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NSF > carbs > Flashcards

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
Q

gluconeogenesis

A

formation new glucose

26
Q

type I diabetes

A

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
Q

diabetes II

A

normal insulin but no response to glucose = insulin resistance

28
Q

type III diabetes

A

normal insulin, normal/delayed response to glucose loading + delayed return normal (>60min)
* characterised high fasting glucose levels

not much is known

29
Q

hyperinsulinism

A

pancreatic tumours in dogs = β cells dividing uncontrollably = too much insulin = persistent hypoglycaemia

30
Q

hypoglycaemia as disease in own right

A

due inadequate syth gluc at birth (baby pigs) + rapid use liver glycogen

aggravated by cold + also in puppies

31
Q

alpha mannosidosis

A

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
Q

beta mannosidosis

A

defects in beta mannosidase - inherited some goats + cattle
* causes severe neurodegeneration

33
Q

fucosidosis

A

defects α-L-fucosidase springer spaniels
* progressive neuronal degeneration, fatal

34
Q

sources ATP w intermediates

diagram

A
35
Q

monosaccharide sources E

A

mainly glucose, also fructose + galactose

36
Q

glycolysis key stages

diagram

A
37
Q

what to coat test tube w when testing blood glucose

A

fluoride as inhibitor enz in glycolysis pathway = stops glycolysis so can accurately measure glucose levels
* otherwise readings falsely low

38
Q

use acetyl CoA

A

add 2 Cs onto mol - add acetyl + CoA recycled

39
Q

carb metabolism ruminants

A
  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
Q

gluconeogensis is + when used + where in bod

A

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
Q

diffs glycolysis + gluconeogensis

A
  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
Q

propionate –> pyruvate/oxaloacetate

diagram

A

in ruminants

43
Q

fate pyruvate after glycolysis

A
  1. aerobic glycolysis = enter mitochond -> acetyl coA -> Krebs’ cycle
  2. anaerobic fermentation (yeast) -> ethanol
  3. anaerobic glycolysis -> lactate (+ NADH back to NAD+)
44
Q

anaerobic glycolysis

A
  • 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
Q

aerobic glycolysis

A

pyruvate -> acetyl CoA -> tricarboxylic acid cycle (= citric acid cycle = Krebs’ cycle)
* each cycle turn creates 3NADH,1FADH2, 1ATP

46
Q

oxidative phosphorylation

A

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
Q

advantages aerobic glycolysis over anaerobic

A

-> 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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