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GI > Iron, Lipid, and metabolic interrelationships > Flashcards

Iron, Lipid, and metabolic interrelationships Flashcards

1
Q

In which forms is iron present?

A

porphyrin bound: hemoglobin, haptoglobin, hemopexin, myoglobin, cytochromes; non-heme enzymes: transferrin (serum transport protein), ferritin (major storage form of iron, liver), hemosiderin (deposit form of iron in iron excess) and free iron (very little)

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2
Q

How is iron absorbed in the intestine?

A

transported across the membrane in the ferrous form (FE2), can be stored in the cells as ferritin or transported by ferroportin into the blood, after iron is converted to ferric form (FE3) it is bound by apotransferrin

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3
Q

How are iron levels in the body regulated?

A

transport of iron across the intestine; no regulation of excretion lost only by normal bleeding and sloughing of cells

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4
Q

What conditions cause a need for an increase in iron?

A

pregnancy, rapid growth, and lactation

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5
Q

What does the hormone hepcidin do? When is it upregulated? Inhibited?

A

inhibit ferroportin release of iron into the blood, upregulated by increased iron in the blood and inhibited by active erythropoiesis

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6
Q

What does transferrin do? what is it?

A

deliver iron to cells needing it for heme biosynthesis or to the liver for storage as ferritin; glycoprotein made in the liver, bind 2 iron atoms, only 30% saturated in normal conditions

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7
Q

How do macrophages recycle iron?

A

take up RBC, heme oxygenase converts iron to ferric form and porphyrin ring is converted to biliverdin, when more iron is needed it will be excreted by ferroportin

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8
Q

What is ferritin? What does it do?

A

complex protein composed of 24 polypeptide chains, form a hollow sphere and iron in the form of ferric hydroxide and ferric phosphate can penetrate this shell-like structure

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9
Q

How is heme biosynthesis initiated and regulated? Process?

A

ALA synthase in mitochondria initiates heme biosynthesis, can be inhibited by its ultimate product protoporphyrin; ALA synthase levels are induced by hypoxia and erythropoietin; 2 ALA molecules condense to form PBG and 4 molecules of PBG form one heme

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10
Q

What does lead due to porphyrin biosynthesis?

A

inhibits both ALA-dehydratase and ferrochelastase, causing severe anemia and reduce heme biosynthesis

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11
Q

What are porphyrias?

A

group of diseases associated with loss of enzymes of porphyrin biosynthesis; acute- have anemia and neurological damage, cutaneous- are associated with accumulation of porphyrin precursors in skin causing damage upon exposure to sunlight

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12
Q

What can iron deficiency cause?

A

most common nutritional deficiency; small birth weights and pre-term delivery, delay motor function and neurological development, cause fatigue and impair mental function in adults

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13
Q

How does iron deficiency anemia show up?

A

most common cause of anemia; microcytic, hypochromic anemia, bone marrow aspiration will show no storage of iron and blood transferrin will be elevated and relatively unsaturated with iron

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14
Q

What is hemochromatosis?

A

iron toxicity; accumulation of too much iron in the body, casuses: excess dietary iron, multiple transfusions in anemia or abnormal iron absorption, gene mutation, or cooking in iron pots; ability of ferritin to store iron in tissues is overwhelmed and hemosiderin deposits form, containing ferritin, denatured ferritin and iron; treat with phelobotomy or iron chelation through injection or oral

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15
Q

What is hemosiderosis?

A

damage to an organ from the accumulation of hemosiderin

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16
Q

what are two reasons a metabolic action may occur? examples?

A

satisfy needs of cell (glycolysis, TCA, ETS) or satisfy needs of distant tissue (lipolysis in adipocytes, glycogenolysis or gluconeogenesis in liver)

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17
Q

What are the key aspects of the Anabolic phase?

A

feed; insulin is the primary hormone, plasma substrates: increased glucose, triglycerides and branched chain AA, decreased free FA and ketones; substrate flux from the splanchnic bed to storage and utilization sites; active process- glycogen storage, protein synthesis, triglyceride formation

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18
Q

What are the key aspects of the catabolic phase?

A

fast (4hrs); glucagon; plasma- decreased glucose and triglycerides, increased free FA, ketones, alanine and glutamine; substrates from storage sites to the liver and utilization sites; glycogenolysis, gluconeogenesis, proteolysis, lipolysis and ketogenesis

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19
Q

What can cause an anticipatory increase in insulin secretion?

A

gastrin, secretin, CCK, and GIP

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20
Q

What things increase the secretion of insulin?

A

glucose, AA, Fatty acids, ketones, ACh, GI hormones, glucagon

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21
Q

What things decrease the secretion of insulin?

A

somatostatin, epinephrine, norepinephrine

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22
Q

What things increase the secretion of glucagon?

A

AA, ACh, epinephrine, norepinephrine, VIP, CCK

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23
Q

What things decrease the secretion of glucagon?

A

glucose, insulin, somatostatin, ketones, FFA

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24
Q

How does the body respond to a carbohydrate meal?

A

glucose to the liver first, here it becomes either glycogen or acetyl CoA then some to triglycerides; some glucose bypasses and goes to the brain, muscle and adipose; the triglycerides formed by the liver are released as VLDL and go to the muscle and adipose

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25
Q

How does the body respond to a protein meal?

A

AA to the liver become pyruvate->glucose-> brain, muscle and adipose; glycogen in liver->glucose-> periphery; AA can also become acetyl CoA in the liver->triglycerides-> adipose and muscle; AA-> muscle from intestine, adipose releases FA->muscle and to the liver->triglycerides to be released

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26
Q

How does the body respond to a fat meal?

A

absorbed fat->adipose and muscle; muscle releases AA to the liver-> pyruvate or ketone bodies; adipose releases fatty acids to the liver-> ketone bodies->periphery and brain or triglycerides->periphery; glycogen and pyruvate in the liver-> glucose->periphery and brain

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27
Q

What happens in the postabsorptive/fasting state?

A

energy and glucose(for brain and RBC) must be supplied, blood glucose and insulin down, glucagon up; glucose first supplied from liver glycogen and then by gluconeogenesis (from lactate, glycerol, and amino acids), muscles use fatty acids and ketone bodies

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28
Q

What happens in starvation?

A

hormones change: insulin down, glucagon, GH, and cortisol up, T4->T3 down; after 2 days glucose usage only by the brain, RBC and renal medulla; brain starts to use ketone bodies; glucose is supplied by gluconeogenesis in the liver and the kidney; release AA from muscle decreased, glutamine and alanine at a higher proportion than whats in muscle; glutamic acid taken up by muscles; decreased urea production and increased ammonia production

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29
Q

What causes the increase in ammonia production in starvation?

A

changing alpha ketoglutarate to glucose increases the level of CO2 and H

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30
Q

How are lipids transported in the body?

A

in lipid protein aggregates called lipoproteins

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31
Q

What is the general composition of lipoproteins?

A

single layer of phospholipids, free cholesterol and associated proteins are the outside “shell”, the inside is cholesteryl esters and triacylglycerides

32
Q

What are apolipoproteins?

A

protein molecule unassociated with lipid

33
Q

What makes a cholesteryl ester?

A

cholesterol esterified at hydroxyl by fatty acid

34
Q

What are triacylglycerides?

A

fatty acid donor for cholesteryl esters; results in lysolecithin

35
Q

What happens to FA less than 12 carbons long in the intestinal cell?

A

can be absorbed into blood stream and bound to albumin and transported to tissues

36
Q

What happens to longer chain FA in the intestinal cell?

A

reform triacylglycerides, make a chylomicron with other lipids and proteins which enter the lymphatics and then the blood

37
Q

What is the exogenous pathway for cholesterol and Triacylglycerides?

A

chylomicrons in the capilaries release FA via lipoprotein lipase which is anchored to the capillary wall by proteoglycans, FA taken up into muscle or adipose for B oxidation or storage glycerol released and taken up by the liver for gluconeogenesis leaving cholesterol rich chylomicron remnants (marker protein B48)

38
Q

What is the endogenous pathway involving transport to peripheral tissues for triacylglycerides and cholesterol?

A

Tryacylglycerol and cholesterol from liver to tissues via VLDL; FA released and IDL are either recovered by liver or converted to LDL the major cholesterol carrier in plasma can either deliver cholesterol or return to the liver (marker protein B-100 and enzyme lipoprotein lipase)

39
Q

What is the endogenous pathway involving removal of cholesterol from peripheral tissues?

A

HDLs synthesized in liver/serve to scavenge extra cholesterol from periphery; uptake is aided by activity of lecithin;cholesterol acyltransferase (LCAT) which transfers lecithin to cholesterol resulting in cholersteryl ester that reside in center of HDL, it is transferred to IDL and VLDL in exchange for triglycerides

40
Q

What is the major core lipid of a chylomicron? apoprotein? function? mechanism of delivery?

A

dietary tryglycerides; B-48; absorption of dietary fat; hydrolysis by lipoprotein lipase

41
Q

What is the major core lipid of a chylomicron remnant? apoprotein? function? mechanism of delivery?

A

dietary cholesterol esters; B-48; delivery of dietary fat to liver; receptor mediated endocytosis by liver

42
Q

What is the major core lipid of a VLDL? apoprotein? function? mechanism of delivery?

A

triglycerides; B-100; transport of triglycerides from liver to other tissues; hydrolysis by lipoprotein lipase

43
Q

What is the major core lipid of a IDL? apoprotein? function? mechanism of delivery?

A

cholesterol esters; B-100; initial product formed in VLDL catabolism; receptor mediated endocytosis by liver and conversion to LDL

44
Q

What is the major core lipid of a LDL? apoprotein? function? mechanism of delivery?

A

cholesterol esters; B-100; cholesterol ester transport; receptor mediated endocytosis by the liver and other tissues

45
Q

What is the major core lipid of a HDL? apoprotein? function? mechanism of delivery?

A

cholesterol esters; A-1; removal of excess cholesterol from tissues and lipoproteins; transfer of cholesterol esters to IDL and LDL

46
Q

What happens when LDL is taken up by cells?

A

apo-B100 protein binds to cell surface LDL receptor and is endocytosed; acidification of endosome, LDL receptor recycled to surface, LDLs degraded in lysosomes releasing cholesterol

47
Q

What are the three mechanisms by which cholesterol production is blocked?

A

1)intracellular cholesterol inhibits production and accelerates degradation of HMG CoA reductase (rate limiting step in de novo synthesis) 2) inhibits synthesis of LDL receptors, reducing the import of cholesterol into cell thus subsequent production of VLDLS 3) activates AcylCoA-cholesterol acyl transferase, promoting storage as cholesteryl ester droplets, using acylCoA as FA donor

48
Q

what happens when scavengers take up LDL?

A

macrophage scavenger receptors bind oxidized LDL; these receptors are not regulated like LDL receptors; cholesterol deposition from elevated LDL, macrophage uptake of oxidized LDL and accumulation of a thrombi at sites of wall damage lead to atherosclerotic plaques

49
Q

What role do antioxidants play in atherogenesis?

A

thought to be due to reduction in oxidized LDL

50
Q

What is bilirubin derived from?

A

RBC breakdown 80% 20% from heme containing proteins (ex. cytochromes);

51
Q

How does the liver conjugate bilirubin? What is principle enzyme required? Typical product? What happens to it next?

A

adds polar group, 90% glucuronic acid, or taurine or glycine; UDP-glucuronyl transferase; bilirubin glucuronide; released into bile; little reabsorbed, some altered via colon flora

52
Q

How is hemoglobin broken down? by what system?

A

take up by reticuloendothelial system; iron from hemoglobin returned to plasma traveling bound to transferrin which goes to the bone marrow to be used or stored or to the liver to be stored

53
Q

How is heme changed chemically to bilirubin?

A

heme via hemoxygenase to biliverdin (green) via biliverdin reductase to bilirubin(red); this occurs in hepatocytes

54
Q

How is bilirubin transported from the reticuloendothelial system to the liver? why?

A

attached to albumin in the blood; so the liver can conjugate it and excrete it via bile

55
Q

Why must it be conjugated?

A

conjugation makes it water soluble and reduces cytotoxicity, unconjugated uncouples oxidative phosphorylation to inhibit RNA and protein synthesis

56
Q

What does the intestinal bacteria do to bilirubin glucuronide?

A

reduces it to urobilinogen, now unconjugated and will either be excreted or some is reabsorbed and returned to the liver

57
Q

What does the liver do with urobilinogen?

A

transported to systemic circulation where it is oxidized in the kidney

58
Q

What accounts for the color of urine and feces?

A

oxidized urobiligen form urobilin and stercobilin which are pigments

59
Q

What causes jaundice?

A

excessive break down of RBC or release of cytochromes can cause increased load of bilirubin; hemolysis, hematoma or intra-abdominal blood collection, ineffective erythropoiesis (inability of marrow to use all hemoglobin formed during RBC prod

60
Q

What is gilberts syndrome?

A

clinical disorder due to reduced bilirubin uptake by liver after it is bound to albumin; may be related to decrease in UDP-GT so bilirubin cant be conjugated, 5% college students, men more than women; intermittent jaundice, fluctuates with stress

61
Q

What is neonatal jaundice?

A

physiological jaundice, 50% of newborns, either excessive bilirubin production (RBC break down more rapid from short life span of neonatal RBC), or immature hepatocyte function (limited uptake or conjugation, impaired excretion or excessive reuptake); treat with UV, white fluorescent or blue light

62
Q

What is crigler-Najjar syndrome?

A

rare genetic defect, absence of UDP-GT; marked elevation of bilirubin; life expectancy normal for the most part unless there is excessive deposition of bilirubin in brain (toxic); phenobarbital can induce UDP-GT

63
Q

What is the amount of dietary uptake of lipids vs. endogenous on daily basis?

A

120-15 dietary; 40-50 endogenous

64
Q

What does bile contain?

A

primary bile acids, lecithin, phosphitidalcholine, cholesterol, bilirubin, bicarbonate

65
Q

Where and by what are secondary bile salts formed? Why is this important?

A

distal SI and colon by normal flora; must be done to recirculate

66
Q

What is the function of bile?

A

emulsify fats, absorption of fats by forming miscelles, excretion of bilirubin and cholesterol

67
Q

How does the gall bladder concentrate the bile?

A

Na reabsorption through N/H exchange on apical side and Na/K ATPase basal side; CL reabsorption via CL/HCO3 exchanger on the apical side and Cl channel on basal side; H2O follows the osmotic gradient created either transcellular or paracellular path

68
Q

How are gallstones formed? Predisposition?

A

cholesterol stones most common, can be bilirubin; typically precipitation of cholesterol from ultraconcentration; possibly genetic predisp; females more likely

69
Q

What are the various mediators of intestinal lipolysis?

A

pancreatic lipase, colipase, secretory phospholipase A2, cholesterol esterase, and breast milk lipase

70
Q

What is the source and activity of pancreatic lipase?

A

pancreatic acinar cells; hydrolyze 1 and 3 positions on triglyceride

71
Q

What is the source and activity of colipase?

A

preform secreted by acinar cells, cofactor for lipase, binds to lipase and augments its activity; also binds to bile acids

72
Q

What is the source and activity of secretory phospholipase A2?

A

preform secreted by acinar cells; hydrolyzes fatty acid at position 2 of tryglyceride; requires calcium for activity

73
Q

What is the source and activity of cholesterol esterase?

A

pancreatic acinar cells; broad substrate specificity-cholesterol and vitamin esters; requires bile acid for activity

74
Q

What is the source and activity of breast milk lipase?

A

mammary glands, related to cholesterol esterase; important in neonates

75
Q

What does gastric lipase do?

A

tri to di more than mono; not as active as pancreatic lipase

76
Q

How are miscelles absorbed in the intestine?

A

small aggregates of mixed lipids and bile acids; suspend in unstirred layer, bump into brush border repeatedly, lipids are taken up into epithelial cells

77
Q

What happens to lipids after being absorbed into the enterocyte?

A

triglycerides synthesized, chylomicrons formed; pinocytosed on basal side and absorbd into lacteals

GI (9 decks)

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