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PHAR 412
Metabolism of Carbohydrates, Lipids, Proteins, and Amino Acids
| Question | Answer |
|---|---|
| What is the function of LCAT (lecithin-cholesterol acyltransferase)? | It converts free cholesterol to cholesterol esters. |
| What is the function of ABCA1A (ATP binding cassette protein A1)? | Incorporates phospholipid and unesterified cholesterol into apoA-I. |
| What is the function of SR-BI (class B scavenger receptor BI)? | Mediates cholesterol uptake in liver via apo A-I. |
| What is the function of PLTP (phospholipid transfer protein)? | Transfers phospholipids from apoB-containing remnant particles to HDL. Removes excess phospholipid from shrinking apoB particles and replaces phospholipids on HDL that are consumed by LCAT. |
| What is the function of CETP (cholesterol ester transfer protein)? | Transfers cholesterol esters from mature HDL to remnant apoB particles in exchange for triacylglycerol. |
| What are three bile acid sequestrants? | Cholestyramine, Colestipol, Colesevelam |
| What do bile acid sequestrants do? | Bind bile acids in intestine preventing reabsorption ---> increases bile acid production in liver (7a-hydroxylase activity) ---> decreases hepatic cholesterol ---> increases LDL receptors ---> decreases LDL |
| How does Tricor affect lipid levels? | Fibrates activate PPARa (peroxisome proliferator-activated receptor), a nuclear receptor ---> increases LPL expression ---> decreases triglycerides and increases HDL |
| What is the mechanism of action for Niacin? | Increases apoA-1 half-life ---> increases HDL |
| What is the threshold of glucose concentration that will stimulate insulin secretion? | 80 mg/dL |
| How soon after a carbohydrate-rich meal do insulin levels reach their peak? | ~1 hour |
| How long do insulin levels stay elevated? | ~3 hours |
| How is insulin metabolized? | The serum half-life of insulin is 5-7 minutes. It is broken down by degrading enzymes in the liver. |
| What are the target tissues of insulin? | Muscle and adipose |
| What stimuli trigger glucagon secretion? | Amino acids, epinephrine & norepinephrine, cortisol |
| True/False: Much less insulin is secreted in response to amino acids than is secreted in response to carbohydrates. | True |
| What happens to glucagon levels after a carbohydrate-rich meal? | Decreases |
| What happens to glucagon levels after a protein-rich meal? | Increases |
| What are the target tissues of glucagon? | Liver and adipose |
| How does the glucagon receptor work? | Glucagon binds GPCR ---> activates PKA |
| What is the cause of adrenergic symptoms? | Blood glucose lower than 60 mg/dL causes adrenergic hormone release (epinephrine & norepinephrine). |
| What is the cause of neuroglycopenic symptoms? | Severe hypoglycemia lower than 60 mg/dL causing a lack of glucose to neurons. |
| What is postprandial/reactive hypoglycemia? | Low blood sugar 2-4 hours after a meal due to prolonged/elevated insulin response. |
| What symptoms does postprandial/reactive hypoglycemia cause? | Adrenergic symptoms |
| True/False: Fasting hypoglycemia may result in both adrenergic and neuroglycopenic symptoms. | True |
| What are possible causes of fasting hypoglycemia? | Disorders in glucose mobilization, hypersecretion of insulin, drug-induced hypoglycemia |
| What are disorders in glucose mobilization? | Glycogen storage diseases, classical galactosemia, hereditary fructose intolerance, gluconeogenesis disorders, severe liver disease, glucagon or epinephrine deficiency. |
| What can cause hypersecretion of insulin? | Tumor of the B-cells (insulinoma), neonatal hypoglycemia |
| What is neonatal hypoglycemia? | Immature glycogen stores and deficiencies of gluconeogenesis enzymes. Occurs in infants of mothers with gestational diabetes (hyperinsulinemia). |
| What is drug-induced hypoglycemia? | Exogenous insulin administration, alcohol-induced hypoglycemia |
| What are biochemical abnormalities that could lead to diabetes? | Pancreatic disorders, endocrine disorders, drugs & toxins, autoimmune destruction of B-cell (Type I diabetes), insulin resistance followed by loss of B-cells (Type II diabetes). |
| What is cystic fibrosis? | Fibrotic destruction of islets |
| Diabetes is diagnosed as a result of a fasting plasma glucose greater than or equal to: | 126 mg/dL |
| What dosage of glucose is given to the patient during an OGTT? | 75 g |
| "Impaired glucose tolerance" or "pre-diabetes" is diagnosed when a blood glucose sample is measured between what range? | 140 to 200 mg/dL |
| What are common symptoms of diabetes? | Polydipsia, polyuria, weight loss, hunger and blurred vision. |
| True/False: Glucose binds to the terminal amino groups of hemoglobin. | True |
| What would glycogen storage diseases cause? | Hypoglycemia |
| What would classical galactosemia cause? | Hypoglycemia |
| What would hereditary fructose intolerance cause? | Hypoglycemia |
| What would gluconeogenesis enzyme deficiency cause? | Hypoglycemia |
| What would sever liver disease cause? | Hypoglycemia |
| What would glucagon/epinephrine deficiency cause? | Hypoglycemia |
| What would insulinoma cause? | Hypoglycemia |
| What would immature glycogen stores cause? | Hypoglycemia |
| What condition would infants of mothers with gestational diabetes have? | Hypoglycemia |
| What would an insulin overdose cause? | Hypoglycemia |
| What would alcoholism with poor food intake cause? | Hypoglycemia |
| What would pancreatitis cause? | Hyperglycemia |
| What would cystic fibrosis cause? | Hyperglycemia |
| What would hemochromatosis cause? | Hyperglycemia |
| What would an adrenal gland tumor cause? | Hyperglycemia |
| What would Cushing's syndrome cause? | Hyperglycemia |
| What would glucagonoma cause? | Hyperglycemia |
| What would glucocorticoids cause? | Hyperglycemia |
| What would loss-of-function of insulin receptor mutations cause? | Hyperglycemia |
| What is the order of origin of blood glucose from phase I to phase V? | (I) Exogenous, (II) glycogen, (III) gluconeogenesis, (IV) gluconeogenesis (from glucose & ketone bodies), (V) gluconeogenesis (from ketone bodies & glucose) |
| What tissues use glucose in what phases? | (I) All, (II) all but liver, (III), all but liver, muscle, adipose, (IV) brain, RBCs, muscle, (V) brain (diminished), RBCs |
| What molecule does the liver use for ketogenesis? | Acetyl-CoA |
| What tissue supplies acetyl-CoA for ketogenesis? | Adipose |
| Which is more active in the fasting state: HSL or LPL? Why? | HSL. HSL is activated by glucagon and stimulates fatty acid release. LPL breaks down dietary fat in chylomicrons to be taken up in adipose tissue. |
| What tissue provides ketone bodies to fuel muscle and brain in the fasting state? | Liver |
| Does the muscle proteolysis rate tend to increase or decrease during the late fasting state? | Decrease |
| Glargine (Lantus) | Slow |
| Glulisine (Apidra) | Rapid |
| What factors contribute to the slow action of insulin glargine (Lantus)? | Mutation of 3 amino acids decreases absorption at neutral pH. |
| What modification accounts for the prolonged action of insulin detemir (Levemir)? | Attachment of a fatty acid causes aggregation with themselves and albumin. |
| Glargine (Lantus) | Slow |
| Glulisine (Apidra) | Rapid |
| What factors contribute to the slow action of insulin glargine (Lantus)? | Mutation of 3 amino acids decreases absorption at neutral pH. |
| What modification accounts for the prolonged action of insulin detemir (Levemir)? | Attachment of a fatty acid causes aggregation with themselves and albumin. |
| What two insulin delivery devices are compact and discreet? | Insuiln pens, pumps, and inhalation devices |
| What two insulin delivery devices are most expensive? | Jet injectors and insulin pumps |
| Which insulin delivery device requires regular cleaning? | Jet injectors |
| Which insulin delivery device can cause pain and bruising? | Jet injectors |
| Which insulin delivery device can result in rapid loss of glycemic control of there is a malfunction? | Insulin pump |
| Which insulin delivery device requires frequent monitoring of blood sugar? | Insulin pump |
| What three insulin delivery devices have needles? | Syringes, pens, and pumps |
| Why would insulin secretagogues be a poor treatment choice for type 1 diabetes? | Type 1 diabetics have a deficiency of B-cells. |
| True/False: Insufficient insulin to induce the lipoprotein lipase of adipose cells contributes to increased blood triglyceride levels in untreated diabetics. | True |
| True/False: Amino acids from muscles can be converted to glucose by gluconeogenesis in a patient with untreated type 2 diabetes? | True |
| What is the function of incretins? | Hormones that enhance glucose-stimulated insulin release, reduce glucagon, and slow gastric emptying. |
| What is an example of a thiazolidinedione? | Pioglitazone (Actos) |
| What is an example of a meglitanide? | Nateglinide (Starlix) |
| What is the mechanism of action for a-glucosidase inhibitors? | Inhibition of carbohydrate digestion |
| What is the mechanism of action for DPP-IV inhibitors? | Stimulation of glucose-dependent insulin secretion, reduction of glucagon, delay gastric emptying |
| What are two examples of a-glucosidase inhibitors? | Acarbose (Precose), Miglitol (Glyset) |
| What are three examples of DPP-IV inhibitors? | Sitagliptin (Januvia), Saxagliptin (Onglyza), Linagliptin (Tradjenta) |
| What is the mechanism of action for biguanides? | Inhibits gluconeogenesis |
| What is an example of a biguanide? | Metformin (Glucophage) |
| What is the mechanism of action for sulfonylureas? | Stimulates insulin secretion |
| What is an example of a sulfonylurea? | Glimepiride (Amaryl) |
| What is the mechanism of action for hormone mimetics? | Mimics a euglycemic hormone |
| What are three examples of hormone mimetics? | Exentide (Byetta), Luraglutide (Victoza), Pramlintide (Symlin) |
| What is Canagliflozin (Invokana)? | SGLT2 inhibitor |
| What diabetes treatments have the risk of hypoglycemia? | Hormone mimetics, sulfonylureas, meglitanides |
| What diabetic treatment has an ADR of causing or worsening congestive heart failure? | Thiazolidinediones |
| What diabetic treatment should not be used in patients with renal dysfunction? | Biguanide and SGLT2 treatment |
| Which class of drug is associated with tachyphylaxis? | Sulfonylureas |
| What does gastrin do? | Stimulates release of HCl and pepsinogen. |
| What does secretin do? | Stimulates HCO3 secretion from pancreas. |
| What does cholecystokinin do? | Stimulates enzyme secretion and release of bile. |
| Where is trypsinogen synthesized? | Small intestine |
| What activates trypsinogen to trypsin? | Enterokinase/trypsin |
| Where is pepsinogen synthesized? | Chief cells in stomach. |
| What activates pepsinogen to pepsin? | Low pH |
| Where is chymotrypsinogen synthesized? | Small intestine |
| What activates chymotrypsinogen to trypsinogen? | Enterokinase/trypsin |
| Where is proelastase synthesized? | Small intestine |
| What activates proelastase to elastase? | Enterokinase/trypsin |
| What is the function of trypsin, pepsin, chymotrypsin, elastase, and enterokinase? | Hydrolyze peptide bonds within chains (endopeptidases). |
| What is the function of carboxypeptidase A and B? | Remove amino acids at C-terminus (exopeptidase). |
| What are the sources of protein in the intestine and their contribution? | Food (50%), pancreatic secretions (25%), desquamated mucosal cells (25%). |
| What is the cofactor for transaminases? | Amino group (NH4) |
| What cofactors are required for glutamate dehydrogenase? | NAD+ |
| What cofactors are formed from glutamate dehydrogenase? | NADH, NH3 |
| What direction is favored if GDP and ADP levels are high, glutamate or a-ketoglutarate? | a-ketoglutarate |
| How can nitrogen in alanine provide free NH4? | Alanine in muscle ---> blood ---> liver, then converted to pyruvate, giving NH3 to glutamate. Glutamate yields free NH4. NH4 is free before used as a cofactor the urea cycle. |
| What cofactors are required for glutamine synthesis from glutamate? | NH4 and ATP |
| How does phenylbutyrate work to lower ammonia levels? | Phenylbutyrate combines with glutamine and is excreted. |
| True/False: Glutamate dehydrogenase can incorporate and release free nitrogen. | True |
| True/False: Hyperammonemia is likely due to an imbalance in the equilibrium of the reaction catalyzed by glutamate dehydrogenase. | True |
| Where is orotate derived from? | Carbamoyl phosphate |
| True/False: The liver produces significant quantities of heme for cytochrome P450s. | True |
| True/False: Creatinine is used as a measure of kidney function because it is produced at a regular rate and is constantly being excreted by the kidney. | True |
| True/False: Ferrous iron is reduced and inserted into protoporphyrin IX to form heme. | True |
| What two molecules come together for form heme? | Glycine and succinyl-CoA |
| How many molecules of an amino acid are required to form one molecule of heme? | 8 |
| True/False: An increase in unconjugated bilirubin could result from increased hemolysis. | True |
| What bilirubin derivatives are found in urine and feces? | Urobilinogen, urobilin, stercobilin |
| What is the ligand for adrenergic receptors? | Epinephrine or norepinephrine |
| Why does histamine cause vasodilation via H1 coupled to Gq when Gq normally causes vasoconstriction? | Gq activates PLC, which increases IP3, increasing calcium, activating eNOS, which increases nitric oxide. Nitric oxide causes relaxation of smooth muscle (vasodilation). |
| What do adrenergic a receptors cause? | Vasoconstriction |
| What do adrenergic B receptors cause? | Bronchodilation |
| What are the receptor types for adrenergic receptors? | Gq (a1), Gi (a2), Gs (B) |
| What is the ligand for nicotinic receptors? | Acetylcholine |
| What do nicotinic receptors cause? | Depolarization/excitation in PNS & CNS. |
| What is the receptor type for nicotinic receptors? | Ion channel (Ca2+, Na+, K+) |
| What does muscarinic M3 cause? | Vasoconstriction, saliva stimulation |
| What are the serotonin receptor types and what do they cause? | 5HT1 (Gi) ---> vasoconstriction, 5HT2 (Gq) ---> hallucinations, 5HT3 (ion channel) ---> depolarization/excitation, 5HT4 (Gs), 5HT5 (Gs), 5HT6 (Gs), 5HT7 (Gs) |
| What is the effect of D1 receptors? | Vasodilation |
| What is the effect of D2 receptors? | CNS - motor function, emotion reward, impulse |
| What is the effect of H2 receptors? | Increase gastric acid secretion |
| True/False: An antagonist of D2 receptors is more likely to be associated with extrapyrmamidal symptoms. | True |
| By what mechanism does GABAb hyperpolarize? | Decreases intracellular K+ |
| What does an agonist of 5HT3 cause? | Nausea and vomiting |
| eNOS is activated by: | Calcium |
| What is required to maintain benzodiazepine binding at GABAa? | y2 |
Created by:
sdeck86
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