BIOENERGETICS - CHOLESTEROL Flashcards
(358 cards)
G protein that promotes activation and
intracellular signaling
A. Ion channel
B. cAMP second messenger
C. Phospholipase C second messenger
D. AOTA
D. AOTA
Least describes eicosanoids
A. Derived from C18 eicosanoids
B. Ibuprofen inhibits cyclooxygenase
C. Prostacyclin inhibits platelet aggregation
D. Group 3 eicosanoids include PGD3, TXA3 and
LTB5
A. Derived from C18 eicosanoids
Arachidonate and some other C20
polyunsaturated fatty acids give rise to
eicosanoids, physiologically and
pharmacologically active compounds known as
prostaglandins (PG), thromboxanes (TX),
leukotrienes (LT), and lipoxins (LX) (see Chapter
21). Physiologically, they are considered to act as
local hormones functioning through G-protein-
linked receptors to elicit their biochemical
effects.
Transfer of fatty acids from cytoplasm to the
mitochondrial matrix requires:
A. ATP, carnitine, co-enzyme A
B. ATP, co-enzyme A, hexokinase
C. ATP, carnitine, pyruvate dehydrogenase
D. ATP, co-enzyme A, pyruvate dehydrogenase
A. ATP, carnitine, co-enzyme A
In the presence of ATP and coenzyme A, the
enzyme acyl-CoA synthetase (thiokinase)
catalyzes the conversion of a fatty acid (or FFA)
to an “active fatty acid” or acyl-CoA, using one
high-energy phosphate and forming
AMP and PPi (Figure 22–1).
Long-chainacyl-CoA (or FFA) cannot penetrate
the inner membrane of mitochondria. In the
presence of carnitine, however, carnitine
palmitoyl transferase-I, located in the outer
mitochondrial membrane, transfers long-chain
acyl group from CoA to carnitine, forming
acylcarnitine and releasing CoA. Acylcarnitine is
able to penetrate the inner membrane and gain
access to the β-oxidation system of enzymes via
the inner membrane exchange transporter
carnitine-acylcarnitine translocase.
Correct order of fxn of enzymes in beta
oxidation
1. Thiolase
2. Enoyl CoA hydratase
3. Beta hydroxyacyl CoA dehydrogenase
4. Acyl CoA dehydrogenase
A. 1,2,3,4
B. 4,3,1,2
C. 4,2,3,1
D. 2,4,3,1
C. 4,2,3,1
Not true of oxidation of 1 mol palmitate in
B oxidation, beginning with free fatty Acid in
cytoplasm.
A. 8 mol of acety CoA formed
B. 2 ATPs required for activating fatty acids
C. Inorganic pyrophosphate (PPi) is produced
D. Carnitine functions as an electron acceptor
B. 2 ATPs required for activating fatty acids
In the presence of ATP and coenzyme A, the
enzyme acyl-CoA synthetase (thiokinase)
catalyzes the conversion of a fatty acid (or FFA)
to an “active fatty acid” or acyl-CoA, using one
high-energy phosphate and forming AMP and
PPi.
Fatty acids with odd number of carbon
enters the citric acid cycle as acetyl coA and
A. Alpha keto glutarate
B. Succinyl coA
C. Acetyl CoA
D. Citrate
B. Succinyl coA
Fatty acids with an odd number of carbon atoms
are oxidized by the pathway of β-oxidation
described above producing acetyl CoA until a
three-carbon (propionyl-CoA) residue remains.
This compound is converted to succinyl-CoA, a
constituent of the citric acid cycle (see Figure 16–
2). Hence, the propionyl residue from an odd-
chain fatty acid is the only part of a fatty acid
that is glucogenic.
Every cycle of beta oxidation of FA yield
A. 1 FAD, 1 NADH, 2 CO2 molecules
B. 1 FADH2, 1 NADH, 1 Acetyl coA
C. 1 FADH2, 1 NAD+, 1 Acetly coA
D. 1 FAD, 1 NAD+, 2 CO2 molecules
B. 1 FADH2, 1 NADH, 1 Acetyl coA
Jamaican vomiting sickness, hypoglycin,
what mechanism?
Jamaican vomiting sickness is caused by
eating the unripe fruit of the akee tree, which
contains the toxin hypoglycin. This inactivates
medium- and short-chain acyl-CoA
dehydrogenase, inhibiting β-oxidation and
causing hypoglycemia.
In extrahepatic tissues, the activation of
acetoacetate to acetyl-coa
A. Acyl CoA synthase
B. HMG CoA lyase
C. CoA transferase
D. Acyl CoA dehydrogenase
C. CoA transferase
In extrahepatic tissues, acetoacetate is activated
to acetoacetyl-CoA by succinyl-CoA-
acetoacetate CoA transferase. CoA is
transferred from succinyl-CoA to form
acetoacetyl-CoA.
Function of lipoprotein lipase
A. Intracellular lipid breakdown of lipoprotein
B. Intestinal uptake of dietary fat
C. Hydrolysis of TAG to supply the fatty needs of
the different tissues of the body
D. Lipoprotein breakdown
C. Hydrolysis of TAG to supply the fatty needs of
the different tissues of the body
Both phospholipids and apo C-II are required as
cofactors for lipoprotein lipase activity, while
apo A-II and apo C-III act as inhibitors. Hydrolysis
takes place while the lipoproteins are attached
to the enzyme on the endothelium.
Triacylglycerol is hydrolyzed progressively
through a diacylglycerol to a monoacylglycerol
and finally to FFA plus glycerol.
Major sphingolipids that lacks in lungs
causing respiratory distress syndrome.
A. Glycospingolipid
B. Inositol Phospholipid
C. Ceramide
D. Dipalmitoyl phosphatidylcholine
D. Dipalmitoyl phosphatidylcholine
Deficiency of Lung Surfactant Causes
Respiratory Distress Syndrome
Lung surfactant is composed mainly of lipid with
some proteins and carbohydrate and prevents
the alveoli from collapsing.
The phospholipid dipalmitoyl
phosphatidylcholine decreases surface tension
at the air-liquid interface and thus greatly
reduces the work of breathing, but other
surfactant lipid and protein components are also
important in surfactant function. Deficiency of
lung surfactant in the lungs of many preterm newborns gives rise to infant
respiratory distress syndrome (IRDS).
Administration of either natural or artificial
surfactant is of therapeutic benefit.
Which of these are a correct match?
A. Krabbes- ceramide
B. Niemann-pick- B-glucosidase
C. Fabry Disease- A- galactosidase
D. Tay-sachs- sphingomyelinase
C. Fabry Disease- A- galactosidase
Least correct of ceramide
Ceramide (see Chapter 21) is synthesized in the
endoplasmic reticulum from the amino acid
serine as shown in Figure 24–7.
Ceramide is an important signaling molecule
(second messenger) regulating pathways
including programmed cell death (apoptosis),
the cell cycle, and cell differentiation and
senescence.
VLDL main lipid component
A. TAG
B. Cholesterol
C. Cholesterol ester
D. Phospholipid
A. TAG
Apoprotein exclusively found in
chylomicron
A. B48
B. B100
C. AOTA
D. NOTA
A. B48
Accumulation of acetyl-coA in the
mitochondria of the liver
A. Broken down into FFA
B. Used as an energy source
C. Converted into oxaloacetate
C. Converted into oxaloacetate
Glycolysis (see Chapter 17), the pentose
phosphate pathway (see Chapter 20), and fatty
acid synthesis (see Chapter 23) all occur in the
cytosol. In gluconeogenesis (see Chapter 19),
substrates such as lactate and pyruvate, which
are formed in the cytosol, enter the
mitochondrion to yield oxaloacetate as a
precursor for the synthesis of glucose in the
cytosol.
Which of the following hormone is not used
in the hydrolysis of lipids?
A. ACTH
B. TSH
C. Glucagon
D. Insulin
D. Insulin
The rate of release of FFA from adipose tissue is
affected by many hormones that influence either
the rate of esterification or the rate of lipolysis.
Insulin inhibits the release of FFA from adipose
tissue, which is followed by a fall in circulating
plasma free fatty acids. Insulin also enhances
lipogenesis and the synthesis of acylglycerol and
increases the oxidation of glucose to CO2 via the
pentose phosphate pathway.
Action of hormone sensitive triacylglycerol
lipase
A. Synthesis of FFA in adipose tissue
B. Hydrolysis of FFA in adipose tissue
C. Synthesis of FFA in liver
D. Hydrolysis of FFA in liver
B. Hydrolysis of FFA in adipose tissue
Triacylglycerol undergoes hydrolysis by a
hormone-sensitive lipase to form FFA and
glycerol. This lipase is distinct from lipoprotein
lipase, which catalyzes lipoprotein triacylglycerol
hydrolysis before its uptake into extrahepatic
tissues.
How are primary bile acids converted to
secondary bile acids?
A. Enzyme produced by exocrine pancreas
B. Enzymes present in duodenum
C. Enzymes present in gallbladder
D. Bacterial oxidation in small intestines
D. Bacterial oxidation in small intestines
Primary bile acids are further metabolized in the
intestine by the activity of the intestinal bacteria.
Thus, deconjugation and 7α-dehydroxylation
occur, producing the secondary bile acids,
deoxycholic acid, and lithocholic acid.
Intracellular cholesterol upregulated by this
transcription factor
A. HMG coA
B. SREBP
C. Sterol proteolytic enzymes
D. HMG coA reductase
B. SREBP
Cholesterol and metabolites repress
transcription of the HMG-CoA reductase via
activation of a sterol regulatory element-
binding protein (SREBP) transcription factor.
SREBPs are a family of proteins that regulate
the transcription of a range of genes involved in
the cellular uptake and metabolism of
cholesterol and other lipids
Dyslipoproteinemia with increased HDL
concetration
A. Familial hypertriacylglycerolemia
B. Familiar hyperalphalipoproteinemia
C. Tangier disease
D. Abetalipoproteinemia
B. Familiar hyperalphalipoproteinemia
Synthesis of glucose from lactate, glycerol
A. Glycolysis
B. Lipolysis
C. Gluconeogenesis
D. Glycogenesis
C. Gluconeogenesis
Gluconeogenesis is the process of synthesizing
glucose or glycogen from noncarbohydrate
precursors. The major substrates are the
glucogenic amino acids (see Chapter 29), lactate,
glycerol, and propionate.
Formed from glucose, used for lactating
mammary gland.
A. Fructose
B. Glucose
C. Galactose
D. Maltose
C. Galactose
Galactose is derived from intestinal hydrolysis of
the disaccharide lactose, the sugar found in milk.
It is readily converted in the liver to glucose.
Oxidation, amination of amino acid alanine
in the liver produces
A. A molecule of pyruvic acid and a molecule of
ammonia
B. A molecule of pyruvic acid and carbon dioxide
C. A molecule of pyruvic acid and water
D. A molecule of pyruvic acid and lactate
A. A molecule of pyruvic acid and a molecule of
ammonia
Most of this is transaminated to alanine, at the
expense of amino acids arising from breakdown
of muscle protein. The alanine, and much of the
keto acids resulting from this transamination are
exported from muscle, and taken up by the liver,
where the alanine is transaminated to yield
pyruvate. The resultant amino acids are largely
exported back to muscle, to provide amino
groups for formation of more alanine, while the
pyruvate provides a substrate for
gluconeogenesis in the liver