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31 Cards in this Set

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Name the essential FA's
Linoleic 18:2 (n-6)
alpha-linolenic 18:3 (n-3)
Trans fatty acids occur in modest amounts in meat and dairy products as result of bacterial fermentation. Catalytic hydrogenation of polyunsaturated vegetable oils to convert these oils to a hardened form of margarine that has the texture of butter is a significant source of trans fatty acids.
saturated fatty acids and trans unsaturated fatty acids raise levels of LDL (low density lipoprotein), which increases risk of coronary heart disease (CHD). But, unlike the saturated fatty acids, the trans acids also lower blood levels of HDL (high density lipoprotein) a molecule deemed protective against CHD
Essential FA deficiency
scaly dry skin

RBC fragility, decreased myocardial contracitlity and resistance to capillary blood flow, decreased ATP from liver mito

skin fixed through omega-6 more than omega-3
Diagnosis of essential FA deficiency
FA oleate is elongated and desaturated to make 20:3 omega-9, the closest approximation to the eicosanoid 20:4

TRIENE/TETRAENE ratio 20:3 to 20:4
ratio above .1 = eFA deficiency
Who gets it
geriatrics on poor diets
fat malabsorption syndromes(surgical bowel resection)
parenteral nutrients deficient in eFA
Burn patients
eFA and pregnancy
Should be 1% of total energy

in preg should be 3%
What breaks down triglycerides?
cholesterol oleate?
Tg, lipase
phospholipid, phospholipase
cholesterol, esterase
Explain digestion and absorption of TG's (LCFA)
TG combine with bile acids and phospholipids to emulsified droplets

add in lipase and esterase and get mixed micelles (LCFA, 2-MG(monoacylglycrol))

these are absorbed by intestinal villus cells (bile acids leave to be reabsorbed in the enterohepatic circ)

FA+MG -> TG -> chylomicrons (VLDL,LDL,HDL) which empty into lymph -> thoracic duct -> blood
digestion/abs of Tg is almost complete, sterols are not
sterols and CE incorp into mixed micelles

most CE is secreted,
digestion and absorption of TG's(MC/SCFA)
abs dir into cells. FFA go to portal vv (bound by albumin)

4X as efficient abs
do not facilitate lipid-soluble vit
Lingual lipase
dont do much with LCFA

pancreatic lipase and colipase, max activity above pH7
1:1 molar ratio
colipase - binds lipase to TG droplet displacing bile salt
bile salts activate what enz
cholesterol esterase, rate of hydrolysis is much less than for TG's
specificity of sterol absorption
beta sitosterol from plants abs poorly, plant sterols interfere with cholesterol abs
1/3 of dietary sitosterol is abs(instead of 5%) --> deposits found in many tissues, plasma CE is normal
fatty malodorous stools
what are some situations assoc with steatorrhea
1)pancreatic disease
2) insuff bile production(duct obstruction)/poor liver secretion(hep)
3) loss of small intestine segm
4) celiac disease and sprue (immune response to gluten, damage to intestinal villi)
how can you diagnose celiac disease/sprue
measure fat soluble vit in blood, test stool for fat
metal soaps
FA in lumen bind divalent cations like Ca Mg and Zinc

can't abs them
decrease Ca in intestine means increase abs of plant oxalates, a major source of kidney stones
what can you give a patient who has steatorrhea
remove dietary fat and replace with MC triglycerides (MCT), can be abs w/o pancreatic lipases

octanoic and decanoic acids are abs dir via portal vv
cholesterol usual uptake
200-600 mg/day
macronutrients abs'd where?
B12/bile salts abs'd where
water soluble vitamins absorbed where
upper intestine
whats more important in atherosclerosis and diet

dietary fat or cholesterol
dietary fat
diet can effect
LDL/HDL ration, want low LDL

and changes in suseptibility to thrombosis(clotting)
P/S ratio
polyunsat/ sat FA's
What type of fatty acid do you want to be eating? (sat vs unsat) and why
saturated = more atherogenic

PUFA's (and oleic)are less atherogenic

Fish oil omega-3 are more antiatherogenic than other PUFA's
Blood cholesterol
200 mg/day is risk factor, over 240 requires serious intervention

measure LDL levels, HDL not a risk
soft or hard margarine
hard margarines are worse
Homocysteine and atherosclerosis
effects not well understood, may be from superoxide radicals,

Hcys levels determined by the rates with which it is recycled to met(using 5,methylTHF-->THF and B12) or cysteine(B6)

Tetrahydrofolate - normalize Hcys

B6/B12 defic = hyperHomocysteinemia