Final Flashcards
carb sources
- diet
- breakdown of glycogen/glycerol
- propionate in liver (in ruminants)
carb metabolism
in cystoplasm through catabolism + anabolism
carb metabolism pathway
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)
glucose
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)
glycolysis
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
aerobic respiration
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
glycogen synthesis (glycogenesis)
excess consumed glucose is converted to glycogen (glycogenesis) -> stored in liver + muscle
- glycogen synthase forms bond b/w glucose using UTP as energy source
glycogen breakdown (glycogenolysis)
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)
gluconeogenesis (glucose from noncarb)
lactate/some aminos/glycerol -> pyruvate -> glucose
- 90% in liver
cori cycle
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
hormonal control of carb metabolism
- insulin
- in pancreas
- decreases blood glucose (increases glycogen formation)
- increases cells absorbing glucose
- increases synthesis of glycogen + fatty acids + proteins
- stimulates glycolysis - glucagon
- in pancreas
- increases blood glucose
- activates glycogen breakdown in LIVER - epinephrine
- in medulla
- increases blood glucose
- stimulates glycogen breakdown in MUSCLE
lipids
C O H
- insoluble in water, soluble in other lipids
ex. triglyceride, neutral fat
triglycerides
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
triglyceride metabolism
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
fat mobilization
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
fasting metabolism
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
triglyceride synthesis
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
amino acid pool
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
nitrogen catabolism
- transamination (in mitochondria)
- amino acid transferred to keto acid via enzyme (‘transaminase’) -> new amino acid - deamination (liver)
- removal of amino group -> ammonia + keto acid + NADH produced
- keto acid used in: transamination OR krebs - urea formation (liver)
- ammonia -> urea -> exits liver via blood -> kidneys filter urea out -> urine
liver + kidney failure
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
carbon skeleton catabolism
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
protein biosynthesis
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
starvation
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
carb digestion
= sugars, starches, cellulose
- starches
- amylase breaks starch down to smaller glucose chains
- other enzymes break saccharides into glucose - sugars
- broken into glucose - cellulose
- can’t be broken down by body
- bacteria + cellulase break it down
fermentation
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
carb metabolism in ruminants
- 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)
herbivore (‘hindgut fermentors’) metabolism
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
ketosis in herbivores
- 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
carnivore metabolism
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
