nutrition Flashcards
triglycerides
saturated (meat, dairy, trans fats)
unsaturated (seeds, nuts, olive and vegetable oils)
cholesterol
egg yolk
meats
organ meats
shellfish
milk
essential fatty acids
linoleic (omega 6) and linolenic (omega 3) acid->helps lower chances of heart disease
found in vegetable oil
functions of lipids
help absorb fat-soluble vitamins
major fuel of hepatocytes and skeletal muscle
cholesterol stabilizes membrane (precursor of bile salts and steroid hormones)
prostaglandins-> SM contraction, BP control, inflammation
phospholipids essential in myelin sheaths and all cell membranes
adipose tissue-> protection, insulation, fuel storage
complete proteins
contain all needed AA’s
eggs, milk, fish, most meats, soybeans
legumes+cereal grains= contain all essential AA’s
incomplete proteins
lack some essential AA’s
legumes, nuts, cereals
structural materials of proteins
keratin
collagen
elastin
actin
myosin
functions of proteins
enzymes
some hormones
nitrogen balance
rate of protein synthesis=rate of breakdown and loss
positive nitrogen balance
synthesis exceeds breakdown
in children, pregnancy, and tissue repair
negative nitrogen balance
breakdown exceeds synthesis
in stress, burns, infection, injury, starvation, poor dietary proteins
starch
complex carb
in grains and vegetables
sugars
fruits
sugarcane
sugar beets
honey
milk
insoluble fiber
cellulose
provides roughage
soluble fiber
pectin in apples and citrus fruits
lowers blood cholesterol
water-soluble vitamins
vitamins B and C
not stored in body->excreted if not used within 1 hr
vitamin C
aka ascorbic acid
promotes the laying down of collagen in CT
antioxidant->neutralizes free radicals
deficiency can result in scurvy (degeneration of skin, teeth, blood vessels)
overdose can result in GI upset
vitamin B6
aka pyridoxine
coenzyme used in AA metabolism
deficiency linked w/ neurological symp.
overdose can result in numbness of hands/feet and unstable gait
vitamin B3
aka niacin
deficiency can cause pellagra
overdose can result in liver damage and skin flush
vitamin B12
coenzyme in nucleic acid metabolism
deficiency can lead to pernicious anemia
fat-soluble vitamins
vitamins A, D, E, K
stores in body except for vit. K
vitamins A and E neutralize free radicals (antioxidants)
broccoli, cauliflower, brussel sprouts= good source of vit. A and C
vitamin A
provitamin A (B-carotene)
structural comp. of visual pigment retinol
antioxidant
deficiency can lead to night blindness
overdose can result in blurred vision, liver toxicity, alopecia
vitamin D
converted to calcitrol via PTH in kidneys
increases role of intestinal Ca2+ and phosphates absorption
deficiency can lead to osteomalacia in adults and rickets in children
overdose can result in brain, CV, and kidney damage
common cause of deficiency is steatorrhea (fat malabsoprtion syndrome)
vitamin E
stabilizes intracellular membranes
needed for hair/skin maintenance
helps prevent damage to cell membranes
antioxidant
vitamin K
aquamephyton, antihemorrhagic vitamin
synthesizes 3 clotting factors and prothrombin
produced by bacteria in LI
overdose can result in liver damage and anemia
coumatin (anticoagulant)= blocks vit. K uptake and utilization to decrease prothrombin formation by liver and prolong clotting times
minerals
inorganic ions released by dissociation of electrolytes
work w/ nutrients to ensure proper body functioning
Ca2+, phosphorous, K+, sulfur, Na+, Cl-, Mg2+, iron, iodine
vegetables, legumes, milk, some meats
carb metabolism
oxidation of glucose (C6H12O6+6O2->6H2O+6CO2+32 ATP + heat)
glucose enters cells via FD
phosphorylated to glucose-6-phosphate
most cells lack enzymes for reverse rxns-> traps glucose inside cell (intestines and kidneys)->liver can reverse rxn and release glucose
keeps intracellular glucose conc. low for continued glucose entry
glycolysis
10 steps
anaerobic
occurs in cytosol
glucose->2 pyruvic acid
final products are 2 pyruvic acid, 2 NADH+H+, 2 ATP, 2 H2O
if O2 present, moves onto krebs cycle in mitochondria
if no O2 present, pyruvic acid is reduced to lactic acid-> may be converted to glucose-6-phosphate for storage as glycogen in liver or de-phosphorylation
krebs cycle
aerobic, but does not directly use O2
NADH molecules must be oxidized to NAD+
pyruvic acid from glycolysis converted into acetyl coA (acetic acid+coenzyme A) and then enters krebs cycle
acetyl coA combines with oxaloacetate to form citrate
forms 4 CO2, 6 NADH, 2 FADH2, 2 ATP as products
chemiosmotic process
couples movement of substances across membrane to chemical rxns
energy used to pump H+ across mitochondrial membrane (flows through ATP synthase membrane channel->energy used to phosphorylate ADP)
ETC
oxidative phosphorylation
NADH++H+ and FADH2 oxidized to NAD+ and FAD
electrons passed along chain to final electron acceptor (O2)
H+ pumped into intramembrane space (establishes proton gradient)
water is byproduct
ATP synthase
produces ~30 molecules of ATP at the end of ETC
glycogenolysis
formation of glucose form glycogen
gluconeogenesis
glucose is formed via AA’s
glycogenesis
glucose is polymerized into glycogen
stored in liver and skeletal muscles
coenzyme A
facilitates the transfer of carbon molecule
dehydrogenation
oxidation of molecules (H+ is removed from molecules and transfered)
NAD+ and FAD becomes reduced into NADH and FADH2->provides electrons to ETC
occurs in krebs cycle
decarboxylation
carboxyl group is removed from a molecule in order to form CO2
occurs in krebs cycle and results in acetic acid and CO2
calcium
most abundant mineral in human body
oxaloacetic acid
4-carbon molecule that starts krebs cycle
micronutrients
vitamins
minerals
macronutrients
proteins
carbs
fat
protein metabolism
not stored in body
oxidized for energy or converted to fat for storage if in excess
transamination
transfer of an amino group (-NH2) from one amino acid to a ketoacid, typically an α-keto acid (turns into glutamic acid)
oxidative deamination
in liver
rids body of toxic ammonia
glutamic acid converted to a-ketoglutaric acid
urea excreted in urine via kidneys
amino acid pool
body’s total supply of free AA’s
proteins lost in urine, hair, skin cells
source for resynthesizing body proteins, forming AA derivatives, gluconeogenesis
carb and fat pools
oxidized directly to produce energy
excess carbs are stored
absorptive state of carbs
anabolism exceeds catabolism
nutrients stored
glucose is the major source of energy and is converted in the liver to glycogen or fat which is released to the blood for storage in adipose tissue as VLDLs
absorptive state of lipids
chylomicrons transport lipids to muscle and fat
most glycerol and fatty acids converted to triglycerides for storage which can used by adipose tissue, liver, skeletal muscle as energy source
absorptive state of proteins
excess AA deaminated and used for ATP synthesis or stored as fat in the liver
most AA used in protein synthesis
insulin
controls absorptive state
stimulated by increased BG and AA levels and intestinal GIP and parasymp NS
DM
inadequate insulin production or abnormal insulin receptors
glucose unavailable to most body cells
increased BG levels
glucose is lost in urine
fats and proteins used for energy->metabolic acidosis, protein wasting, weight loss
glucagon
stimulated by decreased BG and increased AA levels
hyperglycemic hormone
hypoglycemia
too much insulin in relation to amount of glucose
decreased serum glucose levels to 50 mg/dL or below
triggers SNS stimulation via E from adrenal medulla (fight or flight response)
triggers the release of GH, thyroxine, sex hormones, corticosteroids
postabsorptive state
catabolism of lipids, carbs, and proteins exceed anabolism
makes glucose available to blood
promotes use of fats for energy (glucose sparing)
triggered by reduced insulin release as BG levels drop (controlled via symp NS)
sources of glucose
glucogenolysis in liver and skeletal muscle
lipolysis in adipose tissue and liver
catabolism of cellular protein
lipoproteins
transport water-insoluble cholesterol and triglycerides in blood
regulate lipid entry/exit of target cells
contain triglycerides, phopholipids, cholesterol, and protein
increased percentage of lipid= decreased density
VLDLs
mostly triglyceride
transport triglycerides from liver to peripheral tissues (mostly adipose)
LDLs
cholesterol rich
transport cholesterol to peripheral tissues for membrane, storage, or hormonal synthesis
HDLs
highest protein content
transport excess cholesterol from peripheral tissues to liver to be broken down and secreted into bile
provide cholesterol to steroid producing organs
saturated fatty acids
stimulate liver synthesis of cholesterol
inhibit cholesterol excretion from body
unsaturated fatty acids
enhance excretion of cholesterol
enhance cholesterol catabolism to bile salts
trans fats
type of unsaturated fat
ex. margarine
worse than saturated fats
increases LDLs and decreases HDLs
energy intake
energy liberated during food oxidation
energy output
~60% lost as heat
used to do work via ATP
stored as fat or glycogen
metabolic rate
total heat produced by chemical rxns and mechanical work of body
influenced by body SA, age, gender, body temp, stress, thyroxine
measured in post-absorptive state (reclining position, relaxed mentally and physically, room temp 25-25 C)
BMR increases as ratio of body SA to volume increases
chylomicrons
lowest density
composed of triglycerides, cholesterol, phospholipids
formed in intestines after the absorption of dietary fats
transport dietary lipids from the intestines to various tissues via lacteals in the body to be stored or used
lipid metabolism
fats mostly transported via chylomicrons via lacteal
hydrolyzed into fatty acids and glycerol
triglycerides used for energy
converted to glucose if carbs deficient, but oxaloacetic acid must be present
(w/o it, converted by ketogenesis in liver to ketone bodies)
glycerol
enters glycolysis as glyceraldehyde 3-phosphate
produces half the amount of ATP carbs do from oxidative phosphorylation
fatty acid
chains broken into 2-carbon acetic acid fragments and reduced co-enzymes (acetic acid->acetyl coA->krebs cycle->reduced coenzymes->ETC)
lipogenesis
triglyceride synthesis
lipolysis
glycerol and fatty acids used for fuel
ketosis
increased ketones in blood
increases acidity of blood=metabolic acidosis
symp. include fruity breath, increased RR to release CO2 and increase pH
ketone bodies excreted in urine
commonly found in starvation, unwise dieting, and DM
cholesterol
total recommended levels= less than or equal to 200 mg/dL
HDL= greater than 60 is good; less than 40 is not good
LDL= less than or equal to 100 mg/dL is good; greater than or equal to 130 mg/dL is not good
lactic acid fermentation
allows cells to make ATP w/o the involvement of O2
pyruvic acid->lactic acid (regenerates NAD+ and NADH)
allows glycolysis to continue to produce ATP by maintaining the necessary supply of NAD+
