11. Kevin Bryan Reviewer Flashcards
organelle responsible for packaging proteins
golgi apparatus
organelle - ATP production
mitochondria
Unfolding of a molecule ≈ effects in entropy
large increase ÎÎ in entropy
decrease the activation energy of rxn
enzymes
the lower the Km of an enzyme ≈ effect on affinity
higher affinity
competitive inhibition can be overcome by
increasing the substrate
site of ETC (electron transport chain)
mitochondria
cyanide inhibits what COMPLEX of ETC?
Complex 4
Blocks electron transport and ATP synthesis by inhibiting the exchange of ATP and ADP across the inner mitochondrial membrane
ATP ADP
atractyloside
catalyzes rxn that yields wate and hydrogen peroxide
superoxide dismutase
- unpaired electron
- persist for short period of time
- ex. superoxide dismutase
free radicals
glucose and galactose are epimers on
carbon 4
glucose and mannose are epimers on
carbon 2
Blocks electron transport and proton pumping at Complex III
azide
carbon monoxide
Blocks electron transport and proton pumping at Complex I.
rotenone
Blocks ATP synthesis without inhibiting electron transport by dissipating the proton gradient
DNP
Blocks electron transport and proton pumping at Complex II.
antimycin A
can be lethal because it binds to the ferric form of cytochrome oxidase and thereby inhibits oxidative phosphorylation
cyanide
mechanism for nitrite as an antidote to cyanide
Nitrite converts ferrohemoglobin into ferrihemoglobin, which also binds cyanide. Thus, ferrihemoglobin competes with cytochrome oxidase for cyanide. This competition is therapeutically effective because the amount of ferrihemoglobin that can be formed without impairing oxygen transport is much greater than the amount of cytochrome oxidase.
- higher Km
- not easily saturated
- isoenzyme of hexokinase
- ACTIVE in fed state
glucokinase
T/F
Acety Coa can be converted to pyruvate in gluconeogenesis
FALSE
Fatty acids and ketogenic amino acids cannot be used to synthesize glucose. The transition reaction is a one-way reaction, meaning that acetyl-CoA cannot be converted back to pyruvate. As a result, fatty acids can’t be used to synthesize glucose, because beta-oxidation produces acetyl-CoA.
•Acety CoA - oxidized to CO2and H2O in TCA cycle
•used to synthesize cholesterol
•used to synthesize ketone bodies
5 cofactors of alpha ketoglutarate
- Thiamine pyrophosphate (derived from thiamine)
- flavin adenine dinucleotide (derived from riboflavin)
- lipoic acid (derived from lipoic acid)
- pantothenic acid as part of Coenzyme-A (CoA)
- nicotinamide adenine dinucleotide NAD+ (derived from niacin
which of the following enzymes catalyze a rxn that yield FADH2 in citric acid cycle
succinate dehydrogenase
which TCA cycle intermediate participates in heme formation
succinyl CoA
Heme formation
•co-factor of the committed step
vitamin B6
the intermediate that links gluconeogenesis and ketogenesis in the liver
pyruvate
glucose 6 phosphate participates in all processes except •pentose phosphate pathway •gluconeogenesis •ketogenesis •glycogenolysis
ketogenesis
these processes occur inside the mitochondria except •pentose phosphate pathway •TCA cycle •beta oxidation •ketogenesis
pentose phosphate pathway
what is the mechanism of hypoglycemia in acute ethanol intoxication
conversion of PYRUVATE to lactate
branching enzyme of glycogen metabolism is
glycogen branching enzyme AKA
amylo-(1,4→1,6)-transglycosylase
•branching enzyme that catalyzes the transfer of alpha-1,4-linked glucosyl units from the outer end of a glycogen chain to an alpha-1,6 position on the same or a neighboring glycogen chain.
is a state of glucose 6 phosphatase deficiency
Von Gierke’s
T/F
glycogenolysis occurs in muscle
TRUE
glycogen phosphorylase catalyzes the cleavage of glycogen to yield
glucose-1- phosphate
- ptx with deficiency of glycogen phosphorylase in the liver
- expected manifestations EXCEPT:
- hepatomegaly
- ketosis
- lactic acidosis
- marked hyperglycemia
FALSE-
•marked hyperglycemia
deficiency of glycogen phosphorylase is
Hers’ disease
glycogen storage disorder associated with hyperuricemia
Von Gierke’s disease
enzyme deficient in Von Gierke’s disease
glucose 6 phosphatase
pregnant woman with classic galactosemia
•at risk for
premature ovarian failure
High fructose in diet is unhealthy because if is metabolized faster than glycose because it bypasses step catalyzed by
phosphofructokinase 1
- night sweats and tremors after fruit juice ingesiton
- (+) fructose in urine
- enzyme deficieny?
aldolase A
metabolic consequences of aldolase A deficiency
- INCREASE FRUCTOSE 1 phosphate levels
- hyperuricemia
- allosteric inhibition of glycogen phosphorylase
- depletion of ATP
which sugar contribute to cataract formation
sugar alcohol
which causes flatulence in lactose intolerance
bacteria in the gut
the main FATTY ACID in coconut milk
lauric acid
trans fats are manufactured by altering SATURATED fats usig
hydrogenation
end product of FATTY ACID synthsis
palmitic acid
what is the mechanism behind FATTY LIVER in chronic alcohol use
inc ÎÎ NADH prevents fatty acid oxidation forming triacylglycerols
ketone bodies
acetone
acetoacetate
beta hydroxybutyrate
steroid nucleus has ___ carbons
17
steroid nucleus resembles this ring
phenanthrene ring
cholesterol has a side chain at position
17
the consumption of cholesterol should be only up to ___ mg per day
300 mg
WELL FED STATE ≈ effect HMG-CoA reductase
HMG-CoA reductase - dephosphorylated
fate of short and medium chain FA after digestion
absorbed in the hepatic portal vein
Apolipoprotein C-II functions in breakdown of
VLDL and chylomicrons
which apoprotein is closely associated with alzheimer’s disease due to its capacity to avidly bind to beta amyloid plagues
Apo E-4
what is the basis of intestinal expression of apo B-48 lipoprotein
tssue specific RNA editing puts a stop to apoB mRNA translation
this component is responsible for transfer of CHOLESTEROL from tissues to other lipoproteins into HDL as esterified cholesterol allowing it to function in REVERSE CHOLESTEROL TRANSPORT
LCAT
T/F
•hypothyroidism
•diabetes mellitus
•nephrotic syndrome
-all are associated with abnormal lipoprotein patterns
TRUE
what familial disorder of lipoprotein metabolism has elevated levels of LDL
type 2
which familial lipoproteinemia gives
HIGH : chylomicron and VLDL
LOW : HDL, LDL
Type 1
presents as •overproduction and increased levels of VLDL •glucose intolerance •associated with coronary heart disease •type 2 DM •obesity
familial hypertriglyeridemia
ASA given low dose for coronary artery disease exerts its beneficial effect by
inhibition of cyclooxygenase required for synthesis of THROMBOXANE
product of lipid metabolism —> platelet aggregatiion
TXA2
most basic amino acid
arginine