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119 Cards in this Set
- Front
- Back
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What is the central molecule involved in atherosclerosis?
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cholesterol
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Animals resistant to atherosclerosis carry most of their cholesterol as _____.
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HDL (whereas humans carry it as LDL)
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The atherosclerosis lesion is located in what tissue layer?
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arterial intima
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Atherosclerosis affects what arteries?
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Large arteries (coronary, aorta, cerebral, iliac)
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Circulating fatty acids bound to ______ supply the tissues.
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serum albumin.
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There is about ____ per mL of fatty acid bound albumin. However, a special class of lipoproteins can carry FAs in the form of TAG at a concentration of ___ per mL.
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1 mg; 3 mg
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What are the two kinds of lipoproteins?
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1. triglyceride rich
2. cholesterol-phospholipid rich |
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What is the structural apoprotein of the chylomicron?
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Apo B-48
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Apo E on the chylomicron is a ligand for ___ receptors.
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liver
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Apo C-II is a co-factor for the enzyme ______. _____ inhibits Apo C-II.
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lipoprotein lipase (breaks down the chylomicron); Apo C-III
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The structural protein of chylomicrons is _____, while the structural protein of VLDL and LDL is ___. HDL does not have Apo B protein.
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apo-B-48; apo B-100
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Which apoproteins do both chylomicrons and VLDL have?
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Apo E, Apo C-II and Apo-CIII
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Where do VLDL's come from?
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the liver
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Almost all LDL in the system is made from ____ in circulation.
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VLDL
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Cholesterol ester is derived in circulation through the action of the enzyme _____.
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LCAT
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Rank in size, small to large:
LDL, chylomicron, HDL |
HDL < LDL < chylomicron
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What are the cholesterol-ester rich lipoproteins?
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LDL and HDL
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What are the triglyceride rich lipoproteins?
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Chylomicrons and VLDL
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___ has Apo-A1.
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HDL
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Any liproprotein that has ____ is atherogenic.
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Apo-B
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Capillary endothelial cells in
tissues extract the fatty acids from the TG via the enzyme _______. |
lipoprotein lipase
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What is left of the chylomicron after lipoprotein lipase action?
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chylomicron remnants
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What happens to VLDL remnants?
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Most become LDL via the action of two enzymes
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80% of the cholesterol in the blood is in the form of ___.
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LDL
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The residence time of fatty acids in the blood is about 90 sec. The residence time of LDL is about ___.
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5 days
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What might happen if there was a mutation of apo B100?
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LDL would not be taken up by the liver, and blood cholesterol would be far too high. It is deadly.
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The number of liver receptors for LDL is regulated by ____ levels. If there is too much, then new receptors will not be made.
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intracellular cholesterol
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During feeding, uptake of chylomicron remnants by the liver is followed by lipolysis to fatty acids, re-esterification, and secretion as _____.
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VLDL-TG
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Where is HDL taken up by cells?
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the kidney
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What is the main determinant of LDL levels in the blood?
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The number of LDL receptors in the liver.
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HDL is poor in ___ but rich in ____. VLDL is the opposite.
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TAG; CE
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The enzyme ____ allows CE to be transferred from HDL to VLDL.
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CETP (cholesterol ester transfer protein)
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What happens to a VLDL remnant?
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It is taken up by the liver, the CE hydrolyzed, and the C converted to bile acids. The rest becomes LDL.
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How is LDL formed?
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from the hydrolysis of VLDL
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How is HDL formed?
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The liver makes Apo A-1, which combines with cholesterol from peripheral cells. The A-1/cholesterol is esterified via LCAT. It is now a mature HDL.
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What is Tangier disease?
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Body can't make Apo-A-1, and so have very low HDL, and therefore have high incidence of atherosclerosis.
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Apo-B containing lipoproteins, especially LDL, penetrate the subendothelial space of ______.
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large arteries
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Oxidized LDL in arterial intima is take up by ____ receptors in macrophages.
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scavenger
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Once ox-LDL has been taken up by macrophages, they are called ___ cells. The initial lesion is called a _____.
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foam; fatty streak
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The macrophages involved in atherosclerosis secrete cytokines and initiate an ______.
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inflammatory response
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What happens to SMCs during atherosclerosis?
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The smooth muscle in the media secrete collagen and bone matrix proteins, creating a plaque, which will be calcified and mineralized.
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An advanced atherosclerosis lesion is called an ____.
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atheroma
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An ____ may rupture, exposing collagen to platelets, which starts thrombosis and occlusion of the lumen.
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unstable plaque
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Where do early atherosclerosis lesions form?
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Where there is turbulent flow, such as branch points and valves.
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When does atherosclerosis begin?
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in childhood
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What must one have to be diagnosed as having metabolic syndrome?
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Three of four:
1. obesity 2. high TAG or low HDL 3. insulin resistance 4. hypertension |
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Obesity and periodontal disease are common in people with _____.
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diabetes
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Most people on dialysis will eventually die from ______.
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coronary heart disease
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High dental scores are associated with high HbA1c levels, which are both associated with high incidence of _______.
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coronary heart disease
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What percentage of the US pop has DM?
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2-5%
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What are the two kinds of Type 1?
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immune mediated (>90%), idiopathic (<10%5)
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Which viruses have been implicated in immune mediated Type 1?
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mumps and coxsackie
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If a patient has increased urination, increased appetite, weight loss, and reduced muscle mass, what would you expect?
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Type 1 DM
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Which type of DM is subject to ketoacidosis?
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Type 1
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By definition, in Type 2, circulating insulin is sufficient to prevent _____, but not enough to prevent _____.
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ketoacidosis; hyperglycemia
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Most ____ type 2 DM is idiopathic.
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non-obese
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Which type of DM is best described as having an insidious onset?
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Type 2
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What fungal infection might indicate diabetes?
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thrush (oral candida)
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Which type of DM is more likely to have polyuria and thirst?
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Type 1
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Which type of DM is more likely to have nocturnal enuresis?
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Type 1
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Which type of DM is more likely to be asymptomatic?
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Type 2
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Which type of DM is more likely to develop peripheral neuropathy?
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Type 2
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What will a diabetes urinalysis check for?
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glucosuria and ketonura (glucose and ketone bodies in the urine)
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What is the plasma glucose level of someone with DM?
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>126 mg/dl (fasting)
>200 mg/dl (2 hrs after load) |
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What is HbA1c?
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glycosylated hemoglobin
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HbA1c reflects glycemic control over a period of 8-12 wks. What are good and bad numbers?
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<7% = good
7-9% = fair >9% = poor |
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What are normal blood glucose levels?
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<110 (fasting)
<140 (2 hrs after eating) |
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Which type of of DM could suffer a hyperosmolar nonketotic coma?
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Type 2
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What are some occular complications of diabetes?
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glaucoma, cataracts, retinopathy
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Which complication of diabetes is characterized by microaneurysms?
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retinopathy
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What are oral hypoglycemics?
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Drugs that can stimulate insulin secretion, alter insulin action, or alter glucose uptake.
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Who needs injectable insulin?
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Type 1s. And type 2s whose diabetes is not well controlled with diet and oral hypoglycemics.
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What are some oral complications of diabetes?
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-glossodynia
-xerostomia -increased caries -lichen planus -candidiasis -parotitis |
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When should you schedule appts with diabetic patients?
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Short AM appts after breakfast
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Avoid elective treatment on someone with blood glucose levels over ____.
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400 mg/dl
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Which measure of diabetes control are dental treatment recommendations based on?
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HbA1c levels
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Glucagon and insulin are both synthesized in ______, a gland in the pancreas.
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Islets of Langerhans
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Which type of diabetes is characterized by primary beta cell failure?
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Type 1
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As blood glucose increases, insulin is released. What metabolic pathways are affected?
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Glycogen, fatty acid, and TAG synthesis all increase. Liver glycolysis also increases (I'm not sure, but I assume to make building blocks for fat.)
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As blood glucose goes down, glucagon is secreted. What pathways are affected?
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Glycogenolysis, gluconeogenesis, and lipolysis will all increase. Liver glycolysis will go down (I assume because building blocks are not needed).
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What is the most numerous cell type in the islets of Langerhans?
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beta
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Where will you find the alpha cells in the islets of Langerhans?
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on the periphery
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What are the precursors of insulin? Where in the cell are these precursors and insulin synthesized?
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Pre-proinsulin is synthesized in the nucleus.
Pre-proinsulin is converted to proinsulin in the RER. Proinsulin is cleaved to make insulin in the Golgi. (Glucagon is processed in much the same way.) |
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Which cells have glucagon receptors?
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liver
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Glucagon signaling occurs through the ____ pathway.
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cAMP
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Will insulin or glucagon stimulate uptake of potassium and phophate?
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Insulin stimulates uptake of ions.
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In uncontrolled diabetes, what two metabolic pathways are noticeably upregulated?
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gluconeogenesis and lipolysis
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Which Krebs intermediate can be shunted off to gluconeogenesis?
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malate
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What is MODY?
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It's type 2 caused by glucokinase mutation.
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What are AGEs?
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advanced glycation end products. They are carbs that attach to proteins. They mess everything up, cause crosslinking and inelasticity.
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In a diabetic, the acetyl coA from lipolysis is used for what? The oxaloacetate from TCA is used for what?
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Acetyl CoA: ketogenesis
OAA: gluconeogenesis This puts a big damper on TCA. |
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We cannot synthesize ____ from acetyl CoA.
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glucose
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Why can't acetyl coA replenish TCA cycle intermediates?
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Both acetyl CoA carbons are lost as CO2 during TCA.
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What is coordinate regulation?
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Two pathways regulated at the same time to avoid futile cycles, e.g. glycogen synthesis does not occur at the same time as glycogen phosphorolysis
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What can happen to pyruvate?
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1. reduced to lactate
2. aminated to alanine 3. becomes acetyl CoA |
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What are some systemic regulators we have discussed?
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insulin, glucagon, epinephrine
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What are some important local regulators?
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energy charge (e.g. AMP levels), redox ratio (e.g. NAD+ vs NADH)
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What are two examples of feed-forward regulation we discussed?
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PFK-2/F-2,6-BP, and NAG/CPS1
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What is a glucose tolerance test?
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Your glucose levels are measured over time after a glucose load. It should spike up, then go down slightly below normal, then come back up and level up.
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How is insulin stimulation of glycolysis an example of systemic regulation overriding local regulation?
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A cell would normally not do glycolysis when it has high energy levels (as it probably would when insulin is secreted), however, insulin needs acetyl CoA, the product of glycolysis, for fatty acid synthesis, so glycolysis proceeds.
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What is an RTK? What important systemic regulator binds to one?
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receptor tyrosine kinase. insulin.
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What can happen to acetyl CoA?
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1. aminated to amino acid
2. enters TCA 3. used for ketone synthesis 4. used for cholesterol/steroid synthesis 5. used for fatty acid synthesis |
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Which hormone upregulates PFK-2?
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insulin
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What is AMPK?
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It's a kinase that senses energy levels in a cell. It's activated by AMP, deactivated by ATP.
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Where does your fat come from if you don't eat any?
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You use acetyl CoA from carbs to make it?
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Why does Atkins decrease expression of acetyl CoA decarboxylase?
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This is the enzyme that makes malonyl CoA for FA synthesis. You don't need to synthesize FA when you are already eating a lot of it.
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Three examples of coordinate regulation.
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Glycogen synthesis/glycogen phosphorolysis.
Malonyl CoA induces FA synthesis, prevents FA degradation Glycolysis/gluconeogenesis |
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What is VO2max?
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The maximal rate at which you can get oxygen from the air to your tissues.
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The muscles can do anaerobic glycolysis, but the ____ is not.
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liver
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How does the liver deal with the waste products of anaerobic metabolism?
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It can put lactate in the Cori cycle to make glucose.
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What is the Cori cycle?
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The process by which lactate from muscles is converted to glucose in the liver, with the glucose going back to the muscle.
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How is blood glucose maintained during starvation?
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gluconeogenesis
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Under fed conditions, what happens to citrate?
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It can be shunted away from TCA to become acetyl CoA for FA synthesis.
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During starvation, why are TCA intermediates in short supply?
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They are used for gluconeogenesis.
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What is happening with acetyl-CoA during starvation?
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It builds up. It can't be used in TCA. CoASH is removed. It is converted to ketone bodies.
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What is the basal metabolic rate?
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Amount of energy the body requires to do nothing (to live).
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Energy expenditure is the sum of what three things?
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1. basal metabolic rate
2. diet induced thermogenesis (energy required to digest food) 3. physical activity |
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Which cells secrete leptin?
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adipocytes
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What are the two effects of leptin?
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1. decreased food intake
2. increased metabolism (should lead to ineffecient burning, which is good) |
