Chapter 27 Flashcards
caloric homeostasis
adequate but not excessive energy
appetite suppression signals
CCk and GLP-1
Appetite Enhancing Signal
Ghrelin
CCK mechanism
released by intestine into brain . binds g-protein. causes feelings of satiety. releases bile salts.
GLP-1 hormone mechanism
released by intestine into pancrease . binds g-protein. causes increased insulin secretion and b-cell proliferation.
long term caloric homeostasis is controlled by ? (2)
Leptin and insulin
Leptin Mechanism
Leptin is an adipokine released by adipocytes. signals the status of TAG stores.
mice that lack leptin are ?
obese
leptic active at high/low AMP concentration
high
neurons associated with Leptin pathway
NPY, agRP, and POMC
NPY and agRP are appetite stimulants/supressors
stimulants
POMC is appetite stimulants/supressors
suppressing
SOCS aka
supressors of cytokine signalling
SOCS interfere with ? and ?
leptin and insulin signalling
obese have high/low leptin levels. implicated to be caused by ?
high. SOCS
insulin signalling pathway
insulin signals phosphorylation/activation of IRS. Activates P13K. Activates PDK. Activates AKT. Activates GSK-3. Phosphorylates/deactivates glycogen synthase.
activation of glycogen synthase
PP1 phosphatase dephosphorylates
diabetes type 2 cause
excess TAG in adipose as a result of caloric excess. Causes insulin resistance
basic strategy of catabolism
make NADH, ATP and build blocks for biosynthesis
basic strategy of anabolism
use NADPH, ATP and building blocks for biosynthesis
Three major pathways that occur in cytoplasm
glycolysis, pentose phosphate, fatty acid synthesis
major pathway in mitochondrial inner membrane
oxidative phosphorylation
Three major pathways in mitochondrial matrix
CAC, b-oxidation of fatty acids, ketone body formation
PFK regulation
activated by F26BP and AMP. Inhibited by ATP and citrate.
fructose 1,6-bisphosphatase
activated by citrate. inhibited by AMP and F26BP.
Reciprocal control by PFK2
phosphorylation of by PKA turns off glycolysis. dephosphorylation makes F26BP turning glycolysis on.
pentose phosphate primarily regulated by availability if ?
NAD+
glycogen phosphorylase and ? are under reciprocal control
glycogen synthase
major control point in fatty acid synthesis
citrate stimulates acetyl CoA carboxylase and provides substrate for commited step
fatty acid degradation control point
inhibited by fatty acid synthesis
four fates of G6P
G1P, F6P, 6PG, glucose
G6P makes G1P when ? for ?
G6P and ATP are high. glycogen synthesis
G6P makes F6P when ? for ?
ATP or carbon skeletons are needed. Glycolysis.
G6P makes 6PG when ? for ?
cell needs NADPH or ribonucleotides. pentose phosphate.
Brain Energy.
Use 60% of bodies glucose in maintaining membrane potential. Ketone bodies replace glucose as fuel during starvation.
Kidneys transport 60 volumes of blood driven by cotransport of ? using ?
Na+ using Na+/K+ ATPase
adipose tissue is specialized for ?
esterification of fatty acids to form TAGs and breakdown
preferred fuel in resting muscle
fatty acids
preferred fuel in of muscle in times of high ATP use
glucose
glycolysis outpaces TCA when large amounts of ATP are needed leading to production of ?
lactic acid
muscle produces alanine by transamination of ?
pyruvate
metabolic hub that gets first call on nutrients and distributes fuel to other tissues
liver
regulates lipid metabolism
liver
takes up most of the glucose in blood and stores it as glycogen
liver
well fed state conditions
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.
early fasting state conditions
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
adaptations in starvation
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.
ketone body sythesis from acetyl CoA
(thiolase)> acetoacetyl CoA >(HMG CoA synthase)> HMG-CoA >(HMG CoA Lyase)> acetoacetate
type 1 diabetes
lack of insuline
ATP and creatine-P supply enough ATP for ? seconds of sprinting
6
slowest method of ATP production
utilization of fatty acids
as distance running increases, we rely more on aerobic/anaerobic ATP production
aerobic
Alcohol metabolism
ethanol oxidized to acetaldehyde in the cytoplasm and to acetate in mitochondria increasing NADH
Alcohol effects on liver metabolism
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.
ethanol induced P450 pathway
consumes NADPH as it oxidizes ethanol. generates damaging free radicals and reduces ability to generate antioxidant reduced glutathione.
scurvy
disease from vitC deficiency. insufficient hydroxylation of proline in collagen.
