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38 Cards in this Set

  • Front
  • Back
carbs
carbs:
- cheapest E source, not often essential
- sugars, starches, cellulose, gums
- CF: cellulose, hemicellulose, lignin
- NFE: starch, simple sugars
monosaccharides
monosaccharides:
- cannot be further hydrolyzed
- form stable rings in soln
1. pentose (5C): ribose, xylose
2. hexose (6C): glc, fru, gal
disaccharides
disaccharides:
- 2 monos with loss of water
1. sucrose: glc + fru
2. lactose: glc + gal
bonds b/w sugars
bonds b/w sugars:
1. alpha 1,6 and 1,4: starch and glycogen, bonds digested
2. beta 1,4: cellulose, cannot be hydrolyzed by mammalian or avian enzyme
trisaccharides
trisaccharides:
- raffinose: glc, fru, gal
polysaccharides
polysaccharides:
- polymers of many sugars
1. starch:
- amylose (20-30%): alpha 1,4
- amylopectin (70-80%): alpha 1,6
2. cellulose: beta 1,4
mouth digestion
mouth digestion:
- salivary amylase
1. starch ---> dextrin
2. maltose, sucrose, and lactose remain intact
stomach digestion
stomach digestion:
- salivary amylase
1. dextrin and maltose --> maltose, glc
2. sucrose and lactose intact
small intestine digestion
SI digestion:
- enzymes: pancreatic amylase, sucrase, lactase, maltase
1. maltose + glc --> glc
2. sucrose --> fru + glc
3. lactose--> glc + gal
carb abs NR
carb abs NR:
- monos primarily in duodenum and jejunum
- little in stomach or LI
- only newborns (24-48 hr) can abs di, tri or polysaccharides
glc and gal transport
glc and gal transport:
1. Na-dependent glc transporter:
- active, across SI
2. GLUT proteins in intestine and other cells:
- facilitative, passive glc transport
- specific mechanisms for other sugars not well defined
conversion into glc
conversion into glc:
- glc is majority digested carb
- conversion of gal and fru to glc in mucosal cells and hepatocytes
BG homeostasis
BG homeostasis:
- normal NR: 80-100 mg/dl
- preferred E source: CNS, RBC, gonads
- GIT --> liver --> peripheral tissue use:
1. E sources for cells
2. muscle glycogen
3. fat synthesis
met after meal
met after meal:
1. inc BG and insulin: lasting 1-2 hours
2. glycogen synthesis
3. glucose oxidation: for E in other cells
4. adipose in mammals, liver in birds: fat syn (glc--> Ac --> Icfa --> TG)
fasting situation
fasting situation:
- several hours post meal
- glc still essential for many cells
- low normal glc: stimulates glucagon secretion
1. glycogenolysis
2. lipolysis and gluconeogenesis
3. proteolysis
glycogenolysis
glycogenolysis:
- inc by glucagon, depleted rapidly
- hydrolysis of glycogen stores to increase BG
lipolysis
1. lipolysis: mobilization of fat stores to provide E for other tissues
- inc by glucagon and epi
- TG --> glycerol + 3 fa's (54C)
gluconeogenesis
gluconeogenesis :
- synthesis of glc from non-carb sources
- glycerol from lipolysis can be used
proteolysis
proteolysis:
- breakdown of body proteins
1. ketogenis aa's: good E source
- production of ketone bodies= acetone, acetoacetic acid, beta hydroxybutyric acid
2. glucogenic aa:
- via gluconeogenesis: gives off NH2
dietary carbs and R
dietary carbs and R:
- higher in F than NR
- more complex carbs
1. non-structural: sugars, starches, fructosans
2. structural: cellulose, hemicellulose, pectins, ligin
R carb met
R carb met:
- all fermented except that bypassed to SI
- no salivary but pancreatic amylase
- VFA's: main abs end product of fermentation, little glc abs
- R and NR cell req same: R constantly undergoing gluconeogenesis in liver
R BG homeostasis
R BG homeostasis:
- low 40-60 mg/dl
- less fluctuation than NR:
1. constant eating
2. continuous VFA production
3. continuous digesta flow
4. continuous gluconeogenesis
R acetate met
R acetate met:
- 2 C organic acid: CH3COOH
- Ac in rumen--> rumen wall --> portal v --> liver --> gen circulation
- Ac used as:
1. E source
2. substrate for fa's
3. meat, milk modification
R proprionate met
R proprionate met:
- 3 C organic acid: CH3CH2COOH
- rumen:
1. 85% prop, 15% lactate --> liver
--> low prop in blood or glc gen circulation
2. gluconeogenesis sites: liver and kidneys
R butyrate met
R butyrate met:
- 4 C organic acid: CH3(CH2)2COOH
- 25% but in p vein, 75% betaBHBA--> liver--> ketones
- little butyric acid ends up in gen circ
ketones
ketones:
- sources: rumen wall and liver
- 2-3% diff b/w blood and milk
1. E source
2. substrate for fat syn
ketosis
ketosis:
- met dz common in dairy cows soon after calving
- early lactation during active lipolysis
- hypoglycemia, ketonuria, anorexia, lethargy, depressed milk production
carb met R vs NR
carb met R vs NR:
- not very different
1. R: high CF--> VFA abs --> GNG --> glc, acetate and BHBA in blood
2. NR: high sol carbs--> abs of glc --> BG
respiration
respiration:
1. mobilization of AcCoA: glycolysis, beta oxidation or proteolysis to form ketogenic aa
2. TCA gen H+
3. e- transport and oxidative phosphorylation: final E acceptor O2, yields 2-3 ATP
- CO, H2S and CN can stop ET
glycolysis
glycolysis:
1. monosacc met to triose: glc --> pyruvate --> lactate
2. all cells, cytoplasm
3. E consumed, ATP gained
4. numerous substrates can contribute C
5. begins with phosphorylation (hexokinase)
6. yield 2 ATP/ glc oxidized
TCA
TCA:
1. mitochondria
2. input AcCoA: from activation of acetate from blood or pyruvate from glycolysis:
pyruvate + CoA --> AcCoA + CO2 + 2H
3. acetate oxidation: condensation of OAA (4C) with AcCoA (2C) --> citric acid (6C)
- BHBA can also be converted to AcCoA
4. output: citric acid oxidized to OAA + 2CO2 + 4H+ + 1 GTP
E of glc oxidation and respiration
E of glc oxidation and respiration:
glc + 6O2 --> 6CO2 + 6H2O + 36ATP
- net yield: 36 ATP/ glc
- reverse of photosynthesis: 673 kcal solar E--> 36 ATP
gluconeogenesis
gluconeogenesis:
- glc gen from non carb precursors
- more continuous in R
- kidney, liver only
- major precursors: proprionate, lactate, glucogenic aa, glycerol, NOT fa's
- glucogenic aa converted to lactate or alpha keto glutarate
key enz in hepatocytes
key enz in hepatocytes:
1. pyruvate carboxylase (PC) converts pyr--> OAA
2. PEP carboxykinase (PEP-CK): rate-limiting enz converting OAA to PEP
3. glc-6-phosphatase: glc-6-P to glc
met R vs NR
met R vs NR:
1. primary E substrate abs from GIT:
NR glc and R vfa
2. primary substrate for fat syn:
NR glc vs R acetate
3. extent of glc abs from gut:
NR extensive vs R little
4. cellular demand for glc:
NR and R high
5. importance of gluconeogenesis:
NR important (glycerol, aa) vs R very important (proprionate, glycerol, aa)
6. ketone production:
NR abnormal (any =ketosis) vs R normal (excessive= ketosis)
crossroads in met pathways
crossroads in met pathways:
1. glc
2. glc-6-P
3. pyruvate
4. acetate
5. AcCoA
main gluconeogenesis to-knows
main gluconeogenesis to-knows:
- main substrates: propionate, lactate, GNG-aa
- PEP CK: OAA--> PEP
- glc-6-phosphatase: glc-6-P --> PEP
- PC: pyruvate--> OAA
- OAA <--> malate
- 2C: AcCoA
- 4C: succinate, fumarate, malate, OAA
- 5C: alpha keto glutarate
- 6C: citrate, isocitrate
carb digestion in R
carb dig in R:
1. mouth: starch, sol sugars, cellulose, h cellulose --> simple sugars
2. stomach: microbial fermentation, vfa abs, pyr--> acetate, succinate, lactate -->proprionate, butyrate
3. SI: pancreatic amylase, maltose and lactose (calf)
4. intestinal mucosa: maltase and lactase--> glc, gal
- with exception of milk-fed calf, relatively little glc abs in GIT