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IASM > IAS12 > Flashcards

IAS12 Flashcards

1
Q

functions of carbs beyond energy production

A

support brain function as brain relies on glucose
contribute to nucleic acid formation
involve in immune system function, connective tissue structure i.e. HA in connective tissue

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2
Q

glycosidic linkage

A

1-4: no branch / 1-6: branch
affect branching, shape & chars

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3
Q

amylase v amylopectin

A

both are glucose polymers & starch
amylase: 1-4 glycosidic links only
amylopectin: branched, 1-4 & 1-6 bonds

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4
Q

alpha-amylase

A

cleave 1-4 glycosidic linkage in amylose & amylopectin releasing single glucose, eventually forms glucose, maltose, isomaltose, maltotriose & alpha limit dextrins (short chain branched amylopectin remnant)

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5
Q

glycosidase

A

break down disaccharides into monosaccharides for absorption:
lactase, maltase, sucrase

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6
Q

carb digestion except villi

A

mouth: salivary alpha amylase digests alpha-1,4 bonds in amylase forming alpha dextrins -> inactivated in stomach
sucrose & lactose digested in stomach
intestine: pancreatic alpha amylase further cleaves 1,4 bonds in maltose, etc. to release free glucose & form tri-/oligosaccharides, maltose & isomaltose
further cleavage of branched forms in intestinal wall to form mono-
undigested carbs go to ileum, fermented in bacteria & egested in feces

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7
Q

fate of sugars after absorption

A

absorbed via hepatic portal vein
stored in liver or transported to cells

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8
Q

intestinal villi structure

A

basal side connected to many blood & lymph vessels
brush borders face lumen
digestive enzymes attach to brush borders i.e. membrane lining of enterocytes

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9
Q

digestion at villi

A

disaccharides digested to monosaccharides by glycosidases (small intestinal disaccharidases, produced by enterocytes) at brush borders

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10
Q

monosaccharide absorption at villi & why

A

water-soluble mono cannot directly transport through hydrophobic plasma membrane (repelled)
only absorb monosaccharides –> hence single units of glucose must be cleaved from polymers in GI tract
glucose & galactose uptake by symporter SGLT1 against conc. grad. by coupling with transport of Na
fructose uptake by GLUT5, less efficient in large amts since uptake not coupled to Na+

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11
Q

monosaccharide exiting cell

A

some retained for metabolic uses
fructose transport to capillary through GLUT5 in basolateral membrane
glucose, galactose, fructose transport out thru GLUT2 in basolateral membrane

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12
Q

types of cellular glucose transport

A

active: SGLT (intestine, kidney tubule, choroid plexus) (IKC)
facilitated & insulin insensitive
GLUT4: (my friend) muscle & fat cells
facilitated & insulin sensitive:
GLUT1: (bumble bee’s best) almost all tissues but highly abundant in blood cell, blood-brain barrier, baby / fetus
GLUT2: (last known phrase is) liver, kidney, pancreas, intestine // also bidirectional
GLUT3: (no problem): neurons, placenta

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13
Q

sites that use glucose as major or sole fuel

A

sole: RBC & brain (almost, can use KB)
major: muscle (also use FA & KB)

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14
Q

glucose phosphorylation

A

entry mediated by GLUT1
after entry, converted irreversibly to G6P, traps G6P in cell

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15
Q

glycolysis, energy investment phase

A

ATP hydrolyzed & donate phosphate group to glucose by hexokinase, forming G6P, provide energy to push Rx forward
G6P isomerically arranged to form F6P using G6P isomerase / PGI
ATP hydrolyzed, F6P -> F-1,6-BP using PFK

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16
Q

glycolysis, energy generation phase

A

F-1,6-BP splits to form G3P then 1,3-BPG, release of Pi, produces 2 ATP & 1 NADH per G3P
pyruvate is end product

17
Q

fate of pyruvate

A

converted to acetyl-coA -> TCAC & OP if O2 present
converted by lactic dehydrogenase A (LDHA) to lactate -> exported from cell by MTC (no NADH formed)

18
Q

fate of lactate

A

blood lactate enters heart muscles, skeletal muscles, etc. & converted to pyruvate -> enter TCAC
or enter cori cycle

19
Q

glucose use in heavy exercise & oxygen debt

A

glycogen oxidized anaerobically when muscles undergo strenuous exercise -> lactate
heavy breathing continues after exercise to take more O2 for OP to rebuild proton gradient & replenish ATP for cori cycle

20
Q

cori cycle

A

glycogen consumed by muscle anaerobically to form lactate -> blood lactate taken up by liver -> GNG to form glucose -> blood -> muscle to convert back into glycogen
to prevent harmful accu. of lactate (that causes muscle pain) & restore muscle glycogen conc.

21
Q

sites of glucose storage

A

liver (as glycogen OR fatty acids & glycerol as TAG), stores glycogen need for whole body
when glycogen storage full, liver can make FA from glucose using acetyl coA
muscle (glycogen), for use by themselves in demand
adipocyte (TAG)

22
Q

adipocyte carb storage

A

insulin induce GLUT4 expression on adipocytes -> promote uptake & utilization of glucose
2 fates: oxidized into acetyl-coA for FDNS to form FA or conversion to glycerol-3P for backbone of TAG

23
Q

pentose phosphate pathway

A

parallel to glycolysis
produce ribose-5-P for nucleotide biosynthesis
produces NADPH as biochem reactant for glutathione mechanism
produce glutathione against oxidative stress i.e. neutralize harmful peroxide into water

24
Q

UDP-glucose pathway

A

UDP-glucose used to produce:
UDP-glucuronate for glucuronides in detox
intermediate compounds for glycogen
glycoproteins, glycolipids & proteoglycans for EC structures in cell surface
used in molecular constructions e.g. adding sugars to proteins in PTM

25
Q

fructose & galactose conversion to glucose

A

fructose taken up by liver, converted to glucose, glycogen, lactate or pyruvate, FA
small amt exit liver & enter blood
galactose -> glucose in liver -> glycogen for storage

26
Q

glucose de novo synthesis & glycogenolysis

A

synthesized by lactate, TCAC intermediates, AA in dietary protein, glycerol, pyruvate & others
takes place in liver & kidney (slightly), almost reverse of glycolysis
GL: glycogen -> G1P -> G6P -> glucose

27
Q

blood glucose level regulation

A

rise in BGL -> activate insulin-secreting cells in pancreas -> blood insulin lvl inc. -> insulin binds to insulin receptor -> intercellular signal cascade -> stimulate GLUT-4 expression on cell surface -> take up glucose into cell -> BGL lowered

28
Q

abnormal glucose metabolism indication

A

from blood glucose level: in diabetic high BGL for prolonged time w/o going down

29
Q

glucose tolerance

A

ability to dispose of glucose load, tight controls in homeostasis governs to keep regular pattern of glucose tolerance upon dietary intake or sustain fine balance of glucose availability to meet tissue demands
deviated glucose tolerance pattern -> poor glucose homeostasis

30
Q

glucose tests

A

FOR: fasting plasma glucose (FPG) test: BGL in person fasted for >8 hours
OGTT: BGL after person fasts >8 hours & 2h after person drinks glucose containing beverage, measure body response to glucose & BGL regulation
random plasma glucose test: BGL measured at any time w/o fasting

31
Q

maintaining standard basal metabolic state prior to OGTT:

A

DMAIP
diet: >150g of carb for 3 days
medication: withhold non-essential drugs for 3 days
alcohol: no for 3 days
illness: no fever as fever stimulate GH -> increase glucose release into blood -> diabetic-like response i.e. false positive
physical activity: suitable amounts as too little / much impairs glucose tolerance

32
Q

OGTT procedures

A

begins in morning (glucose tolerance decreases sig. in afternoon)
8:00 fasting blood taken as baseline sample
8:10 glucose challenge, drink glucose dose of 1.75g/kg body weight in 1 min
10:10 blood sample taken -> analysis

33
Q

enzyme based glucose detection

A

enzymatic assay coupled to chromogenic agent
glucose catalysed to form H2O2 -> O2 by peroxidase
tag chained chromogenic Rx -> observe O2
O2 oxidises dianisidine to brown
measure optical density changes accu. via spectrophotometry -> glucose conc. known
specific, quick, economical

34
Q

glucose assay preparation

A

enzymes kept in lyophilized form -> printed on dipstick w/ chem. buffers
water reconstitute proteins -> buffers help enzymes catalyse

35
Q

malabsorption effect

A

unabsorbed materials in colon cause osmotic effect -> water draws into bowel -> large volume of water accelerate transit time for food through intestine -> diarrhoea

36
Q

lactose intolerance

A

pain, nausea, flatulence after ingestion of dairy products containing lactose
caused by defective lactase, low lactase lvl or intestinal injury
undigested lactose exposed to bacteria in ileum & colon -> fermentation -> gases produced -> bloating, cramps & diarrhoea

IASM (15 decks)

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