads to continual activation of glycogen synthase which means more glycogen will be produced (glucose is stored)
T or F: Insulin has no influence on skeletal muscle metabolism
FALSE Glucagon has no influence on skeletal muscle metabolism
T or F: Glucagon has a very high half-life
FALSE Half life of only about 3-5 minutes Glucagon is rapidly metabolized in the liver and kidneys
T or F: The increase in intracellular Na+ stimulates the fusion of insulin-containing exocytotic vesicles with the plasma membrane, resulting in insulin secretion
FALSE Increase in Ca2+
T or F: Membrane depolarization due to inhibition of K+ channel stimulates release of glucagon
FALSE Increased membrane polarization due to activation (or less inhibition) of K+ channels stimulates release of glucagon Low glucose produces less ATP therefore ATP/ADP ratio decreases - Less inhibition of K+-ATP (K+ goes out) - increases membrane polarization
T or F: Insulin only affects glucose levels
FALSE Insulin binding to receptor also affects lipid and protein synthesis
T or F: In addition to its storage function, insulin increases fatty acid synthesis and cell growth
FALSE Insulin increases PROTEIN synthesis and cell growth
T or F: Insulin is rapidly removed from the circulation and degraded by the kidney so blood insulin levels decrease rapidly once the rate of secretion slows.
FALSE Insulin is rapidly removed from the circulation and degraded by the liver so blood insulin levels decrease rapidly once the rate of secretion slows. Kidney and muscle do degrade insulin to some extent
T or F: Once the threshold of 80 mg glucose/dL is reached, insulin is secreted in an all or nothing response
FALSE Insulin secretion is not all or nothing. Insulin secretion is proportional to the glucose concentration up to about 300 mg/dL
T or F: The amount of insulin released during a high-protein meal is the same as the amount released by a high-carb meal
FALSE Less is released after a high-protein meal
T or F: Glucagon site of action is principally the liver and skeletal muscle cells
FALSE Liver and adipose tissue
T or F: The "pre" sequence of preproinsulin is located on the C-terminal
FALSE N-terminal
What organ degrades insulin?
Liver
What is insulin?
Major anabolic hormone that promotes storage of nutrients - Glucose storage as glycogen in liver and muscles (glycogenesis) - Conversion of glucose to TAG in the liver and their storage in adipose tissue - Amino acid uptake and protein synthesis in skeletal muscle Insulin also increases synthesis of albumin and other proteins by the liver Inhibits fuel mobilization Release of insulin is dictated by the level of glucose in the blood
What cells release glucagon?
alpha cells of pancreas
What cells release insulin
beta cells of pancreas
What does MAP Kinase signaling activation lead to?
cell growth and gene expression
Name 2 catecholamines
epinephrine and norepinephrine —> Act as neurotransmitters or as hormones
Insulin binding to receptor activates MAP Kinase signaling leading to fusion of GLUT vesicles with membranes
FALSE Activates PI-3K which leads to fusion of GLUT vesicles with membrane
When does insulin levels return to basal levels?
About 2 hours after a meal as blood glucose levels fall
What are the 3 principal ways to achieve metabolic homeostasis?
1. Concentrations of nutrients and metabolites in the blood determine the rate at which they are used or stored 2. Hormones carry messages to target tissues about the physiologic state of the body and nutrient level supply or demand 3. The central nervous system uses neural signals to control tissue metabolism. Either directly or through release of hormone
Describe the signal transduction by glucagon
1. Glucagon binds to receptor causing associated G-protein to exchange GDP for GTP. 2. α-subuits/GTP dissociates and binds to adenylate cyclase 3. Binding to AC activates cAMP synthesis (Increase cAMP) 4. cAMP activates PKA 5. PKA initiates phosphorylation cascade leading to: - Gluconeogenesis - Glycogenolysis: Glycogen → Glc-1-P 6. Signal terminated - cAMP phosphodiesterase —> rapid degradation of cAMP - Inactivation of G-protein via GTP hydrolysis on α-subuit and reformation of α,β,γ -GDP complex
Describe the secretion/release of insulin from B-cells
1. Glucose enters the β-cell via specific glucose transporter proteins known as GLUT 2 2. Glucose is phosphorylated through the action of glucokinase to form glucose 6-phosphate. - Glucose-6-P is metabolized through glycolysis, TCA cycle, and OP. - Results in an increase in ATP levels within the β-cell 3. As the β-cell ATP/adenosine diphosphate (ADP) ratio increases, the activity of a membrane-bound ATP-dependent K+ channel (K+ATP) is inhibited (the channel is closed) 4. The closing of the K+ channel leads to a membrane depolarization which activates a voltage-gated Ca2+ channel that allows Ca2+ to enter the β-cell such that intracellular Ca2+ levels increase significantly 5. The increase in intracellular Ca2+ stimulates the fusion of insulin-containing exocytotic vesicles with the plasma membrane, resulting in insulin secretion **Thus, an increase in glucose levels within the β-cells initiates insulin release**
Describe secretion of glucagon
1. Glucose transported by GLUT1 of alpha cell 2. Low glucose produces less ATP 3. ATP/ADP ratio decreases - Less inhibition of K+-ATP (K+ goes out) - increases membrane polarization 4. Increased polarization - activates voltage gated Ca2+ channels - activates voltage gated Na+ channels 5. Intracellular [Ca2+]↑ 6. Glucagon vesicles fuse with cell membrane 7. [Na+] ↑ restores potential and Ca2+ influx stops
Describe the process of signal transduction by insulin
1. Insulin initiates its action by binding to an insulin receptor on the plasma membrane 2. On binding of insulin, the tyrosine kinase portion of the β-subunits phosphorylate tyrosine residues on each other (autophosphorylation) as well as several other enzymes within the cytosol. 3. The activated phosphorylated receptor binds IRS-1 3. The IRS protein becomes phosphorylated at multiple sites creating an SH2 domain with multiple binding sites 4. Activated/phosphorylated IRS binds to PI-3 kinase at one of the SH2 domains 5. Activated PI-3 kinase will phosphorylate/activate membrane bound PI-3,4,5-trisP 6. PI-3,4,5-trisP is a binding site for PDK 1 and PKB in the membrane 7. PDK1 will bind to PI-3,4,5-trisP in the membrane and phosphorylates/activate PKB. 8. Activated/phosphorylated PKB will dissociate from membrane PI-3,4,5-trisP 9. PKB will travel in cytosol and phosphorylate/INACTIVATE Glycogen Synthase Kinase 3 (GSK-3) 10. Active GSK3 deactivates/phosphorylates glycogen synthase, therefore, PKB inactivating GSK-3 leads to continual activation of glycogen synthase which means more glycogen will be produced (glucose is stored)
What are the 5 Principles of hormonal signaling mechanisms
1. Specificity of action in tissues is conferred by the receptor on target cell for glucagon. - The major actions of glucagon occur in liver, adipose tissue, and certain cells of the kidney that contain glucagon receptors. 2. Signal transduction involves amplification of the first message. - Glucagon and other hormones are present in the blood in very low concentrations. - These minute concentrations of hormone are adequate to initiate a cellular response because the binding of one molecule of glucagon to one receptor ultimately activates many PKA molecules, each of which phosphorylates hundreds of downstream enzymes. 3. Integration of metabolic responses. - For instance, the glucagon-stimulated phosphorylation of enzymes simultaneously activates glycogen degradation, inhibits glycogen synthesis, and inhibits glycolysis in the liver 4. Augmentation and antagonism of signals. - An example of augmentation involves the actions of glucagon and epinephrine - Although these hormones bind to different receptors, each can increase cAMP and stimulate glycogen degradation. 5. Rapid signal termination. - In the case of glucagon, both the termination of the Gs-protein activation and the rapid degradation of cAMP contribute to signal termination.
What are the 3 basic types of signal transduction for hormones binding to receptors on the plasma membrane?
1. receptor coupling to adenylate cyclase - produces cAMP - cAMP sets off phosphorylation cascade 2. receptor kinase activity - Initiates phosphorylation cascade - Phosphorylation can either turn off or turn on enzymes 3. receptor coupling to hydrolysis of phosphatidylinositol bisphosphate (PIP2). - Hydrolysis producing PIP3 and DAG second messengers - Phosphorylation producing PI-3,4,5-trisP - All initiate a phosphorylation cascade
When do the highest of levels of insulin occur?
30 - 45 min after a high carb meal Slightly lagging plasma glucose
What is a normal blood glucose level
80-100 mg/dL
How many different types of adrenergic receptors are there?
9
Prohormone
A physiologically inactive precursor to a hormone Ex: Proinsulin
Glucagon
Act to maintain fuel availability in the absence of dietary glucose by stimulating the release of glucose from liver glycogen (glycogenolysis) Stimulates gluconeogenesis from lactate, glycerol, and amino acids Stimulates mobilization of fatty acids from adipose triacylglycerols to provide an alternate source of fuel Site of action = liver and adipose tissue Message carried by glucagon = "glucose is gone"
What does PI-3K signaling pathway lead to?
Activation of PI-3K signaling pathway leaders to synthesis of lipids, proteins, and glycogen It also leads to cell survival and proliferation It activates fusion of GLUT vesicles with membranes. Increases flux of glucose into cell
B-1 adrenergic receptors
Adenylate cyclase - cAMP system β1-receptor is the major adrenergic receptor in the human heart and is primarily stimulated by norepinephrine. On activation, the β1-receptor increases the rate of muscle contraction, in part because of PKA-mediated phosphorylation of phospholamban
B-2 Adrenergic Receptor
Adenylate cyclase - cAMP system β2-receptor is present in liver, skeletal muscle, and other tissues and is involved in the mobilization of fuels (such as the release of glucose through glycogenolysis). It also mediates vascular, bronchial, and uterine smooth muscle contraction. Epinephrine is a much more potent agonist for this receptor than norepinephrine, whose major action is neurotransmission. Ex: Albuterol
B-3 adrenergic receptor
Adenylate cyclase - cAMP system β3-receptor is found predominantly in adipose tissue and to a lesser extent in skeletal muscle. Activation of this receptor stimulates fatty acid oxidation and thermogenesis, and agonists for this receptor may prove to be beneficial weight-loss agents.
When is the glucagon level the lowest?
After a high-carb meal Begins to rise in earnest about 4-5 hours after high carb meal
Describe the response to a high-carb meal from a normal patient vs a diabetic patient
After high carb meal: Normal: Blood glucose peaks after about 1 hour and drops back to normal blood glucose levels Diabetic: Blood glucose peaks about an hour after eating but takes a lot longer to lower the blood glucose levels
Describe what occurs between insulin/glucagon after a high protein meal
Both insulin and glucagon increase to some extent after a high-protein meal Amino acids also induce insulin secretion but not to the same extent that glucose does Insulin release stimulates amino acid uptake by tissues and enhances protein synthesis. However, because glucagon levels also increase in response to a protein meal, the critical factor is the insulin-to-glucagon ratio Sufficient glucagon is released that gluconeogenesis is enhanced (at the expense of protein synthesis) and the amino acids that are taken up by the tissues serve as a substrate for Gluconeogenesis.
Name the 3 minor up-regulators of insulin
Certain amino acids GIP and GLP-1 —> gut hormones released after ingestion of food Neural input
T or F: As the β-cell ATP/adenosine diphosphate (ADP) ratio increases, the activity of a membrane-bound ATP-dependent Na+ channel (Na+ATP) is inhibited (the channel is closed)
FALSE ATP-dependent K+ channel is inhibited
T or F: The a-1 adrenergic receptors worth through adenylate cyclase-cAMP system
FALSE A-1 = PIP2 system B 1,2,3 = adenylate cyclase-cAMP system
T or F: Adenylate Cyclase converts cAMP to ATP
FALSE ATP to cAMP. AC increases synthesis of cAMP
T or F: Cortisol can only activate genes
FALSE Activate or regress Transactivation/Transregression
T or F: Insulin binding to insulin receptor activates fusion of GLUT vesicles in cytosol
FALSE PI-3K activates fusion of GLUT vesicles in cell membrane GLUT 1, 2, 3, 4 = glucose transport proteins. Transports glucose into the cell. Tissue specific
T or F: The "pre" sequence of preproinsulin gets cleaved off in the cytosol
FALSE RER
T or F: Insulin and glucagon are not prohormones
FALSE They are both polypeptide hormones synthesized as prohormones
True or False: During insulin secretion, the increased polarization of the cell activates voltage gated Ca2+ channels and voltage gated Na+ channels
FALSE This occurs during glucagon secretion
T or F: Insulin receptor is a adenylate cyclase receptor
FALSE Tyrosine Kinase receptor
T or F: Mg2+ is transported in the Golgi complex storage vesicles with proinsulin because when proinsulin is cleaved at the "connecting peptide" region, Mg2+ coprecipitates with insulin
FALSE Zinc (Zn) not Mg2+
T or F: Phosphodiesterase catalyzes ATP to cAMP
FALSE cAMP —> ATP. Decreases cAMP concentration
T or F: The alpha subunit has tyrosine kinase activity
FALSE the cytosolic part β-subunit has tyrosine kinase activity.
T or F: Glucagon decreases after consuming a high protein meal
False Glucagon increases well beyond fasting level
T or F: During the secretion of insulin, the ATP/ADP ratio decreases resulting in the inhibition of K+ channels
False Increased ATP/ADP ratio ATP/ADP ratio decreases in glucagon secretion
T or F: Glucose only has a direct effect on inhibiting glucagon
False Indirect and direct effect of inhibiting glucagon. Glucose increases secretion of insulin which also inhibits glucagon
T or F: Insulin binding to receptor activates MAP Kinase signaling leading to synthesis of lipids, proteins, and glycogen
False Leads to cell growth and gene expression
T or F: The removal of the "pre" sequence of preproinsulin results in the formation of biologically active insulin
False Removal of pro "C-peptide" results in biologically active insulin It leaves the Golgi complex in storage vesicles where a protease removes the biologically inactive "connecting peptide" (C-peptide) and a few small remnants, resulting in the formation of biologically active insulin.
What hormones are insulin counter-regulatory hormones
Glucagon - stimulated by low blood glucose Epinephrine - stimulated by ACTH and released from adrenal medulla NorEpinephrine - Released from nerve endings Cortisol - stimulated by ACTH and released by adrenal cortex They oppose actions of insulin by mobilizing fuels
Discussed signal transduction by epinephrine and norepinephrine via B adrenergic receptors
G-protein - Adenylate Cyclase - cAMP system The binding of epi/norepinephrine stimulates mobilization of fuel cAMP production activates PKA Actived PKA activates numerous cellular processes involved in Fight-Flight response
What are the names of the larger glucagon-containing fragments that are produced after proteolytic cleavage of preproglucagon
GLP-1 and GLP-2 GLP = Glucagon-Like-Protein
What 2 gut hormones affect insulin stimulation?
Gastric Inhibitory Polypeptide Glucagonlike Peptide 1 Both are released after ingestion of food and aid in the onset of insulin release
Glycogen Synthase Kinase 3 (GSK-3)
Glycogen synthase = glycogen synthesis Active GSK-3 phosphorylates glycogen synthase and knocks out its activity - Subsequently, phosphatases are binding to phosphorylated glycogen synthase and removing P causing glycogen synthase to become activated again Phosphatases and GSK3 are competing with each other When insulin binds to its receptor, GSK-3 is deactivated/phosphorylated - Therefore, phosphatases are unopposed and activate glycogen synthase - 3 binding sites for P. Each P that's added makes glycogen synthase slower
Where does the "pre" sequence of preproinsulin get cleaved off?
In the RER
Phosphodiesterase is inhibited by methylxanthines, a class of compounds that includes caffeine. Would the effect of a methylxanthine on fuel metabolism be similar to fasting or to a high-carbohydrate meal?
Inhibition of phosphodiesterase by methylxanthine would increase cAMP and have the same effects on fuel metabolism as would an increase of glucagon and epinephrine, as in the fasted state. Increased fuel mobilization would occur through glycogenolysis (the release of glucose from glycogen) and through lipolysis (the release of fatty acids from triacylglycerols).
Describe the synthesis of insulin
Insulin is synthesized as a preprohormone that is converted in the rough endoplasmic reticulum to proinsulin The "pre" sequence is a short hydrophobic signal sequence at the N-terminal end that is cleaved as it enters the lumen of the RER After cleavage of the pre sequence, proinsulin folds into proper conformation and disulfide bonds are formed between the cysteine residues It is then transported in microvesicles to the Golgi Complex It leaves the Golgi complex in storage vesicles where a protease removes the biologically inactive "connecting peptide" (C-peptide) and a few small remnants, resulting in the formation of biologically active insulin. Zinc is included in the storage vesicles because cleavage of the C-peptide decreases the solubility of the resulting insulin, which then coprecipitates with zinc.
Describe the response of insulin and glucagon after a high protein meal
Insulin: - Peaks >20% of high carb meal - Stimulates A.A uptake and protein synthesis Glucagon - Increases well beyond fasting level - Stimulates gluconeogenesis - Amino acids —-> glucose - Protein degradation - High glucagon/insulin ratio - Gluconeogenesis is favored over protein synthesis - Amino Acids used to synthesize glucose rather than build proteins
What microscopic cluster of small glands in the pancreas releases insulin and glucagon
Islet of Langerhans - Scatted among the cells of the exocrine pancreas Alpha cell —-> Glucagon Beta Cells —-> Insulin
After glucose enters B-cell through GLUT-2, what happens to glucose?
It is phosphorylated to G-6-P and is metabolized via glycolysis, TCA cycle, or oxidative phosphorylation
How does epinephrine effect insulin response ?
Negative effect Epi is secreted in response to fasting, stress, trauma, exercise etc. which signals energy use not energy storage Increase in epi results in decreases release of insulin because insulin signals for glucose storage
What molecules is glucose a precursor for?
Other carbohydrates - fructose, lactoce, etc Non-carb molecules - Non-Essential amino acids - Non-essential fatty acids - Cholesterol and steroid hormones - Nucleic acids
Discussed signal transduction by epinephrine and norepinephrine via A adrenergic receptors
PIP2 system Post-synaptic receptors Vascular and smooth muscle contraction
What enzyme rapidly degrades cAMP to AMP
Phosphodiesterase
Glycogenesis
Polymerization of glucose for storage as glycogen
Describe the structure of insulin
Polypeptide hormone Active form of insulin is composed of 2 polypeptide chains (A-chain and B-chain) linked by two interchain disulfide bonds A-chain has an additional intrachain disulfide bond
Describe structure of glucagon
Polypeptide hormone Synthesized as an α-cells of the pancreas by cleavage of the much larger preproglucagon, a 160-amino acid peptide. Like insulin, preproglucagon is produced on the RER and is converted to proglucagon as it enters the lumen of the endoplasmic reticulum. Proteolytic cleavage at various sites produces the mature 29-amino acid glucagon (molecular weight = 3,500 Da) and larger glucagon-containing fragments (named GLP-1 and GLP-2)
a-1 adrenergic receptors
Postsynaptic receptors Mediate vascular and smooth muscle contraction. They work through the PIP2 system via activation of a Gq-protein and phospholipase C Mediates glycogenolysis in the liver
Describe non-genomic signal transduction pathway for cortisol
Protein carrier delivers glucocorticoid to target tissue Glucocorticoid binds to cell surface receptor (GR) Receptor interacts with other proteins to elicit effect Ex: MAPK PI3K AKT
T or F: Alpha cells release insulin in response to carbohydrate ingestion
TRUE
T or F: Amino acids stimulate release of glucagon
TRUE
T or F: Epinephrine and norepinephrine cause the mobilization of fuels
TRUE
T or F: Signals from the central nervous system are not required for insulin secretion
TRUE
T or F: cAMP is not affected by ATP, ADP, or AMP levels in the cell
TRUE
T or F: Insulin binding to it's plasma membrane receptor can also lead to MAP Kinase Signaling Pathway
TRUE Insulin leads to MAP Kinase signaling activation which leads to cell growth and gene expression
T or F: Epinephrine and Cortisol are insulin counterregulatory hormones
TRUE They have effects on fuel metabolism that oppose those of insulin
What are the 2 ways to terminate the signal transduction of glucagon
Termination of the Gs-protein activation and the rapid degradation of cAMP via cAMP phosphodiesterase contribute to signal termination.
metabolic homeostasis
The balance between substrate need and substrate availability
What are the general effects of Epinephrine and Norepinephrine
The general effect of these catecholamines is to prepare us for fight or flight. Under these acutely stressful circumstances, these "stress" hormones increase fuel mobilization, cardiac output, blood flow,
Describe insulin receptors
The insulin receptor is a tyrosine kinase receptor with two types of subunits: 1. 2 α-subunits to which insulin binds 2. 2 β-subunits, which span the membrane, protrude into the cytosol, and autophosphorylate each other The cytosolic portion of the β-subunit has tyrosine kinase activity. - On binding of insulin, the tyrosine kinase phosphorylates tyrosine residues on the β-subunit (autophosphorylation) as well as on several other enzymes within the cytosol.
Signal transduction
The mechanism by which the message carried by the hormone ultimately affects the rate of the regulatory enzyme in the target cell
How does neural input affect insulin levels
The pancreatic islet is innervated by the ANS via a branch of vagus nerve Neural signals from vagus nerve help coordinate insulin release with secretory signals initiated by ingestion of fuels **Signals from CNS are not required for insulin secretion**
How does glucose enter B-cells to stimulate release of insulin?
Through specific glucose transporter proteins called GLUT-2
Describe cortisol signal transduction with intracellular receptors
Transactivation and Transregression 1. Protein carrier delivers glucocorticoid (Cortisol) to target tissue - Hydrophobic steroids are bound to plasma protein carries and need to dissociate as an unbound hormone to diffuse into cell **Steroid hormone receptors can be in the cytoplasm or on the nucleus** - Some steroids bind to membrane receptors that use second messangers 2. Glucocorticoid transported across membrane 3. Associates with proteins (receptor) in cytosol or nucleus 4. Complex affects gene transcription (turns on or off) - Receptor/Hormone complex binds to DNA and activates or represses one or more genes - Activates genes create new mRNA that moves back into cytoplasm - Translation of the new mRNA creates new proteins for cells
T or F: Both insulin and glucagon increase after a high-protein meal
True
T or F: Glucagon increases well beyond fasting level after consuming a high protein meal
True
T or F: Glucagon is rapidly metabolized in the liver and kidneys
True
T or F: Increase Ca2+ concentration inside Beta cells stimulates insulin release and increased Ca2+ concentration inside Alpha cells stimulates glucagon release
True
T or F: Insulin is rapidly removed from the circulation and degraded by the liver so blood insulin levels decrease rapidly once the rate of secretion slows.
True
T or F: Insulin secretion is proportional to the glucose concentration up to about 300 mg/dL
True
T or F: Insulin stimulates energy storage
True
T or F: The 160 amino acid preproglucagon is cleaved at various sites to produce the mature 29-amino acid glucagon and larger glucagon-containing fragments named GLP-1 and GLP-2
True
T or F: The concentration of fatty acids in the blood is the major factor determining whether skeletal muscles will use fatty acids or glucose as fuel
True
T or F: The synthesis of glycogen and triglycerides is reduced when glucagon levels rise in the blood.
True
T or F: increased levels of circulation glucagon relative to insulin stimulates the mobilization of fatty acids from adipose tissue
True
T or F: Glucagon has no influence on skeletal muscle metabolism
True Muscle cells lack glucagon receptors