Term
| True or false: both the brain and the CNS can use oxidized FFA’s from the liver (acetoacetate, beta-hydroxybutyrate) as an energy source. |
|
Definition
| False, the brain can only use glucose, while the CNS can use ketones from FFAs |
|
|
Term
| True or False: Lack of insulin only results in life-threatening ketoacidosis if blood sugar levels are low. |
|
Definition
| False, ketoacidosis occurs regardless of blood sugar. |
|
|
Term
| List the following events in order during a fasted state - protolysis, lipolysis, gluconeogensis, glycogenolysis, ketogenesis. |
|
Definition
| Glycogenolysis in the liver occurs for first 8-10 hours, then protolysis and gluconeogensis from amino acids, then lipolysis and ketogenesis. |
|
|
Term
| List the three major tissues for glycogen storage. |
|
Definition
|
|
Term
| Both insulin and exercise induce the synthesis of what glucose transporter in muscle and adipose? |
|
Definition
|
|
Term
| Match the following drug types- 1 sulfonylureas, 2 biguanides(metformin), 3 thiazolidines, 4 incretin mimetics - with their respective functions, listed here: a.natural hormone from intestine to increase insulin secretion without weight gain, b.stimulates beta cells to secrete insulin, c.inhibits liver gluconeogensis and enhances GLUT4, d.enhances insulin receptor and GLUT4 in fat cells |
|
Definition
| 1-B, 2-c, 3-d, 4-a; DPP-4 ihibitors also increase the available incretin by preventing degradation. |
|
|
Term
| Dipeptidyl peptidase-4 degrades incretin hormones, how does an inhibitor drug help a diabetic patient? |
|
Definition
| By blocking the enzyme it increase the amount of incretin available to stimulate insulin secretion by beta cells. |
|
|
Term
| True or False: weight loss in even small amounts can prevent T2DM in patients with risk factors and can also treat the disease making medication to lower blood sugar unnecessary. |
|
Definition
|
|
Term
| Which of these does maintaining normal or near-normal blood glucose levels in diabetes patients help prevent, either microvascular or macrovascular degradation? |
|
Definition
|
|
Term
| True or False: lipid lowering drugs like statins and anti-inflammatory/platelet drugs like aspirin are not as important in preventing cardiovascular disease as maintaining blood sugar levels. |
|
Definition
| False, they are equally or more important. |
|
|
Term
| In MODY, patients are lean people who develop a syndrome like T2DM, what type of pattern of inheritance is this? |
|
Definition
| Simple mendelian inheritance, patients have abnormal glucose metabolism with always one parent having diabetes |
|
|
Term
| Arrange the following categories of tissues with the appropriate glucose transporter: 1. RBC’s, blood-brain barrier, basal glucose uptake in all cells 2. intestinal epithelium, liver, beta-cells 3. neurons 4. adipose and striated muscle. |
|
Definition
| 1.GLUT1 2.GLUT2 3.GLUT3 4.GLUT4 |
|
|
Term
| Which of the following tissues have glucose transporters that are either insulin dependent or independent - liver, beta cells, brain, muscle? |
|
Definition
| First three insulin independent, last is dependent |
|
|
Term
| What is the major cause of death for diabetics? |
|
Definition
|
|
Term
| What are the major causes for non-alcoholic fatty liver disease? |
|
Definition
| Obesity, diabetes, high tryglycerides; 24-42% of pop has it, most are asymptomatic |
|
|
Term
| True or False: When TAG/TG breaks down it creates 4 lipids consisting of 3 fatty acids and 1 glycerol. |
|
Definition
| False, glycerol is not a lipid |
|
|
Term
| Which of the following is derived from lipids: steroid hormones(estrogen, cortisol, aldosterone), inositol phosphates (cell signals), bile salts, surfactant, prostaglandins, leukotrienes, adipose tissue? |
|
Definition
|
|
Term
| What molecule does 80-90% of heart muscle energy derive from? |
|
Definition
|
|
Term
| What major lipid is the precursor to steroid hormones and bile salts? |
|
Definition
|
|
Term
| Bile salts with greater than 10% cholesterol tends to form what? |
|
Definition
| Cholesterol crystals which become gall stones |
|
|
Term
| What structure do bile salts form with dietary lipids, like cholesterol and fat-soluble vitamins, to increase the surface area for pancreatic lipases? |
|
Definition
|
|
Term
| TAG is broken down in the lumen of the intestine and some FFA can simply diffuse into enterocyte capillaries, what length is the maximum a FFA can be and still diffuse directly into blood? |
|
Definition
|
|
Term
| Cholesterol absorption requires a transporter called NPC1L1, what drug inhibits its function? |
|
Definition
|
|
Term
| True or False: bile salt resportion requires the Intestinal Bile Acid Transporter. |
|
Definition
|
|
Term
| True or False: in enterocytes long chain FFAs are resynthesized to TAG, cholesterol esters, and phospholipids to create cholymicrons (lipoproteins) that enter the lymph system and enter the blood at the thoracic duct. |
|
Definition
|
|
Term
| How does the dietary lipid that is secreted from the intestine in the form of cholymicrons get to other organs? |
|
Definition
| Lipoprotein lipase, localized to endothelial cells of muscle and adipose tissue, hydrolyses TAG to release FFAs |
|
|
Term
| After dietary lipids are delivered to adipose and muscle tissue via LPL where does the remaining TAG-poor cholymicron remnant target? |
|
Definition
|
|
Term
| The liver does not normally accumulate lipids, because it does what two things regarding lipids? |
|
Definition
| Re-packages lipids into TAG-rich VLDL which is secreted into the blood; and, it secretes lipid into bile. |
|
|
Term
| Name the transporter in the liver that is a cholesterol and phospholipids transporter that is utilized when the liver makes HDL. |
|
Definition
|
|
Term
| What are the two major non-medication ways to raise HDL? |
|
Definition
|
|
Term
| Where is most HDL synthesized? |
|
Definition
| Liver (75%), intestine (25%) |
|
|
Term
| Familial Hypercholesterolemia results in heterozygote LDL of 300-450 and homozygote LDL of 450-1100, what causes this? |
|
Definition
| There is a mutation in the gene encoding the LDL receptor so that it does not cause absorption of LDL from the blood once activated, nor does the cholesterol from LDL repress transcription of the LDL receptor or HMG-CoA reductase genes. |
|
|
Term
| What do statins do and how does it relate to HMG-CoA reductase? |
|
Definition
| Statins partially inhibit HMG-CoA reductase which lowers cell cholesterol levels and thus leads to an increased synthesis of LDL receptor expression resulting in plasma LDL reduction |
|
|
Term
| True or False: metabolic syndrome, a pre-diabetic state, is associated with fasting triglycerides >150 mg/dl. |
|
Definition
|
|
Term
| 75% of LDL receptors are on which organ? |
|
Definition
|
|
Term
| Which glucose transporter is regulated by insulin-dependent translocation? |
|
Definition
|
|
Term
| Why is glucokinase, which is present in the liver and beta-cells, called the glucose sensor? |
|
Definition
| Because when glucose levels in the cell rise glucokinase regulatory binding protein releases glucokinase from the nucleus of the cell allowing it to convert glucose to G6P. |
|
|
Term
| Which of the following are true regarding glycolysis: it is from G6P to pyruvate, occurs in the cytosol, is anaerobic, regulated by allosteric effects and hormones, produces 2 ATP per glucose, and has 8 steps of which 6 are reversible and not subject to regulation. |
|
Definition
|
|
Term
| Why is phosphofructokinase-1, rather than hexokinase or glucokinase, the key control point of glycolysis? |
|
Definition
| PFK-1 catalyzes the first unique and irreversible reaction in glycolysis so it is optimum for regulation |
|
|
Term
| True or False: phosphofructokinase-2 is also a phosphotase enzyme, called a bifunctional enzyme, that once phosphorylated increases kinase activity and decreases phosphotase activity. |
|
Definition
| False, it decreases kinase activity and increases phosphotase activity. |
|
|
Term
| Hormonal regulation of the bifunctional enzyme in glycolysis is done by glucagons and insulin, how do they affect glycolysis? |
|
Definition
| Glucagon inhibits glycolysis, and insulin stimulates glycolysis |
|
|
Term
| How does the bifunctional enzyme in glycolysis differ in the liver versus muscle? |
|
Definition
| In the liver, once its phosphorylated, it reduces glycolysis; the opposite happens in muscle and the heart |
|
|
Term
| When pyruvate is metabolized by a dephosphorylated pyruvate dehydrogenase what molecule is the result? |
|
Definition
|
|
Term
| True or False: gluconeogenesis is simply the reverse of glycolysis and requires 1 ATP for every 1 glucose synthesized. |
|
Definition
| False, gluconeo utilizes unique enzymes requiring 6 ATP for every glucose |
|
|
Term
| How does glucose-6-phosphotase enable the liver to send glucose to other tissues? |
|
Definition
| When dephosphorylated the remaining glucose can be dumped into blood |
|
|
Term
| True or False: gluconeogenesis and glycolysis are reciprocally regulated by F1,6P and PFK-1 respectively. |
|
Definition
|
|
Term
| True or False: Not only is glycogen synthesis and breakdown reciprocally regulated but they are also regulated by allosteric effectors. |
|
Definition
|
|
Term
| What is the difference between phosphorylase and phosphorytase? |
|
Definition
| Lase leaves a phosphate group on a molecule, Tase takes one away |
|
|
Term
| The following point to which disease - low C-peptide, anti-GAD antibodies, insulin autoantibodies. |
|
Definition
|
|
Term
| How is it that high LDL or low HDL promotes lipid plaques in arteries? |
|
Definition
| They allow macrophages to absorb oxidized LDL becoming foam cells and contributing to a lipid-rich nectrotic plaque. |
|
|
Term
| What is the level of K+ in the body with T1DM? |
|
Definition
| Normal or High in plasma, but the body is severely depleted because of cell breakdown and loss of K due to energy starved cells |
|
|
Term
| Which of these cause B-cell mass to increase over normal size - obesity or pregnancy? |
|
Definition
| trick question, both. in a pregnant woman mass of the cells increases with duration of pregnancy. |
|
|