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FSHN 350- Exam 5

Components of TDEE EXee, NEAT, TEF, BMR
What does NEAT stand for? non exercise induced thermogenesis
MET measure expressing the energy cost of a physical activity as a ratio of metabolic rate during the exercise and during a reference
BMR amout 1.2 kcal/minute
Compensators vs. noncompensators eat more when exercise/don’t
Part of the brain that controls satiety hypothalamus
Db/++ parabiosis lean mouse died of starvation (db leptin resistant)
Db/ob parabiosis ob mouse died of starvation (db leptin resistant)
Ob/++ parabiosis ob mouse becomes lean (ob leptin deficient)
Leptin satiety factor (over-produced in most obese individuals); helps some lose weight
Important discovery from leptin resistance adipose tissue is an important endocrine organ
Peptide YY reduces appetite and food intake (increases after feeding)
Ghrelin appetite activating hormone (increased during fast)
POMC neurons decrease food intake (activated by insulin)
NPY/AgRP neurons increase food intake (inhibited by PYY; activated by ghrelin)
POMC signaling pathway problems mutations; autoimmune against MC4 receptor
Obesity associated w/ what in leptin, PYY, and ghrelin? increased leptin (resistance), decreased PYY, decreased ghrelin* inconclusive
PYY obese vs. lean less in both fasting and fed states; not resistant
Satiety and hunger in reduced obese individuals more food & not less hungry
Less than ___% of individuals are able to maintain weight loss for ____ years or longer 10%; 5
Ghrelin before and after weight loss after-> much higher
Change in PYY and ghrelin 62 week after weight loss ghrelin starts to normalize, but PYY continues to fall
Evolutionary perspective of obesity the system is driven to regain weight b/c fear of starving
What causes increased caloric intake after use of THC? snacking
Anorectic POMC neurons
Orexigenic NPY/AgRP neurons
CB1 receptors cannabinoid receptors in CNS
CB2 receptors cannabinoid receptors in in periphery
Mice lacking CB1 receptor lose weight on standard chow and a high fat diet
Acomplia/rimonabant blocked CB1 receptor; taken off market b/c of depression
How do CB1/CB2 receptors modulate appetite? activation of NPY neurons
vitamin A is composed of retinols
other function (than vision) of vitamin A cell differentiation
VADD vitamin A deficiency disorder-> night blindness, hyperkeratosis
vitamin D activation vitamin D3-> semi active form (in liver), then parathyroid hormone converts it to active form in kidneys (**activated by low calcium)
vitamin D and cardiovascular risk significantly higher risk w/ less vitamin D
vitamin D deficiency rickets in children, osteoporosis in adults
vitamin E antioxidant found in cell membranes (prevents oxidation of fatty acids)
regeneration of vitamin E (3 compounds) NADPH, ascorbate, GSSG
B1 thiamin
B2 riboflavin
B3 niacin
B5 panthothenic acid
B6 pyridoxine
B7 biotin
B9 folate
B12 cobalamin
which vitamin is absorbed in the ileum? B12
active form of thiamin (B1) thiamin pyrophosphate
TPP function oxidative carboxylation reactions
3 reactions that require TPP pyruvate-> acetyl coA; alpha ketoglutarate -> succinyl coA; BCAA -> acetyl coA
thiamin deficiency Beri-Beri (weak-weak) and Wernicke-Korsakoss caused by interaction w/ alcohol
riboflavin (B2) central component of FMN and FAD
FMN structure riboflavin + phosphate
FAD structure riboflavin + phosphate + AMP
3 reactions that require riboflavin (FAD or FMN) Kreb's cycle (succinate-> fumarate); ETC electron delivering; beta oxidation
niacin (B3) converted to NAD and NADP
where does NADPH function? MEOS (ethanol-> acetaldehyde) and fatty acid synthesis
niacin deficiency pellaga 4 D's (dermatitis, diarrhea, dementia, death) *occurs where corn is the main staple
pantothenic acid (B5) component of coenzyme A
pyridoxine 3 types pyridoxine (plant), pyridoxal (animal), pyridoxamine (animal)
pyridoxine (B6) many enzymes in protein metabolism; amino acid metabolism (transaminase)
biotin (B7)- 2 reactions coenzyme for carboxylases; pyruvate-> oxaloacetate (gluconeogenesis); acetyl coA -> malonyl coA (FA synthesis)
folate (B9) purine synthesis, cell homeostasis during periods of cell division
folate deficiency neural tube defects (spina bifida)
cobalamin (B12) structure has a cobalt in middle; largest vitamin
cobalamin (B12) function odd chain FA metabolism (methylmalonyl- coA mutase); make methionine from homocysteine (then SAMe can be produced)
cobalamin deficiency if gastric cells stop producing intrinsic factor, pernicious anemia occurs
vitamin C structure resembles glucose (some animals can synthesize it)
vitamin C function antioxidant/reducing agent; cofactor for collagen synthesis
vitamin C is a co-factor for enzymes involved in carnitine and neurotransmitter production
vitamin C is a natural antihistamine
vitamin D function calcium homeostasis
Created by: melaniebeale
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