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carbs Flashcards

1
Q

monosaccharide structure

A

can be in chains but usually rings as active grp either side

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2
Q

starch

A

major storage form in plants
* polysaccharides amylose (single chain) + amylopectin (branched)

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3
Q

glycogen structure

A

highly branched polysaccharide made repeating units glucose

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4
Q

lactose

A

galactose + glucose

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5
Q

sucrose

A

glucose + fructose

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6
Q

maltose

A

a-glucose x2

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7
Q

cellobiose

A

b-glucose x2

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8
Q

isomaltose

A

a-glucose + b-glucose

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9
Q

cellulose

A

cellobiose disaccharide repeat
* b-glucose bonding = most animals can’t digest but ruminants have microbes in digestive sys that allow breakdown
* found plants like grasses

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10
Q

chitin

A

disacc repeat N-acetyl-B-D-glucosamine
found insect exoskeletons = enzs that break down trialled as insecticides bc most animals no have = won’t affect

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11
Q

glycoprots

A

prots w sugar attached by glycosylation then more sugars build up on initial. 2 types:
1. N-linked glycosylation
2. O-linked glycosylation

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12
Q

N-linked glycosylation

A

sugar bonded asparagine as in Asn-X-Ser or Asn-X-Thr
added in RER + modified G. app

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13
Q

O-linked glycosylation

A

sugar attached Ser or Thr residue in Golgi
* 1st residue addded = N-acetylgalactosamine
* aggrecan has loads - found cartilage as high osmotic pot = lots water = spongey = walk w/o pain

aggrecan - bottle brush shape
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14
Q

formation + breakdown glycogen in liver

A

glucose -> glucose-6-phosphate -> glucose-1-phosphate -> glycogen
+ reverse

liver controls blood glucose w hormones insulin + glucagon

glucose also taken up by muscle

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15
Q

formation + breakdown glycogen in muscle

A

same as liver for formation but no glucose-6-phosphatase = can’t breakdown glucose-6-phosphate to glucose = can’t release glucose to blood.
* so glucose-6-phosphate broken down for E

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16
Q

sk muscle fibre type I

A

red/oxidative
* obtains E from circulating glucose by aerobic resp
* slower but efficient (using all gluc in blood)

little glycogen

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17
Q

sk muscle fibres type II

A

white (bc conts so much glycogen)
* obtains E v fast by glycogen breakdown + anaerobic resp
* v fast (glycogen right there) but less efficient

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18
Q

glycogen -> glucose-1-phosphate

A
  1. glycogen -> glucose-1-phosphate up to 4 residues from branch by glycogen phosphorylase
  2. at branch 3 residues moved to end of chain by 4’α glucanotransferase
  3. 1,6-glucosidase removes remaining glucose
  4. glycogen phosphorylase can act on new unbranched chain
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19
Q

UDP-glucose -> glycogen

A

glycogen built on glycogenin enz as sugars added + build up around it

branches created by glucan branching enz

glycogenin forms centre glycogen granule

20
Q

glucose-6-phosphate -> UDP-glucose

A

using UTP-Glucose-1-phosphate uridyltransferase + phosphoglucoisomerase

21
Q

glycogen storage diseases

A
  • Type Ia = classical von Gierke’s disease
  • Type II = Pompe’s disease
  • Type III = Cori’s disease
22
Q

classical von Gierke’s disease

A

glucose-6-phosphatase deficiency = liver can’t convert glucose-6-phosphate -> glucose
* overproduction glycogen + can’t breakdown = hypoglycaemia = lack glucose in blood
* enlarged liver (hepatomegaly) due excessive glycogen storage

can occur maltese puppies

23
Q

Pompe’s disease

A
  • glycogen transferred cyt to lysosomes + broken down to maltose by β-amylase
  • lysosomal glucosidase normally breaks it down but deficient = lysosomal accumulation glycogen

affects beef shorthorn, Brahman cattle, lapland dogs

24
Q

Cori’s disease

A

deficiency debranching enz = shorter + more frequent glycogen branches = too much storage glycogen in liver = can’t be broken down to glucose etc…

german shepherds

25
gluconeogenesis
formation new glucose
26
type I diabetes
autoimmune response selectively destroys pancreatic islet Langerhans cells = can't make insulin = need injecting daily * cause in cats = amyloidosis = deposition amylin in pancreas, causing prot aggregation + destruction pancreatic β cells | initial description = cause in dogs
27
diabetes II
normal insulin but no response to glucose = insulin resistance
28
type III diabetes
normal insulin, normal/delayed response to glucose loading + delayed return normal (>60min) * characterised high fasting glucose levels | not much is known
29
hyperinsulinism
pancreatic tumours in dogs = β cells dividing uncontrollably = too much insulin = persistent hypoglycaemia
30
hypoglycaemia as disease in own right
due inadequate syth gluc at birth (baby pigs) + rapid use liver glycogen | aggravated by cold + also in puppies
31
alpha mannosidosis
alpha mannosidase breaks down N-linked glycoprots * don't have = neurological + skeletal abnormalities inherited in humans, angus cattle + cats acquired by herbivores through ingestion locoweed - conts swainsonine, competitive inhib
32
beta mannosidosis
defects in beta mannosidase - inherited some goats + cattle * causes severe neurodegeneration
33
fucosidosis
defects α-L-fucosidase springer spaniels * progressive neuronal degeneration, fatal
34
sources ATP w intermediates | diagram
35
monosaccharide sources E
mainly glucose, also fructose + galactose
36
glycolysis key stages | diagram
37
what to coat test tube w when testing blood glucose
fluoride as inhibitor enz in glycolysis pathway = stops glycolysis so can accurately measure glucose levels * otherwise readings falsely low
38
use acetyl CoA
add 2 Cs onto mol - add acetyl + CoA recycled
39
carb metabolism ruminants
1. breakdown polysacchs -> monosacchs in digestion 2. glucose, fructose + galactose transported through intestinal epithelial cells 3. fermentation: carbs -> volatile fatty acids inc propionate used make glucose in gluconeogenesis | non-ruminants: 1,2 same then taken up cells + converted ATP
40
gluconeogensis is + when used + where in bod
biosynth glucose * source all E in ruminants * glucose not always available (food/liver glycogen) so maintains blood glucose levels from aas in prots + fatty acids * lactate from anaerobic glycolysis to glucose mostly liver, some in kidney
41
diffs glycolysis + gluconeogensis
1. reverse process 2. gluconeo extra intermediate oxaloacetate synthed from pyruvate 3. diff enzs fructose-1,6-bisphosphate -> fructose-6-phosphate AND glucose-6-phosphate -> glucose
42
propionate --> pyruvate/oxaloacetate | diagram
in ruminants
43
fate pyruvate after glycolysis
1. aerobic glycolysis = enter mitochond -> acetyl coA -> Krebs' cycle 2. anaerobic fermentation (yeast) -> ethanol 3. anaerobic glycolysis -> lactate (+ NADH back to NAD+)
44
anaerobic glycolysis
* regens NAD+ = glycolysis can continue * lactate diffs out muscle into blood + converted glucose in liver (gluconeogenesis) + glucose back to muscle | lactate acidic so gradually acidifies blood in acidosis
45
aerobic glycolysis
pyruvate -> acetyl CoA -> tricarboxylic acid cycle (= citric acid cycle = Krebs' cycle) * each cycle turn creates 3NADH,1FADH2, 1ATP
46
oxidative phosphorylation
via e- transport chain in mitochond 1. active carriers drop stuff in complexes in mem 2. stuff transferred bet complexes in chain using enzsto make ATP 1NADH -> 2.5ATP 1FADH2 -> 1.5ATP
47
advantages aerobic glycolysis over anaerobic
-> oxidative phosphorylation = highly efficient way release E * lots ATP released quickly + w/o animal dies as no enough E continue

NSF (22 decks)

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