Metabolism Overview Flashcards

1
Q

What is metabolism?
a) The process of cellular respiration
b) The linked series of biochemical reactions
c) The synthesis of cellular components
d) The generation of ATP within mitochondria

A

b) linked series of biochem reactions

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2
Q

What is metabolism?

A

Metabolism is the linked series of biochemical reactions, whose pathways are interdependent and highly regulated.

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3
Q

What are the two broad classes of metabolic reactions, and what do they do?

A

catabolic reactions and anabolic reactions. Catabolic reactions convert fuels into cellular energy, while anabolic reactions are energy-requiring reactions used to synthesize cellular components or used for movement.

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4
Q

What roles do the central metabolic pathways play?

A

The central metabolic pathways have both catabolic and anabolic roles. They not only generate ATP through catabolic pathways but also provide building blocks for the synthesis of more complex molecules.

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5
Q

How do cardiac myocytes demonstrate the importance of catabolic metabolism?

A

The constantly beating heart of cardiac myocytes requires a large, continuous supply of ATP to provide the energy for muscle contraction, highlighting the importance of catabolic metabolism.

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6
Q

Where does the majority of ATP generation occur within our hearts, and what is it linked to?

A

The majority of ATP generation occurs within mitochondria in our hearts. It is directly linked to O2 utilization and CO2 generation.

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7
Q

Approximately how much ATP do the mitochondria within our hearts generate each day?

A

~1 kg ATP each day

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8
Q

What happens during a myocardial infarction (MI or heart attack) related to ATP generation?

A

During a myocardial infarction, if the supply of O2 and nutrients is compromised, not enough ATP will be generated, and the affected tissue will die.

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9
Q

Question: What is metabolism?
a) The process of cellular respiration
b) The linked series of biochemical reactions
c) The synthesis of cellular components
d) The generation of ATP within mitochondria

A

b

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10
Q

Which of the following best describes catabolic reactions in metabolism?
a) They synthesize cellular components.
b) They require energy for movement.
c) They convert fuels into cellular energy.
d) They occur within the mitochondria.

A

c

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11
Q

What are the roles of central metabolic pathways?
a) They generate ATP and CO2.
b) They provide building blocks for complex molecules.
c) They regulate cellular respiration.
d) They create anabolic reactions.

A

b

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12
Q

Where does the majority of ATP generation occur in the heart?
a) In the Z lines of cardiac myocytes
b) Within the sarcomeres of the heart
c) Within the nucleus of cardiac cells
d) Within mitochondria

A

d

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13
Q

What is the significance of ATP generation in cardiac myocytes?
a) It provides energy for muscle contraction.
b) It directly links to O2 utilization and CO2 generation.
c) It demonstrates the importance of anabolic metabolism.
d) It requires a large supply of nutrients.

A

a

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14
Q

How much ATP does the mitochondria within our hearts generate approximately each day?
a) 100 grams
b) 500 grams
c) 1 kilogram
d) 10 kilograms

A

c

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15
Q

What happens during a myocardial infarction (MI or heart attack)?
a) The heart muscle contracts more forcefully.
b) The supply of O2 and nutrients to the heart is compromised.
c) The heart rate decreases significantly.
d) The cardiac myocytes stop beating.

A

b

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16
Q

What are the three main macronutrients involved in catabolic metabolism?

A

The three main macronutrients are proteins, carbohydrates, and fats (lipids).

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17
Q

What are the building blocks of proteins, and where are they absorbed?

A

Proteins are broken down into single amino acids, and they are absorbed in the small intestine.

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18
Q

What is the general chemical formula of carbohydrates, and what are their building blocks?

A

The general chemical formula of carbohydrates is (CH2O)n, and their building blocks are monosaccharides, such as glucose, fructose, and galactose.

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19
Q

What is starch, and what is the primary carbohydrate stored in plants?

A

Starch is a polysaccharide made of many glucose monomers, and it is the primary carbohydrate stored in plants.

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20
Q

How is high fructose corn syrup (HFCS) created, and how does its composition compare to sucrose?

A

HFCS is created by hydrolyzing starch into glucose monosaccharides and converting approximately 50% of the glucose into fructose. Like sucrose, HFCS is chemically similar, as both are composed of half glucose and half fructose.

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21
Q

What happens to digestible disaccharides and polysaccharides once they are consumed?

A

All digestible disaccharides and polysaccharides are broken down to monosaccharides before being absorbed in the small intestine.

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22
Q

What defines lipids, and what is the most abundant lipid form in our diets?

A

Lipids are defined by their insolubility in water. The most abundant lipid in our diets is triacylglycerols, commonly known as fat.

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23
Q

What is the major lipid form of energy storage in both plants and animals, and where are large droplets of these lipids found in our bodies?

A

The major lipid form of energy storage is triacylglycerols. Large droplets of triacylglycerols are found in our adipocytes, which are the most common cell type within adipose or fat tissue.

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24
Q

Why does lipid digestion involve hydrolyzing fatty acids from the glycerol scaffold?

A

Triacylglycerols cannot cross cell membranes, so they must be broken down into fatty acids and glycerol to be absorbed into cells.

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25
How do we make ATP?
by oxidizing carbon (removing H+ or electrons or addition of oxygen)
26
What catalyzes the oxidation of a carbon?
Dehydrogenases
27
What reoxidizes NADH and FADH2?
Complexes I and II of the ETC
28
What is the feed-fasting cycle?
We store fuels from foods as fat and glycogen, and proteins as muscle or other cellular components, then slowly release fules as needed.
29
What is insulin
The primary signaling hormone to build and store fuels.
30
What molecules signal the body to release fuel stores?
1. low insulin plus elevated glucagon 2. (nor)epi 3. cortisol
31
What is gluconeogenesis?
The process of glucose synthesis from lactate, glycerol, and amino acids in hepatocytes and kidney cortical cells
32
How are relatively constant blood glucose levels maintained?
1. release of glucose from hepatic glycogen stores 2. gluconeogenesis 3. release of FA from adipocytes and switching of tissues/cells to primarily oxidizing FA instead of glucose
33
What is the primary source of ketones?
From fatty acid oxidation in hepatocytes
34
How do plasma levels of non-esterified fatty acids (NEFAs) change after an overnight fast and a meal
NEFA = free fatty acids
35
What enzyme releases glucose from the liver into the blood?
Hepatic glycogen phosphorylase
36
How does the body make up for limited liver glycogen storage when glocuse is needed in the body?
Adipocytes release fatty acids into the blood and glycerol is released after triacylglycerol lipolysis, absorbed by the liver and converted to glucose via gluconeogenesis. With increased duration, more ketone bodies are made by the liver. Gluconeogenesis decreases and ketogenesis increases.
37
What are the phases of glucose maintenance after eating and through 48 hrs?
1-2 hr - absorption in intestine 2-8 liver glycogen release 6-24 gluconeogenesis 8-48 FA oxidation from adipose tissue delivers glycerol to liver, which makes ketones
38
What is the most abundant ketone body?
beta- hydroxybuterate
39
Compare the timescale of ketogenesis between infants and adults
infants: 2-4 hrs children 2-4: 4-10 hrs children 6-8: 6-24 hrs adult females: 12 hrs -6 days (higher levels than males
40
Can triacylglycerols, FA, and/or glycerol cross membranes?
TG: no FA: yes glycerol: yes
41
Pancreatic lipase
1. stim by CCK 2. released into duodenum 3. normally low in blood 4. high in pancreatitis
42
Lipoprotein lipase
1. tethered to capillary endothelial cells, pointing toward lumen 2. mostly in adipose and muscle tissue 3. can hydrolyze TGs in bloodstream packaged into chylomicrons (dietary TGs) and VLDLs (made in liver) 4. activity is not determined by or reflected by serum lipase measurements
43
What are the major roles of chylomicrons and VLDLs?
deliver FAs (and cholesterol and fat-soluble vitamins) to body's tissues
44
Hepatic lipase
1. similar to lipoprotein lipase 2. localized to luminal surface of hepatic sinusoid capillaries
45
Adipocyte lipases
1. associated w/ lipid droplet 2. series of lipases that release FA from fat storage depots during fasting and physical activity 3. activated by low serum insulin, elevated glucagon and (nor)epi 4. cause for increased NEFAs
46
What are the adipose lipases?
1. adipose triglyceride 2. hormone-sensitive 3. monoacylglycerol
47
How do NEFAs travel in the blood?
Associate w/ serum protein albumin. When they dissociate, taken up by cells throughout body, including liver, where they can be oxidized (usually beta-oxidation) to make ATP
48
What happens in the liver to fatty acids that are oxidized?
Some re-packaged as VLDLs and released in blood
49
What is beta-oxidation?
The primary metabolic pathway humans use to catabolize FA
50
What are the 2 stages of beta-oxidation?
1a. FA activation via attachment of coenzyme A (CoA) 1b. transport into mito matrix by swapping CoA for carnitine 2. Repeated cycles of beta-oxidation w/in mito matrix
51
What is a FA attached to coenzyme A called?
acyl-CoA
52
Can acyl-CoA enter the mitochondrial matrix?
No. So, the long-chain acyl (FA) group is tranferred to carnitine (catylyzed by carnitine-palmitoyl transferase - CPT)
53
What is the major regulatory step in FA oxidation?
The FA group being transferred to carnitine for transport into the mito matrix
54
What can inhibit carnitine-palitoyl transferase (CPT1)?
malonyl-CoA (an intermediate in FA synthesis) -allows for FA oxidation to be inhibited when FA synthesis is activated
55
What is malonyl-CoA?
an intermediate in fatty acid synthesis
56
Under what conditions is FA synthesis activated?
1. High glucose and insulin 2. excessive ethanol 3. fructose catabolism
57
What is considered a long-chain FA?
> 12-carbon
58
What happens to acyl-CoA once
59
What are the basic steps of beta-oxidation?
1. activation of FAs, binding w/ CoA and forming acyl-CoA, which requires ATP and is catalyzed by fatty acyl-CoA synthetase 2. Transport into the mitochondria by forming a carnitine ester catalyzed by carnitine palmitoyltransferase I (CPT1) 3. Translocation across the inner mitochondrial membrane - carnitine ester of the fatty acyl group is transported across the inner mitochondrial membrane into the mitochondrial matrix by a carnitine-acylcarnitine translocase 4. Regeneration of acyl-CoA: atty acyl group is transferred back to CoA from carnitine by the enzyme carnitine palmitoyltransferase II (CPT2) 5. Beta-oxidation cycle: series of reactions that sequentially remove two carbon units from the fatty acyl-CoA chain 6. Repeat cycle 7. Production of acetyl-CoA and energy: acetyl-CoA molecules can enter the citric acid cycle to produce ATP and other forms of energy through oxidative phosphorylation
60
What are the 4 steps of the beta-oxidation cycle?
1. Dehydrogenation: removal of 2 hydrogen atoms from the beta carbon and the alpha carbon of the fatty acyl-CoA by acyl-CoA dehydrogenase, producing a trans-Δ2-enoyl-CoA. 2. Hydration: The trans-Δ2-enoyl-CoA undergoes hydration, adding a water molecule to the double bond. This is catalyzed by enoyl-CoA hydratase, forming 3-hydroxyacyl-CoA. 3. Dehydrogenation: The 3-hydroxyacyl-CoA is dehydrogenated again by 3-hydroxyacyl-CoA dehydrogenase, forming 3-ketoacyl-CoA. 4. Thiolysis: The last step is the cleavage of 3-ketoacyl-CoA into acetyl-CoA and a new, shorter fatty acyl-CoA chain by thiolase.
61
Lactate test
All cells can do anaerobic glycolysis - break down glucose to produce ATP and lactate
62
What would cause high levels of lactic acid
1. shock/sepsis due to poor perfusion causing hypoxic environment 2. Extreme state of stress preventing reuptake of lactate (assumed) 3. Intense exercise 4. pyruvate dehydrogenase deficiency (prevents pyruvate from being hydrolyzed) 5. inborn metabolic disorders that affect the ETC, mitochondrial DNA mutation as the cause (all mito genes code for ETC) or nuclear genes could be a cause too 6. cyanide poisoning
63
Where is oxygen used
Oxidative phosphorylation - the final electron acceptor in the ETC to produce ATP
64
What uses lactate?
1. Gluconeogenesis in the liver - converts lactate to glucose 2. any tissue with mitochondria and enough oxygen can use it, pyruvate to generate glucose?
65
Glucose testing
High - chronic prob: 1. insulin resistance 2. GLUT 4 transporters on muscle and adipose are insulin sensitive Low - acute prob, can -> death
66
Triglycerides
67
What makes uric acid?
purine catabolism
68
What can increase uric acid?
1. tumor lysis syndrome 2. insufficient excretion by kidneys (DM) 3. maybe purine-rich foods
69
Consequences of high uric acid
1. gout - painful arthritis w/ uric acid crystals
70
Urea
Forms from amino acid breakdown -produced by liver in urea cycle
71
What measures urea
BUN - blood urea nitrogen
72
When is BUN high?
1. kidney damage/dysfunction - not excreting it fast enough 2. hypovolemic 3. occult GI bleeding
73
High BUN symptoms
confusion, coma, death
74
Ammonia
Produced from protein metabolism Should be cleared/brken down in liver
75
When could ammonia be high?
1. alcoholism 2. liver damage/dysfunction 3. deficiency in urea cycle
76
High ammonia probs
1. neurotoxin 2. liver disease
77