carbs Flashcards
monosaccharide structure
can be in chains but usually rings as active grp either side
starch
major storage form in plants
* polysaccharides amylose (single chain) + amylopectin (branched)
glycogen structure
highly branched polysaccharide made repeating units glucose
lactose
galactose + glucose
sucrose
glucose + fructose
maltose
a-glucose x2
cellobiose
b-glucose x2
isomaltose
a-glucose + b-glucose
cellulose
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
chitin
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
glycoprots
prots w sugar attached by glycosylation then more sugars build up on initial. 2 types:
1. N-linked glycosylation
2. O-linked glycosylation
N-linked glycosylation
sugar bonded asparagine as in Asn-X-Ser or Asn-X-Thr
added in RER + modified G. app
O-linked glycosylation
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
formation + breakdown glycogen in liver
glucose -> glucose-6-phosphate -> glucose-1-phosphate -> glycogen
+ reverse
liver controls blood glucose w hormones insulin + glucagon
glucose also taken up by muscle
formation + breakdown glycogen in muscle
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
sk muscle fibre type I
red/oxidative
* obtains E from circulating glucose by aerobic resp
* slower but efficient (using all gluc in blood)
little glycogen
sk muscle fibres type II
white (bc conts so much glycogen)
* obtains E v fast by glycogen breakdown + anaerobic resp
* v fast (glycogen right there) but less efficient
glycogen -> glucose-1-phosphate
- glycogen -> glucose-1-phosphate up to 4 residues from branch by glycogen phosphorylase
- at branch 3 residues moved to end of chain by 4’α glucanotransferase
- 1,6-glucosidase removes remaining glucose
- glycogen phosphorylase can act on new unbranched chain
UDP-glucose -> glycogen
glycogen built on glycogenin enz as sugars added + build up around it
branches created by glucan branching enz
glycogenin forms centre glycogen granule
glucose-6-phosphate -> UDP-glucose
using UTP-Glucose-1-phosphate uridyltransferase + phosphoglucoisomerase
glycogen storage diseases
- Type Ia = classical von Gierke’s disease
- Type II = Pompe’s disease
- Type III = Cori’s disease
classical von Gierke’s disease
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
Pompe’s disease
- 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
Cori’s disease
deficiency debranching enz = shorter + more frequent glycogen branches = too much storage glycogen in liver = can’t be broken down to glucose etc…
german shepherds
gluconeogenesis
formation new glucose
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
diabetes II
normal insulin but no response to glucose = insulin resistance
type III diabetes
normal insulin, normal/delayed response to glucose loading + delayed return normal (>60min)
* characterised high fasting glucose levels
not much is known
hyperinsulinism
pancreatic tumours in dogs = β cells dividing uncontrollably = too much insulin = persistent hypoglycaemia
hypoglycaemia as disease in own right
due inadequate syth gluc at birth (baby pigs) + rapid use liver glycogen
aggravated by cold + also in puppies
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
beta mannosidosis
defects in beta mannosidase - inherited some goats + cattle
* causes severe neurodegeneration
fucosidosis
defects α-L-fucosidase springer spaniels
* progressive neuronal degeneration, fatal
sources ATP w intermediates
diagram
monosaccharide sources E
mainly glucose, also fructose + galactose
glycolysis key stages
diagram
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
use acetyl CoA
add 2 Cs onto mol - add acetyl + CoA recycled
carb metabolism ruminants
- breakdown polysacchs -> monosacchs in digestion
- glucose, fructose + galactose transported through intestinal epithelial cells
- fermentation: carbs -> volatile fatty acids inc propionate used make glucose in gluconeogenesis
non-ruminants: 1,2 same then taken up cells + converted ATP
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
diffs glycolysis + gluconeogensis
- reverse process
- gluconeo extra intermediate oxaloacetate synthed from pyruvate
- diff enzs fructose-1,6-bisphosphate -> fructose-6-phosphate AND glucose-6-phosphate -> glucose
propionate –> pyruvate/oxaloacetate
diagram
in ruminants
fate pyruvate after glycolysis
- aerobic glycolysis = enter mitochond -> acetyl coA -> Krebs’ cycle
- anaerobic fermentation (yeast) -> ethanol
- anaerobic glycolysis -> lactate (+ NADH back to NAD+)
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
aerobic glycolysis
pyruvate -> acetyl CoA -> tricarboxylic acid cycle (= citric acid cycle = Krebs’ cycle)
* each cycle turn creates 3NADH,1FADH2, 1ATP
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
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
