PSIO 303 Exam 3 Quiz Questions
T/F: There is a genuine dysfunction in the glucagon secretory mechanism of α-cells of the pancreas in the Metabolic Syndrome.
False
T/F: With increasing resting blood pressure, there are generally increases in fasting plasma insulin and in whole-body insulin sensitivity.
False
Of the following pairs of components, which are the earliest that arise with Metabolic Syndrome? - Hyperinsulinemia and insulin resistance - Impaired glucose tolerance and dyslipidemia - Insulin resistance and hypertension - Dyslipidemia and hyperinsulinemia
Hyperinsulinemia and insulin resistance
Which of the following is neither a core component nor an additional component of Metabolic Syndrome? - Adipocyte dysfunction - Microalbuminuria - Dyslipidemia - Hyperinsulinemia - Hyperkeratosis
Hyperkeratosis
Which of the following is the main site of dysfunction in the myocyte insulin signaling cascade? - PDK1 - PKB/AKT - PIP2 - IRS-1
IRS-1
Which of the following is a correct statement about the liver and glucose homeostasis? - It breaks down stored glycogen to glucose in a process called gluconeogenesis. - It modulates gluconeogenesis and glycogenolysis in response to insulin and glucagon. - It stores glucose carbons primarily as fat in its hepatocytes. - It is able to process nutrients from the intestines via the hepatic-portal circulation, but only after those nutrients are first sensed by endocrine pancreas.
It modulates gluconeogenesis and glycogenolysis in response to insulin and glucagon.
Which of statement about protein phosphorylation is true? - It can be reversed by phosphodiesterases. - It occurs on serine, threonine and tyrosine amino acid residues. - It requires inorganic phosphate in addition to ATP for the enzymatic reaction. - It can only increase the catalytic activity of enzymes.
It occurs on serine, threonine and tyrosine amino acid residues.
Excess SNS signaling to pancreatic α-cells will result in enhanced glucagon secretion. This simulatory effect requires which of the following cell signaling events?
It requires an increase in intracellular Ca2+ levels, causing enhanced exocytosis of glucagon-containing vesicles.
Based on our limited body of knowledge regarding the details of Alpha cell regulation during the development of type 2 diabetes, which of the following is FALSE? - SNS overactivity will affect α-adrenergic receptors on the α-cell, increasing glucagon release. - Just like β-cells, under oxidative stress α-cells are targeted by the apoptotic activity of caspases. - Preserved function of α-cells in the absence of sufficient insulin secretion by β-cells can exacerbate hyperglycemia. - Glucagon release by α-cells can increase as local insulin levels decrease due to a removal of inhibition.
Just like β-cells, under oxidative stress α-cells are targeted by the apoptotic activity of caspases.
Sulfonylureas have beneficial effects on β-cells by binding to __________ and causing them to __________.
KATP channels ; close
Which of the following statements regarding signal transduction is FALSE? - Signal transduction relies exclusively on cell surface receptors in order to change cellular behavior. - Phosphorylation of proteins is a critical (and quite common) component of signal transduction in cells. - Signal transduction is used by the body to change the function of cells. - The use of second messengers allows for signal transduction events to be amplified in the cell.
Signal transduction relies exclusively on cell surface receptors in order to change cellular behavior.
Which of the following statements about HGP in the Metabolic Syndrome is true? - One adaptation contributing to elevated HGP is a greater parasympathetic activation of the α-cells. - An increase in HGP is observed in all individuals with Metabolic Syndrome. - An increase in HGP precedes the phase of compensatory hyperinsulinemia. - One adaptation contributing to elevated HGP is an increase in lipolysis
One adaptation contributing to elevated HGP is an increase in lipolysis
Which of the following proteins is an enzyme which catalyzes one of the rate-limiting steps for gluconeogenesis in liver cells? - hexokinase - GSK-3β - PEPCK - glycogen phosphorylase a
PEPCK
Serine phosphorylation is known to impair the functionality of insulin signaling. Which of the following kinases cannot initiate this effect? - GSK-3beta - JNK - p38 MAPK - PI3K
PI3K
Which of the following enzymes involved in insulin signaling adds phosphates to phospholipids in order to create interaction p artners for other proteins to bind to? - GSK-3β - PDK - PI3K - PKB/Akt
PI3K
Phosphorylation of glycogen synthase kinase 3 (GSK-3) by __________ during insulin ppppp signaling in skeletal muscle, prevents phosphorylation of glycogen synthase (GS) by GSK-3. This results in __________ of glycogen synthesis.
PKB/Akt; stimulation
Which of the following kinases is activated by an increase in plasma FFAs? - JNK - p38 MAPK - PKCθ - IKKβ
PKCθ
Enzymes which remove phosphates from cellular proteins are called __________, whereas enzymes which add phosphates to cellular proteins are called __________.
Phosphatases; kinases
The tissue type primarily responsible for peripheral glucose disposal and for whole-body insulin resistance is:
Skeletal muscle
The insulin receptor is an integral part of the insulin signaling cascade. Which of the following statements is true regarding the insulin receptor? - The insulin receptor is a heterotetramer, consisting of 2 extracellular alpha-subunits that bind the hormone and 2 transmembrane beta-subunits. - The insulin receptor can only phosphorylate itself to stimulate a signal downstream. - The insulin receptor is a tyrosine phosphatase. - Insulin binds to the cystein rich domains of the beta-subunits, thereby enhancing, via a specific conformation change, the tyrosine kinase activity of the alpha-subunits. - The insuline receptor is a monomer, consisting of 2 extracellular alpha-subunits that bind the hormone and two trasmembrane beta-subunits.
The insulin receptor is a heterotetramer, consisting of 2 extracellular alpha-subunits that bind the hormone and 2 transmembrane beta-subunits.
Which of the following statements about Metabolic Syndrome is FALSE? - It is a cluster of pathologies that increases the risk for cardiovascular disease. - The onset of symptoms is typically very rapid - It is also known as Syndrome X and Insulin Resistance Syndrome
The onset of symptoms is typically very rapid
Phosphorylation of which amino acid results in negative modulation of insulin receptor signaling activity when insulin is bound?
Serine
Which of the following statements about adiponectin is false? - The primary form of adiponectin in the plasma is the globular form. - Adiponectin can exist in the plasma as high molecular weight forms, low molecular weight forms, and globular forms. - The globular form of adiponectin has biological action. - Adiponectin is secreted primarily by white fat cells.
The primary form of adiponectin in the plasma is the globular form.
Which of the following statements about the transport of glucose across the endothelium of capillaries in skeletal muscle is/are FALSE? - This transendothelial glucose transport can be directly increased by insulin. - How much glucose is delivered across the endothelium to the skeletal muscle cells can influence the rate glucose transport by the muscle cells - This transendothelial glucose transport is mediated by the GLUT-1 isoform - Increased blood flow to the capillary can increase glucose transport to the extracellular space
This transendothelial glucose transport can be directly increased by insulin.
T/F: Decreases in both circulating adiponectin levels and cellular adiponectin receptor levels can contribute to reduced adiponectin action and to the development of insulin resistance.
True
T/F: GSK-3 and GS are inactive when phosphorylated.
True
T/F: GSK-3 can disrupt insulin signaling in two ways. It can do so by phosphorylating serine residues on IRS-1, and it can also do so by phosphorylating and inhibiting glycogen synthase.
True
T/F: Glucagon stimulates glycogenolysis and gluconeogenesis in the liver.
True
T/F: Increased SNS activity in the Metabolic Syndrome is associated with enhanced renal release of the peptidase renin.
True
T/F: Individuals with a 2-hour glucose level above 200 mg/dL during an OGTT can be diagnosed with type 2 diabetes.
True
T/F: Most of the individuals who have some degree of hypertension also have signs of impaired glucose tolerance and insulin resistance
True
T/F: The onset of the phase of β cell failure coincides with the transition from a state of impaired glucose tolerance to overt type 2 diabetes.
True
T/F: While the glucagon:insulin ratio is enhanced in the Metabolic Syndrome, it underestimates the elevation of HGP because it doesn't take into account insulin resistance.
True
Which of the following statements about IRS proteins is FALSE: - Tyrosine phosphorylation of IRS increases the enzymatic activity of the IRS protein. - IRS proteins are phosphorylated on tyrosine residues by the activated insulin receptor. - Tyrosine-phosphorylated IRS can propogate signaling to modulate numerous aspects of cell metabolism, such as glucose transport, glycogen synthesis, lipid synthesis, and protein synthesis. - Tyrosine-phosphorylated IRS acts as a docking protein to regulated downstream signaling factors.
Tyrosine phosphorylation of IRS increases the enzymatic activity of the IRS protein.
In the transition from a state of impaired glucose tolerance to overt Type 2 diabetes, the individual will experience _____________ insulin secretion and ______________ plasma glucose levels in response to a carbohydrate-containing meal.
decreased, increased
For hepatocytes, which of the following events will not occur in response to excessive serine phosphorylation of IR and IRS? - diminished suppression of glycogenolysis by insulin - diminished HGP - diminished suppression of gluconeogenesis by insu\lin - decreased insulin-dependent tyrosine phosphorylation of IR and IRS
diminished HGP
Which of the following intracellular signaling molecules is NOT involved in the enhanced GLUT4 translocation and glucose transport activity by the interaction of AdipoR1 and APPL1? - P38 MAPK - AMPK - Akt - P13K - eNOS
eNOS
Which organ/tissue is the major one responsible for peripheral disposal of glucose in response to the glucose level rise caused by consumption of a carbohydrate-containing meal? - the hypothalamus - skeletal muscle - adipose tissue - the liver
skeletal muscle
The primary impact of insulin acting on hepatocytes is the ___________ of glycogen synthesis and the _____________ of both glycogen breakdown and gluconeogenesis. Thus overall, insulin leads to a(n) ___________ in hepatic glucose production (HGP)
stimulation; suppression; decrease
Sulfonylureas were developed to help overcome insulin resistance and prevent/control hyperglycemia. These drugs do the job of _____ by binding to and closing a ______.
ATP, K+channel
Adenylate cyclase uses the substrate _____ to form the second messenger chemical _____, and the increase in this second messenger chemical causes the activation of the enzyme named _____.
ATP; cAMP; PKA
High levels of glucose will have all of the following effects on the Alpha cell EXCEPT? - Inhibition of glucagon release. - Activation of Na+ channels and membrane repolarization. - Increased glucose entry via transport using GLUT-1. - Lack of the opening of Ca2+ channels and no change in intracellular Ca2+ levels.
Activation of Na+ channels and membrane repolarization.
Which of the following statements about the secretion and transport of adiponectin is false? - Adiponectin transport across the endothelium of the vasculature in skeletal muscle tissue is by simple diffusion - One mechanism for reduced adiponectin section is increased FFA action on the adipocytes - As adipocytes become larger due to increased lipid storage, the secretion of adiponectin decreases - The transport of adiponectin in the circulation requires attachment to binding globulins such as albumin
Adiponectin transport across the endothelium of the vasculature in skeletal muscle tissue is by simple diffusion
In Metabolic Syndrome, which of the following characteristics of cardiovascular disease (CVD) begins to develop before the deterioration of insulin secretory function (and thus before any transition to a diabetic state)? - Atherogenesis (the formation of fatty plaques in the arteries) - elevated hepatic glucose production (HGP) - microvascular complications such as retinopathy and nephropathy - elevated fasting blood glucose levels
Atherogenesis (the formation of fatty plaques in the arteries)
Which mechanism of cell-cell communication is illustrated by the figure below?
Autocrine
Low levels of glucose, as seen by the pancreas, will result in all of the following, EXCEPT - Beta cell depolarization - Sodium channel activation in the Alpha cell - Glucagon release - Quiescent Beta cells
Beta cell depolarization
Which chemical second messenger is produced by activated phospholipase C (PLC)? - cAMP - Both DAG and IP3 - Ceramide - PIP3
Both DAG and IP3
Which second messenger chemical is a major player in the signal transduction pathway through which glucose stimulates release of insulin by β cells of the endocrine pancreas?
Ca2+
An inhibitor of the serine kinase GSK-3beta will have all of the following effects on insulin-resistant skeletal muscle except: - Cause decreased serine phosphorylation of IRS-1 in the presence of insulin. - Cause increased insulin-stimulated glucose transport. - Cause decreased insulin-stimulated tyrosine phosphorylation. - Cause reduced serine kinase activity of GSK-3beta.
Cause decreased insulin-stimulated tyrosine phosphorylation.
Which of the following is an accurate statement about adiponectin and its relationship to insulin sensitivity? - Circulating adiponectin levels are positively correlated with whole-body insulin sensitivity. - Adiponectin levels are higher in insulin-resistant subjects compared to insulin-sensitive subjects. - Circulating adiponectin levels are positively correlated with % body fat. - Circulating adiponectin levels are positively correlated with fasting insulin levels.
Circulating adiponectin levels are positively correlated with whole-body insulin sensitivity.
T/F: The synthesis and secretion of insulin and glucagon takes place in the exocrine pancreas.
False
When does HGP normally become elevated in the course of the development of the Metabolic Syndrome and type 2 diabetes?
Elevated HGP begins to develop once Beta cell failure starts.
Which of the following is not considered to be an adipokine? - Angiotensinogen - PAI-1 - Adiponectin - Resistin - FFAs
FFAs
T/F: A chemical messenger secreted by one cell and acting on the same cell in the same tissue is an example of paracrine communication.
False
T/F: APPL1 increases glucose transport in skeletal muscle cells by interacting directly with the insulin receptor.
False
T/F: As visceral adiposity begins to increase, there is a parallel increase in the secretion and action of adiponectin.
False
T/F: For Metabolic Syndrome, the increase in insulin resistance happens simultaneously with both the increase in secretion of insulin and the elevation of fasting plasma glucose.
False
T/F: Glucose that enters the bloodstream from the intestines is first processed and detected by the pancreas.
False
T/F: Hormone-mediated effects on HGP occur most rapidly through cellular adjustments to gluconeogenesis, whereas the modulation of glycogenolysis and glycogenesis takes much longer.
False
T/F: Hormones secreted from the respective cells in the pancreas are delivered to the hepatic-portal circulation by the pancreatic duct.
False
T/F: In hepatocytes, decreased tyrosine phosphorylation of the IR and IRS-1 will result in decreased HGP.
False
T/F: Insulin can bind to receptors on the smooth muscle cells of arterioles which supply blood to the capillary beds of the skeletal muscle tissue. In doing so, insulin will activate nitric oxide synthase (eNOS) in those smooth muscle cells, leading to nitric oxide production and vasodilation.
False
T/F: Only IRS-1 is affected by the up-regulation of PKCtheta activity caused by free fatty acids (FFAs).
False
T/F: Pancreatic beta cells are able to sense elevations in blood glucose levels because of increased GLUT-4 translocation to the plasma membrane.
False
T/F: Phosphorylation events become less common throughout the subsequent stages of cellular signal transduction.
False
T/F: Reactive oxygen species cause cellular dysfunction and do not play a role in normal growth and metabolism.
False
T/F: Release of adiponectin from fat cells would promote the development of cardiovascular associated defects and impairments in Metabolic Syndrome.
False
T/F: Skeletal muscle is a major organ for both the removal of glucose from the bloodstream and the delivery of glucose into the bloodstream following glycogen breakdown.
False
T/F: The expression of the adaptor protein APPL1 is increased in insulin-resistant muscle cells and antagonizes the interaction of AdipoR1 and APPL2 to activate cell metabolism.
False
T/F: The movement of glucose into or out of the hepatocyte depends on the hormone-mediated availability of GLUT-2 transporters. Specifically, GLUT-2 is inserted into the plasma membrane, or removed from it, depending on the presence, or absence, of insulin.
False
T/F: The pharmacological inhibition of ACE would lead to an increase in blood pressure.
False
Which of the following events turns a G protein "off" in that it prevents the Gα subunit from interacting with effectors? - The α-subunit of the G-protein dissociates from the βγ-subunit. - The bound GDP molecule is exchanged for a new GTP molecule within the α-subunit. - The G-protein dissociates from the receptor. - GTP is hydrolyzed to GDP on the α-subunit.
GTP is hydrolyzed to GDP on the α-subunit.
Which of the following is not a cell type expressed in the Islet of Langerhans? - Gamma - F - Alpha - Delta
Gamma
When activated by the insulin signaling pathway, PP1G will increase the activity of ______ and decrease the activity of ______.
Glycogen synthase, glycogen phosphorylase a
Exercise results in increased sympathetic nerve activity to the pancreas which is associated with decreased insulin secretion by the Beta cells. Which of the following is NOT involved in that process? - G-protein coupled receptors - cAMP - Norepinephrine - Gq - PKA
Gq
Parasympathetic signaling to β-cells involves the binding of ACh to muscarinic receptors. These receptors are GPCRs that are coupled to a subfamily of G proteins which causes you downstream elevations of Ca2+ in the cytoplasm. Given this information, with which subfamily of G proteins must these GPCRs be coupling? - Gq - Gi - Gs - G12,13
Gq
Sympathetic signaling to α-cells involves the binding of NE to α1-adrenergic receptors. These receptors are GPCRs that are coupled to a subfamily of G proteins which causes downstream elevations of Ca2+ in the cytoplasm. Given this information, with which subfamily of G proteins must these GPCRs be coupling? - Gi - G12,13 - Gq - Gs
Gq
The α subunits of the _____ subfamily of G proteins interact with phospholipase C (PLC) when activated.
Gq,11
The α subunits of the _____ subfamily of G proteins interact with (and stimulate) adenylate cyclase when activated.
Gs
Glucose delivery to skeletal muscle tissue is reduced in the Metabolic Syndrome due to all of the following mechanisms EXCEPT: - Impaired insulin stimulation of eNOS in smooth muscle cells - Less blood flow to the capillaries perfusing the muscle - Decreased transendothelial glucose transport via GLUT-1 - Reduced NO-stimulated vasodilation of arterioles
Impaired insulin stimulation of eNOS in smooth muscle cells
When glucose levels in the blood rise, the resulting increase in ATP concentration within β cells __________ the opening of ATP-sensitive K+ channels in the plasma membrane.
Increases
Insulin increases glucose transport into skeletal muscle cells by:
Increasing translocation of GLUT-4-containing vesicles to the plasma membrane.
When it comes to essential hypertension in Metabolic Syndrome, it is suggested that __________ and __________ may be responsible for the development of this core component by increasing central sympathetic outflow, causing peripheral vasoconstriction, and more.
Insulin resistance; hyperinsulinemia
When a ligand binds to a GPCR, the activated GPCR becomes capable to doing what for G proteins?
It can now enable a new GTP molecule from the cytoplasm to replace the old GDP molecule bound to the α subunit of the G protein.
Which of the following is associated with the short-term (acute) effects of a rise in plasma FFA's? - Decreased mitochondrial production of ATP - β-cell apoptosis - Mitochondrial dysfunction - More insulin release by the β cell
More insulin release by the β cell
ACh receptors are ligand-gated ion channels that permit the movement of what ion when ACh binds?
Na+
In the face of long-term elevations in FFAs and/or glucose, the mitochondrial dysfunction evident in β-cells during the relative β-cell failure phase leads to __________ in ATP production and a corresponding __________ in the release of insulin.
a decrease; decrease
The insulin receptor is which type of catalytic receptor?
a receptor tyrosine kinase
The transcription of the genes for the enzymes PEPCK and G6Pase is the major mechanism for the regulation of gluconeogenesis. Which of the following proteins is not involved in their downregulation (in the reduction of the expression of those genes)? - activated PKA - Ser-phosphorylated GSK-3 - Tyr-phosphorylated IRS-1 - activated insulin receptor
activated PKA
From the list below, identify the adipokine which can positively affect insulin action in a variety of cell types, including myocytes. - TNF-α - resistin - adiponectin - Angiotensinogen
adiponectin
Renin acts to cleave __________ to form __________. This peptide is then cleaved by __________ to form the bioactive peptide __________.
angiotensinogen, ANG I, ACE, ANG II
The Km of GLUT4 is lower than the Km of GLUT2, which means that glucose transport via GLUT4 will saturate...?
at a lower glucose concentration than GLUT2
Metabolic syndrome develops over the course of many years. An increase in __________ likely initiates the condition, with early subsequent defects being __________ and __________. Other core components develop thereafter, resulting in a progressively increasing risk of heart attack or stroke.
central adiposity; insulin resistance; compensatory hyperinsulinemia
Which of the following influences is clearly not involved in the activation of stress kinases which increase insulin resistance in skeletal muscle? - increased concentration of inflammatory factors in the blood - increased concentration of free fatty acids in the blood - decreased activity of eNOS in response to insulin binding in endothelial cells - hyperglycemia
decreased activity of eNOS in response to insulin binding in endothelial cells
Which component (core or additional) of Metabolic Syndrome can be defined as the inability to properly manage an increase in blood glucose levels? - dyslipidemia - impaired glucose tolerance (IGT) - hepatic steatosis - essential hypertension
impaired glucose tolerance (IGT)
Reducing the concentration of FFAs in the bloodstream will lead to less __________ phosphorylation of __________ by PKCθ.
serine; both IR and IRS
To modulate the function of target cells, successful cell-cell communication involves receptor-ligand binding, __________, and __________.
signal transduction via second messengers; modifications to existing proteins as well as modification to gene expression in order to change cell function.
For the signal transduction process, the "transmission and modulation" steps specifically involve
the amplification of intracellular signaling due to multiple steps, for example by the phosphorylation of effector proteins or enzymes.
Which phase of dysfunction in the secretory capacity of pancreatic β-cells in the Metabolic Syndrome is the direct result of acute exposure of these cells to high levels of FFAs and/or glucose in the bloodstream? - the decompensatory hypoinsulinemia phase - the relative β-cell failure phase - the relative β-cell hyperplasia phase - the compensatory hyperinsulinemia phase
the compensatory hyperinsulinemia phase
Which phase of dysfunction in the secretory capacity of pancreatic β-cells in the Metabolic Syndrome is the result of the loss of β-cell mass?
the relative β-cell failure phase
