front 1 Two hormones primarily keep blood glucose near 80–100 mg/dL and
coordinate fuel storage/mobilization: | back 1 B. Insulin and glucagon |
front 2 After a high-carbohydrate meal, plasma insulin is typically highest
at: | back 2 D. 30–45 minutes |
front 3 Intertissue metabolic homeostasis is achieved in three principal
ways; which is NOT one of them? | back 3 A. Lymphatic metabolite signaling |
front 4 Major determinant of whether skeletal muscle oxidizes fatty acids vs
glucose: | back 4 C. Plasma fatty acid level |
front 5 Adult minimum daily glucose requirement is best matched by: | back 5 A. 190 total, 150 brain, 40 others |
front 6 Injected glucagon increases hepatic output but not skeletal muscle
metabolism because muscle: | back 6 C. Lacks glucagon receptors |
front 7 Physiologic targets of glucagon include: | back 7 B. Liver and adipose |
front 8 Poorly controlled diabetes causes weight loss despite appetite
because: | back 8 D. Lipids become main fuel |
front 9 Marked hyperglycemia causes polyuria → dehydration → higher glucose;
the initial urine increase is from: | back 9 A. Osmotic diuresis |
front 10 Confusion and seizures during severe hypoglycemia are: | back 10 B. Neuroglycopenic manifestations |
front 11 Tremor, palpitations, and sweating during hypoglycemia are driven
mostly by: | back 11 C. Epinephrine |
front 12 Correct islet hormone pairing: | back 12 A. α:glucagon β:insulin |
front 13 Islet hormones enter the liver first via: | back 13 D. Hepatic portal vein |
front 14 Insulin is considered anabolic because after carbohydrate ingestion
it promotes: | back 14 C. Fuel use; fat and glycogen storage |
front 15 Insulin and glucagon are synthesized in islet cells as: | back 15 B. Prohormones |
front 16 Preproinsulin is converted to proinsulin in the: | back 16 A. Rough ER |
front 17 During proinsulin folding, disulfide bonds form between: | back 17 D. Cysteine residues |
front 18 After folding and disulfide formation, proinsulin is transported to
the: | back 18 C. Golgi complex |
front 19 Proteolysis in storage vesicles produces insulin plus: | back 19 A. C-peptide |
front 20 Within storage vesicles, insulin is precipitated with: | back 20 B. Zn2+ |
front 21 Biologically active insulin consists of: | back 21 D. Two chains, disulfide links |
front 22 Insulin binding triggers receptor autophosphorylation and downstream
protein phosphorylation through the receptor’s: | back 22 C. Tyrosine kinase domain |
front 23 Glucagon raises cAMP, which activates PKA to: | back 23 A. Phosphorylate regulatory enzymes |
front 24 Compared with glucagon, insulin generally shifts key enzymes
toward: | back 24 D. Increased dephosphorylation |
front 25 Recurrent fasting hypoglycemia with inappropriately high insulin
suggests a tumor producing excess insulin called: | back 25 B. Insulinoma |
front 26 During IV glucose, β-cell uptake primarily uses: | back 26 B. GLUT2 |
front 27 In β-cells, glucose → glucose-6-phosphate via: | back 27 D. Glucokinase |
front 28 β-cell glycolysis→TCA→OXPHOS most directly increases: | back 28 A. ATP levels |
front 29 Teen with new DKA has near-zero insulin. Best mechanism? | back 29 C. Autoimmune β-cell destruction |
front 30 Type 1 DM susceptibility is linked to HLA coding: | back 30 A. MHC II |
front 31 Fasting hypoglycemia suggests insulinoma. As glucose falls: | back 31 B. Insulin rises despite low glucose |
front 32 Approximate glucose threshold for insulin release: | back 32 D. 80 mg/dL |
front 33 Insulin is rapidly removed primarily by: | back 33 B. Liver |
front 34 Cephalic-phase insulin release is enhanced by: | back 34 C. Vagus parasympathetic signals |
front 35 Post-meal hormones that augment early insulin release: | back 35 A. GIP and GLP-1 |
front 36 MODY can result from mutations in: | back 36 C. Glucokinase or transcription factors |
front 37 MODY2 glucokinase mutation reduces activity via: | back 37 D. Higher Km or lower Vmax |
front 38 Neonatal diabetes presents within the first: | back 38 B. First three months |
front 39 Most common mutation in permanent neonatal diabetes: | back 39 A. KCNJ11 |
front 40 A KATP channel stuck open impairs insulin because: | back 40 D. Ca2+ influx stays low |
front 41 Glucagon is cleared by liver/kidney; half-life is: | back 41 C. 3–5 minutes |
front 42 Islet blood flow carries insulin: | back 42 B. β→α across islet |
front 43 Glipizide increases insulin secretion by: | back 43 C. Closing KATP channels |
front 44 High insulin with absent C-peptide suggests: | back 44 A. Exogenous insulin use |
front 45 Primary defect in type 2 diabetes mellitus: | back 45 D. Insulin resistance in tissues |
front 46 In diabetes, glucagon may remain elevated due to: | back 46 B. Alpha-cell insulin resistance |
front 47 NOT a plasma-membrane signaling mechanism: | back 47 A. Nuclear receptor transcription |
front 48 Insulin receptor component spanning into cytosol: | back 48 C. Beta subunit |
front 49 After insulin binding, phosphorylated IRS-1 recruits via: | back 49 D. SH2 domains |
front 50 Increased amino acid uptake into skeletal muscle primarily reflects
which insulin action? | back 50 B. Stimulation of glucose and amino acid transport |
front 51 A patient takes a methylxanthine PDE inhibitor. Which metabolic
pattern is most expected? | back 51 B. Fasted-state fuel mobilization |
front 52 A patient develops tachycardia after sympathetic surge. The dominant
cardiac adrenergic receptor is: | back 52 A. β1 receptor |
front 53 The major agonist stimulating the heart’s dominant β-receptor
is: | back 53 C. Norepinephrine |
front 54 A hepatic cell increases glycogenolysis via an adrenergic receptor
class most associated with fuel mobilization. Which receptor? | back 54 B. β2 receptor |
front 55 Which catecholamine is a much more potent β2 agonist? | back 55 A. Epinephrine |
front 56 Activation of β2 receptors also mediates vascular, bronchial, and
uterine smooth muscle ______. | back 56 A. Contraction |
front 57 A drug aimed at increasing thermogenesis in adipose tissue would
target: | back 57 D. β3 receptor |
front 58 β3 receptor activation most directly increases: | back 58 A. Fatty acid oxidation |
front 59 Postsynaptic receptors mediating vascular contraction via Gq/PLCβ
use: | back 59 B. PIP2 pathway |
front 60 In a healthy person after a high-carb meal, insulin peaks at 30–45
minutes and returns to basal by: | back 60 C. 2 hours |
front 61 Two insulin polypeptide chains are linked by: | back 61 D. Disulfide bonds |
front 62 The insulin chain containing an additional intrachain disulfide bond
is the: | back 62 B. A (α) chain |
front 63 Increased β-cell glucose metabolism raises ATP:ADP, which first leads
to: | back 63 B. Closing KATP channels |
front 64 Closure of β-cell KATP channels most directly causes: | back 64 B. Membrane depolarization |
front 65 Insulin is rapidly cleared primarily by the: | back 65 A. Liver |
front 66 Preproglucagon processing yields mature 29–AA glucagon plus: | back 66 A. GLP-1 and GLP-2 |
front 67 After a high-protein meal, amino acids typically cause glucagon
to: | back 67 C. Remain high or increase |
front 68 During fasting-feeding cycles, which hormone varies more? | back 68 B. Insulin |
front 69 In a binding assay using intact insulin receptors, the subunit that
binds insulin is: | back 69 C. α subunit, extracellular domain |
front 70 A mutation truncating the receptor’s cytosolic kinase region most
directly affects which subunit? | back 70 A. β subunit, transmembrane/cytosolic |
front 71 Minutes after insulin binds, the earliest receptor event is: | back 71 D. Tyrosine autophosphorylation of β |
front 72 In insulin signaling, the principal substrate phosphorylated by the
receptor is: | back 72 B. IRS-1 |
front 73 After IRS-1 phosphorylation, docking occurs through proteins
containing: | back 73 A. SH2 domains |
front 74 A hormone receptor that activates adenylate cyclase to raise cAMP is
best classified as: | back 74 C. GPCR |
front 75 The glucagon receptor most directly couples to which
G-protein? | back 75 B. Gs |
front 76 In hepatocytes, glucagon binding most directly increases: | back 76 D. cAMP |
front 77 cAMP activates PKA by: | back 77 C. Dissociating regulatory from catalytic |
front 78 After activation, PKA phosphorylates key enzymes mainly on: | back 78 A. Serine residues |
front 79 The phosphorylated-enzyme message is primarily terminated by: | back 79 D. Protein phosphatases removing phosphate |
front 80 cAMP is rapidly degraded to AMP by: | back 80 B. Membrane phosphodiesterase |
front 81 Caffeine increases cAMP primarily by inhibiting: | back 81 C. Phosphodiesterase |
front 82 A methylxanthine’s metabolic effect most closely mimics: | back 82 D. Fasted glucagon/epinephrine state |
front 83 A CRE-binding protein directly phosphorylated by PKA is: | back 83 B. CREB |
front 84 CREs that mediate cAMP-hormone transcriptional effects are located
in: | back 84 A. Promoter regions of genes |
front 85 Cortisol signaling is best summarized as: | back 85 D. Intracellular receptor binding → nucleus → gene expression |
front 86 Overall, catecholamines primarily cause: | back 86 C. Increased fuel mobilization |
front 87 β-adrenergic receptors generally signal through: | back 87 B. Gs and adenylate cyclase |
front 88 The major adrenergic receptor in human heart and its primary
agonist: | back 88 A. β1; norepinephrine |
front 89 The adrenergic receptor prominent in liver/muscle fuel mobilization,
with epinephrine > norepinephrine potency: | back 89 D. β2 receptor |
front 90 Receptor that mediates vascular/bronchial/uterine smooth muscle
contraction: | back 90 C. β2 receptor |
front 91 A candidate “weight-loss” agonist increasing thermogenesis would
target: | back 91 A. β3 receptor |
front 92 Increased cardiac contraction with β1 stimulation is partly via PKA
phosphorylation of: | back 92 B. Phospholamban |
front 93 Only 30–40% of “glucagon” is mature; major extra-pancreatic source of
fragments is: | back 93 D. Intestinal L cells |
front 94 A patient receives an α1 agonist and develops increased afterload.
The primary postsynaptic α1 effect is: | back 94 A. Vascular smooth muscle contraction |
front 95 During sympathetic activation, α1 signaling in hepatocytes can
directly increase: | back 95 C. Hepatic glycogenolysis |
front 96 An α1 receptor couples into the PIP2 system. Which G-protein mediates
this pathway? | back 96 B. Gq |
front 97 In α1 signaling, activation of Gq most directly stimulates: | back 97 D. Phospholipase Cβ |
front 98 A clinic measures waist–hip ratio. A high value most strongly
indicates: | back 98 C. Visceral periintestinal adipocytes |
front 99 Visceral periintestinal adipocytes fat distribution pattern is
associated with diabetes risk because it correlates with: | back 99 A. Reduced insulin sensitivity |
front 100 A patient with uncontrolled diabetes reports polyuria and intense
thirst. Which sequence best explains the mechanism described
here? | back 100 D. Osmotic diuresis, dehydration, ↑glucose |
front 101 A newborn develops diabetes within the first 3 months. The most
common permanent form involves an activating KCNJ11 mutation. What is
the key functional consequence? | back 101 C. KATP stays open, Ca2+ blocked |
front 102 Chronic hyperglycemia can distort membrane/serum proteins and slow
degradation via: | back 102 A. Nonenzymatic glycosylation |
front 103 Which long-term complication cluster best fits microvascular diabetic
disease? | back 103 C. Retinopathy nephropathy neuropathy |
front 104 Which complication cluster best fits macrovascular diabetic disease
in these notes? | back 104 B. Coronary cerebral peripheral disease |
front 105 After KATP channel closure in β-cells (by ATP or sulfonylurea), which
event most directly triggers insulin vesicle fusion with the
membrane? | back 105 A. Increased intracellular Ca2+ |
front 106 The pore-forming unit of the β-cell KATP channel is encoded
by: | back 106 B. KCNJ11 |
front 107 The regulatory subunit that binds sulfonylureas is encoded
by: | back 107 A. ABCC8 |
front 108 Connie has fasting hypoglycemia with inappropriately high insulin;
symptoms improve after eating. Most likely diagnosis: | back 108 C. Insulinoma |
front 109 Confusion, fatigue, and blurred vision during hypoglycemia are
classified as: | back 109 D. Neuroglycopenic manifestations |
front 110 Why is C-peptide useful for assessing β-cell function? | back 110 B. Equimolar secretion, slower clearance |
front 111 MODY patients can still produce/release insulin, but typically
require: | back 111 C. Higher glucose levels |
front 112 Glucagon can increase PEPCK gene transcription via cAMP. Insulin
antagonizes this at gene expression via: | back 112 B. IRE in promoter |
front 113 Insulin receptor mediates internalization of receptor-bound insulin
molecules. This causes what pharmacologic phenomenon? | back 113 D. Receptor downregulation |