Exam 3 Flashcards
functions of fat in body
- source of energy (9kcal/g)
- carrier for the fat soluble vitamins
- source of EFA
- insulation
- lubricant
- protection
- precursors for hormones
- structural functions
phospholipid bilayer
- P is polar, and FA is nonpolar
- the structure of cholesterol lends rigidity and helps keep fluidity
- Cholesterol and cis-FA prevent hydrophobic chains from packing too tight
simple lipids
- esters of FA with various alcohols
- Fats and oils are esters of FA with glycerol
- waxes are esters of FA with alcohols other than glycerol
compound lipids
- esters of FA containing non lipid substances
- phosphorus (phospholipid)
- CHO (glycolipids)
- protein (lipoprotein)
gross energy
- 9.45 kcal/g (9 when accounting digestibility)
- most >80% digestible
triglycerides / triacylglycerols
- 95% of dietary fat
- 85% of stored energy in body
- major storage form of energy in the body
- composed of glycerol backbones attached by an ester bond to 3 FA side chains
- typically seen as two or more different FA residues or mixed triglyceride
- when digestion occurs, products are 2 FA and a monoglyceride
phospholipids
- major component of cell membranes
- glycerol backbones with 2 FA and a phosphate group
FA
- FA are the simplest of lipids
- have a polar head group (carboxylic acid) and a hydrophobic tail (hydrocarbon chain)
saturated FA
- all C-C bonds are single
saturated FA C2
acetic
saturated FA C3
propionic
saturated FA C4
butyric
saturated FA C5
valeric
saturated FA C14
myristic
saturated FA C16
palmitic
saturated FA C18
stearic
saturated FA C2-C6
volatile and water soluble in decreasing amounts
saturated FA C4, C6, C8
in milk fat
saturated FA >C8
solid at room temp (C10 mp = 88 F)
saturated FA C16 and C18
are the most common saturated FA
unsaturated FA
- contain one or more C=C double bond
- one C=C bond is called monounsaturated
- 2 or more C=C bonds are polyunsaturated
- double bonds lowers the melting point
nomenclature for FA
- chain elongates from the carboxyl end so start numbering at the methyl group
- C18:2 w6 (example)
EFA
- FA synthetase makes palmitate (C16 saturated)
- cells elongate and desaturate
- however, cannot desaturate between methyl end and 9th carbon
- w3 and w6 must be in diet
- linoleic (w6)- arachidonic acid -> prostaglandins
- linolenic (w3) - EPA and DHA
- need only one tablespoon of oil per day
sources of linoleic
- corn oil, safflower, soybean, cottonseed, sunflower seed, peanut oil.
- arachidonic acid: meats (animal fats)
sources of linolenic
- linseed (flaxseed), canola, small amount in soybean oil
- EPA and DHA: fish oil (cold water fish) and marine algae
hydrogenated fat
- cis typically found in nature
- trans seen in synthetic fats
potential problems with trans
- causes unfavorable lipoprotein profile (HDL decreases and LDL and total cholesterol increases; thus adverse effect on cardiovascular disease)
- can interfere with EFA metabolism
digestion of triglycerides
- pancreatic lipase is major digesting enzyme
- gastric lipase and intestinal lipase play minor role
- nursing ruminants: pregastric esterase from base of tongue starts milk fat digestion in abomasum
- fat enters SI from stomach as a coarse emulsion due to stomach movements
colipase
- lipase cannot attach to lipid droplet when bile salts are present
- acts as an anchor for lipase
- secreted by pancreas as procolipase
- activated by trypsin
- required for lipase activity when bile salt is present
formation of chylomicron
- synthesized in the intestinal epithelial cells
- TAG is produced in the smooth ER
- protein (apo b-48) produced in rough ER
- assembly of lipoprotein in ER and Golgi complex
- secreted into lymphatic system by exocytosis
- it transports absorbed dietary fats from intestine out to tissue
VLDL
- synthesized in liver
- transports synthesized fats from liver out to tissues
fate of chylomicron/ catabolism for chylomicron and VLDL
- C2 is a protein that activates lipoprotein lipase (LPL)
- LPL is on the capillary walls and can bind to the chylomicron and breaks down the lipoprotein
- 3 FA are produced that can enter the muscle, heart, mammary, or adipose
- glycerol is also produced as goes back to the liver (which is the only organ that can use it)
- in adipose tissue: TG is resynthesized and stored; get glycerol from glucose - DHAP - glycerol-p
- in other tissue cells: fat can be oxidized for energy
after breakdown of chylomicron and VLDL
- chylomicron remnant metabolized by liver
- VLDL becomes LDL: LDL can deliver cholesterol to cells. HDL picks up cholesterol from body cells. LDL also accepts cholesterol from HDL. Liver removes LDL from blood and converts cholesterol to bile.
Km
- heart LPL has low Km
- adipose has higher (10x) Km: fed or fasted state, heart enzyme remains saturated, thus redirects uptake of fat from adipose tissue towards heart
fat digestion by ruminants
- TG in diet goes to FA and glycerol
- 70-90% of FA is saturated by bacteria and goes to small intestine to eventually form chylomicron
- glycerol is converted to DHAP to pyruvate to propionate. Most propionate is converted to glucose and goes back to liver.
saturated and trans FA in ruminants
- enough FA escape saturation to prevent EFA deficiency in ruminants
- ruminant fat is more saturated than nonruminants
- trans FA: ruminant meat and dairy products = 1-8% of fat is trans FA; up to 40-50% of hydrogenated vegetable oils are trans FA; 75-90% of trans FA in U.S. diet from hydrogenated oils
conjugated linoleic acid (CLA)
- found in dietary products and other ruminant foods
- formed by microorganisms in rumen
- cis-9, trans-11 octadecadienoic acid most common
- conjugated (c=c-c=c)
- normal (c=c-c-c=c)
- anti-carcinogenic effects: inhibits proliferation of some cancers
- antiatherogenic effects: lowers total and LDL cholesterol
- reduces fat and increases lean body mass
- enhances some immune response
- increases rate of bone formation in growing animals
IDL
- produced in blood (remnant of VLDL)
- endocytosed by liver or converted to LDL
LDL
- produced in blood (remnant of IDL; end product of VLDL)
- contains high concentration of cholesterol and cholesterol esters
- endocytosed by liver and peripheral tissues
HDL
- produced in liver and intestine
- exchanges proteins and lipids with other lipoproteins
- functions in the return of cholesterol from peripheral tissues to the liver
there are several needs that are met by blood glucose
- liver glycogen
- muscle glycogen
- fat formation
- tissue oxidation
- fat cannot be used for net synthesis of glucose **
what happens after you eat?
- dietary glucose enters blood
- some glucose used by liver to replenish liver glycogen supply
- other glucose goes to muscle and other extra-hepatic tissues
what are the primary transports for TG out into tissues?
chylomicron and VLDL
what are the primary glycogen storage areas?
liver and muscle
what two areas use GLUT 4 for glucose uptake in the fed state?
adipose and muscle
these two areas have low Km for glucose
brain and rbc
uses only glucose
rbc
prefers glucose but switches to ketone bodies under starvation
brain
FA synthesis
- in the cytosol of the cell
- acetyl-coa formed in mitochondria
- acetyl-coa cant cross membrane
- it gets across the membrane by citrate
- FA synthesis requires NADPH and gets it from malic enzyme and pentose phosphate pathway
Acetyl-coa to cytosol and generation of NADPH
- pyruvate goes into cell and goes under two reactions to form OAA and acetyl-coa
- OAA and acetyl-coa come together to form citrate
- citrate crosses out of the membrane into cytosol
- once in cytosol, citrate splits back into OAA and acetyl-coa
- OAA is then converted to malate
- malate then is converted back to pyruvate by the malic enzyme which is where NADPH comes from
- NADPH also comes from pentose phosphate pathway by going from G-6-P to F-6-P and G-3-P
what happens between meals (post-absorptive/basal state)
- supply of dietary glucose decreases
- liver takes over in controlling blood glucose by breaking down glycogen
- fattening stops
- gluconeogenesis from AA (also glycerol, and lactate) begins
- some tissues begin shifting to FA as source of fuel (not brain or rbc)
- muscle operates from glycogen glucose and from fat (all muscle glycogen is not depleted, saved for emergency)
most gluconeogenesis is in the __?
liver (some in kidney)
FA binds to ___ and are carried to tissues
blood protein albumin
fat breakdown
- pancreatic lipase
- lipoprotein lipase of wall
- hormone sensitive lipase
common ketone bodies
- acetoacetic acid
- beta-hydroxybutyrate
glucagon
- stimulates breakdown glycogen
- stimulates mobilization of stored TG
- involved in stimulation to make AA available for gluconeogenesis
gluconeogenesis from AA…Entry points of AA
- acetoacetate
- acetyl-coa
- pyruvate
- a-keto-glutarate
- succinyl- coa
- fumarate
- oxaloacetate
gluconeogenesis from pyruvate
- pep converted to pyruvate which crosses into the mitochondria and is converted into OAA
- OAA can’t cross membrane so it is converted to malate which crosses the membrane back into the cytosol to be converted back to OAA which goes back to PEP
Transfer/removal of NH2 group from AA
- transamination
- results in a-keto acid
only organ with deaminases
liver
Alanine’s corresponding keto acid
pyruvate
aspartic acid’s corresponding keto acid
oxaloacetic acid
glutamic acid’s corresponding keto acid
a-keto glutarate
leucine’s corresponding keto acid
a-ketoisocaproic acid
glucose-alanine cycle
- glucose in blood goes to muscle
- glucose then converted to pyruvate
- pyruvate goes to alanine with the addition of NH2, which is transported to liver
- in the liver, alanine loses the NH2 (which goes to urea), and becomes pyruvate
- pyruvate converted back to glucose and glucose exits into the blood to start cycle again
starved state
- all liver glycogen depleted
- glucose is formed from AA (primarily), lactate, and glycerol
- muscle operates largely on fat and animal is loosing weight (muscle glycogen is not depleted except in emergency; muscle glycogen foes not go to blood glucose)
- nerve tissue use ketones primarily for energy
- glucose saved for RBC and some nerve tissue uses
for short term help with ketosis
- iv of dextrose
- injection of glucocorticoids
pregnancy toxemia
- with sheep (practically ketosis, just by different cause)
- sheep have high incidence of twinning. So the fetuses take up a lot of space where rumen normally is. Now ewe cant eat as much, so she starts mobilizing fats instead of ketones and ketone bodies rise.
hardware disease
may swallow nail or other tool/metal object. It falls into reticulum and can poke a hole and cause the contents to spill out in abdominal cavity. Infection can arise due to microorganisms.
reticulum
- called “honeycomb”
- no secretory glands, same cells as esophagus
- 5% of stomach
- provides passage to omasum (particle size is important)
rumen
- no secretory glands, same cells as esophagus
- 80% of stomach
omasum
- “many plies”
- many sheets of tissue
- feed passes through these tissue layers for mainly water removal
- 7-8% of stomach
abomasum
- “true stomach”
- secretes HCl and pepsin
- 7-8% of stomach
reticulo-rumen
- anaerobic fermentation (mostly bacteria and protozoa)
- 25-50 billion bacteria/ml
- 200,000-500,000 protozoa/ml
- numbers/types in population change with diet
- protozoa numbers are higher with forage diet (lower pH)
- near neutral pH
- no digestive secretions - microbial action
- produce CH4, H2, CO2 (bacteria use CO2 and H2 to make CH4)
what happens to feed in ruminants?
- animal bites and bolus swallowed
- enters reticulum/rumen
- musculature of rumen mixes feed with liquid and other contents of rumen
- rumination cycle
- bolus re-enters rumen (more finely chewed)
- while in rumen, microorganisms are digesting feed
rumination
- regurgitation
- remastication
- reinsalivation (saliva high in bicarbonate which is a good buffer)
- redeglutition
- cycle takes ~1 min
- ruminate 7-10.5 hrs/day (avg ~8)
symbolic relationship
- ruminant provides feed and space
- microorganisms digest feed (particularly cellulose) and provide essential nutrients
how long does feed stay in rumen?
- 48-52 hr for roughages (longer for poorer quality)
- 18-22 hr for grain
- particle size is important in allowing feed particles to pass to the omasum
eructation
- gases (mostly CO2 and CH4) must be expelled
- eructation (belching)
- if not, then bloat occurs
- clover and alfalfa have lot of alkaloids. Gases get trapped in bubbles which block the opening to the esophagus and cannot escape, thus bloating occurs.
what causes bloat?
- froth blocks cardia
- gas cant escape
- rumen fills like balloon
- if no relief, death due to suffocation
treatment for bloat
- give surfactant (corn oil)
- tube down throat
- trochar in paralumbar fossa (last resort)
- stick in mouth
- feed poloxalene (bloat guard)
newborn and rumen development
- reticulum, rumen, omasum very small and nonfunctional at birth
- only abomasum is functional (largest part of stomach)
- milk passes straight to abomasum
- by 3 weeks, rumen is developing
- coarse or fibrous feeds hasten development
- by 3-4 months rumen is fully functional
- microbial population introduced through contact with mother, other animals, soil
Thiamin (B1)
- forms thiamin pyrophosphate (TPP)
- catalyzes decarboxylation reactions (lose CO2)
- pyruvate —(TPP)–> acetyl coa
- a ketoglutarate –(TPP)–> succinyl coa
Riboflavin (B2)
- functions in oxidative reduction rxns
- FAD is one coenzyme and can accept 2 H in oxidation rxns
- succinate –(FAD)–> fumarate
- FA –(FAD)–> acetyl coa
- oxidation of some AA
- the reduced form (FADH2) can enter the electron transport system , be oxidized back to FAD, and 2 molecules of ATP will be formed
Niacin
- coenzyme for oxidation reduction rxns
- involved in several rxns in glycolysis and the Krebs cycle
- FA –(NAD)–> acetyl coa
- NADH2 can enter the electron transport system, be oxidized back to NAD and 3 molecules of ATP will be formed.
- another coenzyme, NADPH, is necessary for some synthetic rxns such as FA synthesis
Pantothenic acid
- part of the structure of coenzyme A
- acetyl coa has a central role in metabolism
- FA oxidation begins with the formation of fatty acyl- coa
- coa compounds are necessary for FA synthesis
- a ketoglutarate –(coa)–> succinyl coa
- propionate –(coa)–> succinyl coa
Pyridoxine (B6)
- forms a coenzyme called pyridoxal phosphate which is necessary for several enzymes involved in AA metabolism
- all AA transanimation and deaminations require pyridoxal phosphate. The amino group must be removed before AA can be oxidized via the Krebs cycle for energy or used for gluconeogenesis
- required in the decarboxylation of AA
Biotin
- involved in carboxylation rxns in which CO2 is added to form a new C-C bond
- pyruvate —> oxaloacetate
- acetyl coa —> malonyl coa ( FA synthesis)
- propionate —> succinyl coa
Frolic acid
- involved in the transfer of methyl groups such as in some AA rxns and the synthesis of DNA and RNA
Cobalamin (B12)
- propionate –> succinyl coa
- normal blood cell formation
- transfer of methyl groups
Reticular groove
- located at base of esophagus
- normally open
- closes in nursing calf
- barium sulfate and X-rays
- can be restimulated to close in adult cattle and sheep
Horse digestive tract
- similar to simple stomach animals except for relatively large cecum at the beginning of LI
- microbial fermentation similar to rumen
- cannot use microbial protein (cecum is behind small intestine)
Fistula
- opening from outside into an inner cavity
- rumen fistula
+ paralumbar fossa
+ make incision then suture rumen wall to skin
+ later, cut out area of rumen and insert cannula
+ animal is essentially unaffected
Glucose and ruminants
- only ~15% glucose needed is absorbed
- rely on gluconeogenesis
- intestinal cells use more glucose than absorbed
- have negative drop in glucose across mesentery
Primary source of energy in ruminants
- VFA
Primary carbon source for glucose in ruminants
Propionate
CHO utilization in rumen
- most CHO utilized by rumen microorganisms, this very little glucose absorbed by ruminants
- VFA account for ~70% or more of animals energy needs by 1. Oxidation of VFA via TCA cycle and 2. Conversion of propionate to glucose then oxidize glucose
Acetate and VFA metabolism in ruminants
- extra hepatic
- absorbed from rumen - portal blood - liver - body tissues
- can be used for energy, body fat synthesis, and milk fat synthesis during lactation
Propionate and VFA metabolism in ruminants
- hepatic
- absorbed from rumen - portal blood - liver - very little leaves liver
- can be used for energy, glucose synthesis, synthesis of certain AA
- not used for fat synthesis
Neither __ nor __ can be used for fat synthesis
Propionate; glucose
Butyrate and VFA metabolism in ruminants
- extra hepatic
- converted to b hydroxybutyrate (half during absorption from rumen; and after reaching liver)
- b-oh-butyrate is one of the ketone bodies
- can be used for energy, body fat synthesis, and milk fat synthesis during lactation
FA synthesis in ruminants
- don’t have enough citrate lyase and malic enzyme
- acetate in cytosol can be turned into acetyl coa
- use pentose phosphate pathway for NADPH
Carbon source in FA synthesis in ruminants
Acetate
Primary byproduct of glucose in ruminants
VFA
