Chapter 27

Question 1

caloric homeostasis

Answer 1

adequate but not excessive energy

Question 2

appetite suppression signals

Answer 2

CCk and GLP-1

Question 3

Appetite Enhancing Signal

Answer 3

Ghrelin

Question 4

CCK mechanism

Answer 4

released by intestine into brain . binds g-protein. causes feelings of satiety. releases bile salts.

Question 5

GLP-1 hormone mechanism

Answer 5

released by intestine into pancrease . binds g-protein. causes increased insulin secretion and b-cell proliferation.

Question 6

long term caloric homeostasis is controlled by ? (2)

Answer 6

Leptin and insulin

Question 7

Leptin Mechanism

Answer 7

Leptin is an adipokine released by adipocytes. signals the status of TAG stores.

Question 8

mice that lack leptin are ?

Answer 8

obese

Question 9

leptic active at high/low AMP concentration

Answer 9

high

Question 10

neurons associated with Leptin pathway

Answer 10

NPY, agRP, and POMC

Question 11

NPY and agRP are appetite stimulants/supressors

Answer 11

stimulants

Question 12

POMC is appetite stimulants/supressors

Answer 12

suppressing

Question 13

SOCS aka

Answer 13

supressors of cytokine signalling

Question 14

SOCS interfere with ? and ?

Answer 14

leptin and insulin signalling

Question 15

obese have high/low leptin levels. implicated to be caused by ?

Answer 15

high. SOCS

Question 16

insulin signalling pathway

Answer 16

insulin signals phosphorylation/activation of IRS. Activates P13K. Activates PDK. Activates AKT. Activates GSK-3. Phosphorylates/deactivates glycogen synthase.

Question 17

activation of glycogen synthase

Answer 17

PP1 phosphatase dephosphorylates

Question 18

diabetes type 2 cause

Answer 18

excess TAG in adipose as a result of caloric excess. Causes insulin resistance

Question 19

basic strategy of catabolism

Answer 19

make NADH, ATP and build blocks for biosynthesis

Question 20

basic strategy of anabolism

Answer 20

use NADPH, ATP and building blocks for biosynthesis

Question 21

Three major pathways that occur in cytoplasm

Answer 21

glycolysis, pentose phosphate, fatty acid synthesis

Question 22

major pathway in mitochondrial inner membrane

Answer 22

oxidative phosphorylation

Question 23

Three major pathways in mitochondrial matrix

Answer 23

CAC, b-oxidation of fatty acids, ketone body formation

Question 24

PFK regulation

Answer 24

activated by F26BP and AMP. Inhibited by ATP and citrate.

Question 25

fructose 1,6-bisphosphatase

Answer 25

activated by citrate. inhibited by AMP and F26BP.

Question 26

Reciprocal control by PFK2

Answer 26

phosphorylation of by PKA turns off glycolysis. dephosphorylation makes F26BP turning glycolysis on.

Question 27

pentose phosphate primarily regulated by availability if ?

Answer 27

NAD+

Question 28

glycogen phosphorylase and ? are under reciprocal control

Answer 28

glycogen synthase

Question 29

major control point in fatty acid synthesis

Answer 29

citrate stimulates acetyl CoA carboxylase and provides substrate for commited step

Question 30

fatty acid degradation control point

Answer 30

inhibited by fatty acid synthesis

Question 31

four fates of G6P

Answer 31

G1P, F6P, 6PG, glucose

Question 32

G6P makes G1P when ? for ?

Answer 32

G6P and ATP are high. glycogen synthesis

Question 33

G6P makes F6P when ? for ?

Answer 33

ATP or carbon skeletons are needed. Glycolysis.

Question 34

G6P makes 6PG when ? for ?

Answer 34

cell needs NADPH or ribonucleotides. pentose phosphate.

Question 35

Brain Energy.

Answer 35

Use 60% of bodies glucose in maintaining membrane potential. Ketone bodies replace glucose as fuel during starvation.

Question 36

Kidneys transport 60 volumes of blood driven by cotransport of ? using ?

Answer 36

Na+ using Na+/K+ ATPase

Question 37

adipose tissue is specialized for ?

Answer 37

esterification of fatty acids to form TAGs and breakdown

Question 38

preferred fuel in resting muscle

Answer 38

fatty acids

Question 39

preferred fuel in of muscle in times of high ATP use

Answer 39

glucose

Question 40

glycolysis outpaces TCA when large amounts of ATP are needed leading to production of ?

Answer 40

lactic acid

Question 41

muscle produces alanine by transamination of ?

Answer 41

pyruvate

Question 42

metabolic hub that gets first call on nutrients and distributes fuel to other tissues

Answer 42

liver

Question 43

regulates lipid metabolism

Answer 43

liver

Question 44

takes up most of the glucose in blood and stores it as glycogen

Answer 44

liver

Question 45

well fed state conditions

Answer 45

glucose and AA's transported in blood. insulin released to stimulate energy storage and protein synthesis. glycogen storage in muscle and liver occurs. liver able to trap large amount of glucose because it has a glucokinase with high Km or high affinity for glucose.

Question 46

early fasting state conditions

Answer 46

decreased insulin secretion. increased glucagon levels. liver releases glucose to bloodstream. adipose tissues release fatty acids and muscle and liver use fatty acids as fuels

Question 47

adaptations in starvation

Answer 47

muscle use fatty acids exclusively. pyruvate dehydrogenase turned off. pyruvate, lactate and alanine sent to liver for gluconeogenesis. gluconeogenesis depeletes TCA intermediates. excess acetyl CoA used to produce ketone bodies. less glucose demand decreases protein breakdown.

Question 48

ketone body sythesis from acetyl CoA

Answer 48

(thiolase)> acetoacetyl CoA >(HMG CoA synthase)> HMG-CoA >(HMG CoA Lyase)> acetoacetate

Question 49

type 1 diabetes

Answer 49

lack of insuline

Question 50

ATP and creatine-P supply enough ATP for ? seconds of sprinting

Answer 50

6

Question 51

slowest method of ATP production

Answer 51

utilization of fatty acids

Question 52

as distance running increases, we rely more on aerobic/anaerobic ATP production

Answer 52

aerobic

Question 53

Alcohol metabolism

Answer 53

ethanol oxidized to acetaldehyde in the cytoplasm and to acetate in mitochondria increasing NADH

Question 54

Alcohol effects on liver metabolism

Answer 54

NADH accumulation inhibits gluconeogenesis and fatty acid oxidation. Acetate is converted to acetylCoA which stimulates fatty acid synthesis (b/c NADH inhibits TCA cycle) resulting in "fatty liver". Ketone body production increases which can lower blood ph. acetate processing eventually impaired and acetaldehyde accumulates causing liver damage.

Question 55

ethanol induced P450 pathway

Answer 55

consumes NADPH as it oxidizes ethanol. generates damaging free radicals and reduces ability to generate antioxidant reduced glutathione.

Question 56

scurvy

Answer 56

disease from vitC deficiency. insufficient hydroxylation of proline in collagen.