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Final Flashcards

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1
Q

carb sources

A
  1. diet
  2. breakdown of glycogen/glycerol
  3. propionate in liver (in ruminants)
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2
Q

carb metabolism

A

in cystoplasm through catabolism + anabolism

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3
Q

carb metabolism pathway

A

carb -> monosaccharide (glucose) -> 2 pyruvate (AKA pyruvic acid) -> acetyl CoA -> kreb’s cycle -> electron
transport -> 34 ATP

glucose enters cell and is broken down to pyruvate via glycolysis. enough O? -> aerobic respiration
not enough O? -> pyruvate -> lactic acid (stiff muscles)

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4
Q

glucose

A

primary carb in body

  • absorbed by all cells through facilitated diffusion (form of active transport)
  • quickly metabolize glycogen -> glucose
  • ONLY energy source for RBC and brain cells
  • skeletal muscle cells can use ketones + fatty acids

liver regulates levels
- removes from blood after eating (when high) by converting glucose -> glycogen/triglycerides + storing them
- when low: converts glycogen -> glucose
- can also make glucose from non-carbs!

eg. hypo/hyperglycemia (blood sugar)
- diabetes mellitus (not enough insulin -> cells starve because glucose isn’t being absorbed).
- causes imbalance b/w carb + lipid metabolism
- not enough glucose enters cell -> increased fatty acid metabolism (excess aceteyl coa, increase in ketones)

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5
Q

glycolysis

A

in cytoplasm
- glucose -> 2 pyruvate
- produces 2 ADP + 2 NADH

pathway regulated by 3 enzymes:
1. hexokinase
- inhibited by glucose-6-phosphate
- feedback inhibition
2. phosphofructokinase
- inhibited by ATP + citrate
- activated by ADP + AMP
3. pyruvate kinase
- inhibited by ATP

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6
Q

aerobic respiration

A

in mitochondria
- enzymes and cofactors in cristae

1) krebs cycle
- pyruvate becomes acetyl CoA (acetyl group + coenzyme A), then enters membrane
- acetyl coA binds with oxaloacetate -> citric acid
- converts back to oxaloacetate through cycle, each spin producing 1 ATP, 2 FADH, 3 NADH (+CO2 waste)
- spins 2 times (1 glucose -> 2 pyruvate)

  • entry of acetyl-CoA + rate of spin reduced by high ATP levels
  • if low: cycle stimulated
  • inhibitors: ATP, NADH, succinyl CoA
  • activator: ADP

2) electron transport chain
- NADH and FADH2 donate high energy electrons to chain of e- carrier molecules known as ‘cytochromes’
- at each step energy pumps protons from mitochondrial matrix into intermembrane space making an ‘electrochemical gradient’ -> potential energy
- ATP synthase complex moves protons back to matrix -> energy released
- energy used to combine ADP + P -> ATP

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7
Q

glycogen synthesis (glycogenesis)

A

excess consumed glucose is converted to glycogen (glycogenesis) -> stored in liver + muscle
- glycogen synthase forms bond b/w glucose using UTP as energy source

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8
Q

glycogen breakdown (glycogenolysis)

A

when muscles need energy + when liver restores low blood sugar to normal (needs to provide glucose to blood)
- in liver, kidney, and intestine
- NOT in muscle (missing an enzyme, however can produce glucose-6-phosphate to be used in the pathway)

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9
Q

gluconeogenesis (glucose from noncarb)

A

lactate/some aminos/glycerol -> pyruvate -> glucose

  • 90% in liver
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10
Q

cori cycle

A

anaerobic
- lactate in muscles reconverted to glucose by liver using cori cycle

active exercise:
- lactate increases in muscles -> diffuses into blood -> taken to liver -> liver converts back to pyruvate
- pyruvate -> glucose (gluconeogenesis) -> glucose enters blood -> back to muscles

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11
Q

hormonal control of carb metabolism

A
  1. insulin
    - in pancreas
    - decreases blood glucose (increases glycogen formation)
    - increases cells absorbing glucose
    - increases synthesis of glycogen + fatty acids + proteins
    - stimulates glycolysis
  2. glucagon
    - in pancreas
    - increases blood glucose
    - activates glycogen breakdown in LIVER
  3. epinephrine
    - in medulla
    - increases blood glucose
    - stimulates glycogen breakdown in MUSCLE
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12
Q

lipids

A

C O H

  • insoluble in water, soluble in other lipids
    ex. triglyceride, neutral fat
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13
Q

triglycerides

A

more CH bonds than any other nutrient
- 2x energy of carbs
- store 6x energy than glycogen

  • fat concentrates energy in lightweight form
  • important for birds
  • herbivores don’t eat as much -> convert carbs to fat
  • excess triglyercides in blood go through lipolysis in liver
  • broken down into: 1 glycerol, 3 fatty acid chains
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14
Q

triglyceride metabolism

A

glycerol broken into dihydroxyacetone phosphate in cytoplasm -> glycolysis converts it into pyruvate -> acetyl coa -> krebs -> NADH + FADH enter electron transport chain
* if balance b/w carb + fat metabolism, most will go through krebs cycle

OR pyruvate -> gluconeogenesis

breakdown of fatty acid chains occurs in mitochondria
- beta oxidation: pathway converting fatty acid chain -> acetyl CoA + FADH + NADH
- one fatty acid chain = 18 C -> 148 ATP

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15
Q

fat mobilization

A

more difficult than carbs, so used as reserve energy
- lipids stored in fatty tissue for backup when food is low
- when cells need fatty acids, hormones (eg epinephrine) interact w/adipose
- called on by resting muscle + liver cells to be used as energy source after a few hours of fasting, meanwhile glycogen stores prioritized for RBC and brain cells

  • epinephrine stimulates hydrolysis of triglycerides
  • glycerol + fatty acids enter blood
  • fatty acids form lipoprotein w/albumin -> transported where needed
  • glycerol is water soluble, so dissolves in blood -> carried where needed
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16
Q

fasting metabolism

A

fatty acids become primary energy source
- glycolysis decreases
- oxoloacetate synthesized less
- oxoloacetate used to make glucose, lack of it reduces krebs activity
- more acetyl coa made by fatty acid breakdown than can be processed in krebs -> excess becomes ketone bodies in liver -> carried to brain , muscles, heart via blood

  • ketone body types: acetoacetic acid, acetone, betahydroxybutyric acid
  • can be oxidized for energy

ketonemia: too much ketone bodies in blood
ketonuria: ketones in urine
acetone breath: acetone in blood is so high it is expelled from lungs

ketosis: ketonemia + ketonuria + acetone breath
ketoacidosis: low pH from high ketones

17
Q

triglyceride synthesis

A

excess energy-producing nutrients converted to fatty acids -> fatty acids incorporated into triglycerides -> stored as adipose

  • in liver, adipose, and mammary
  • liver can modify chains: lengthen/shorten, saturate/unsaturate
  • (‘biosynthesis’ in cytoplasm)
  • chains built 2 C at a time
18
Q

amino acid pool

A

total supply of amino acids in body

  • come from digestion of food, degrading tissue, synthesis in liver
  • any excess is not stored, -> degraded -> N atoms excreted (used for N compounds or urea)
  • carbon skeletons used for: energy production, synthesis of glucose, conversion of triglycerides
  • protein turnover: body proteins hydrolyzed + resynthesized
19
Q

nitrogen catabolism

A
  1. transamination (in mitochondria)
    - amino acid transferred to keto acid via enzyme (‘transaminase’) -> new amino acid
  2. deamination (liver)
    - removal of amino group -> ammonia + keto acid + NADH produced
    - keto acid used in: transamination OR krebs
  3. urea formation (liver)
    - ammonia -> urea -> exits liver via blood -> kidneys filter urea out -> urine
20
Q

liver + kidney failure

A

diseased kidney won’t excrete urea effectively.
- uremia: buildup of urea in blood
- high blood urea nitrogen (BUN)

diseased liver won’t convert ammonia to urea
- increased ammonia
- low BUN

21
Q

carbon skeleton catabolism

A

carbon skeleton degraded into pyruvate, acetyl coa, acetoacetyl coa to produce energy
- if energy not needed -> converted into glucose or fat

glucogenic amino acid: can be used to make glucose
- pyruvate -> krebs

ketogenic amino acid: can be used to make ketone bodies+ fatty acids
- acetyl coa and acetacetyl coa

22
Q

protein biosynthesis

A

cell function relies on constant protein synthesis
- amino acids joined by peptide bonds = protein
- instructions for building in DNA

  • can synthesize non-essential amino acids, essential must come from diet
  • starting material: intermediates of glycolysis + krebs
  • can readjust proportions of amino acids to meet needs, diet doesn’t have the exact proportions
23
Q

starvation

A

1) (GLYCOGEN STORES) body lowers basal metabolic rate
- needs less food
- maintains blood glucose levels by using glycogen stores in liver (but only last few hours)
- fat catabolized for glucose -> ketone levels rise
- glucose synthesized from glucogenic amino acids

2) (KETONES) change lets body use ketones + glucose for energy
- stored fat = primary source, continues until depleted

3) (PROTEIN) protein main energy source
- glucose synthesized from glucogenic amino acids
- begin to use protein from liver and plasma
- then uses protein from GIT, heart, muscles
- structures decrease in size
- decreased plasma proteins -> decreased oncotic pressure -> fluids leak -> ascites

malnourished animals have negative N balance

24
Q

carb digestion

A

= sugars, starches, cellulose

  1. starches
    - amylase breaks starch down to smaller glucose chains
    - other enzymes break saccharides into glucose
  2. sugars
    - broken into glucose
  3. cellulose
    - can’t be broken down by body
    - bacteria + cellulase break it down
25
Q

fermentation

A

decomposition and utilization of food (esp carbs) by microbes
- GIT of all animals, but in carnivores/omnivores it doesn’t generate much energy
- herbivores = majority of energy

26
Q

carb metabolism in ruminants

A
  • grains (starch and sugar)
  • grasses (complex carbs -> cellulose, hemicellulose, pectin)

symbiosis: microorganisms in GIT use nutrients for their own growth and produce waste -> ruminants use waste for their growth
- microorganisms can be digested for protein

in reticulorumen:
- bacterial enzymes break carbs through hydrolysis.
- saccharides -> pyruvates
- pyruvates -> volatile fatty acids (VFAs)
eg. acetic acid, propionic acid, butyric acid
- VFAs -> blood

  • VFAS = main energy source
    (glucose main source in monogastric animals)
    glucose still needed:
  • made through gluconeogenesis (using propionate + glucogenic aminos) in liver
  • glucose is conserved in ruminants, not used to make fatty acids (instead made from acetate)
27
Q

herbivore (‘hindgut fermentors’) metabolism

A

eg. rabbits, guinea pig, horse

starch -> glucose for energy
- fermentation in large intestine (bacteria uses cellulose -> VFAs for energy).
- can’t use protein from fermenting microbes

28
Q

ketosis in herbivores

A
  • increased need for starch + cellulose during last trimester and lactation
  • inadequate nutrition = glycogen stores depleted -> compensate by breaking down fat -> ketone bodies form -> ketosis -> eclampsia

eclampsia: fatal metabolic disorder
- sign: hypoglycemic encephalopathy
- eat more carbs!!

lactation: needs lots of glucose to make lactose
- ketosis while lactating is self-limiting: milk production stops -> then glucose drain also stops

29
Q

carnivore metabolism

A

meat high in protein, moderate in fat, low in carbs
- protein = primary energy source

  • more need than omnivores: protein, arginine, taurine, methionine, cysteine, arachidonic acid, niacin, pyridoxine, vit A + D
  • glucose produced through digesting carbs + through gluconeogenesis of amino acids

Chemistry (5 decks)

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