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FSHN 350- Exam 5
| Question | Answer |
|---|---|
| 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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