Exam 3 (glycogenesis, glycogenolysis, cholesterol, steriod hormones, de novo fatty acid synthesis, beta oxidation, lipolysis Flashcards
1
Q
What is the enzyme that converts glucose-6-phosphate to glucose-1-phosphate in glycogenesis?
A
Phosphoglucomutase (isomerase enzyme)
2
Q
What enzyme converts glucose-1-phosphate to UDP-glucose?
A
UDP Glucose pyrophosphorylase
3
Q
Where is glycogen stored?
A
Liver and skeletal muscle
4
Q
When does glycogenesis occur?
A
During the FED state
5
Q
What is the enzyme that continues to add glucose molecules to the glycolytic chain during step 4 of glycogenesis?
A
Glycogen synthase
6
Q
What enzyme cleaves alpha-1,4-glycolytic bonds and creates alpha-1,6-glycolytic bonds in step 5 of glycogenesis?
A
Glycogen branching enzyme
7
Q
What is the enzyme that begins to cleave glycosyl residues off the glycogen chain in the first step of glycogenolysis?
A
Glucose Phosphorylase
8
Q
What state does glycogenesis occur?
A
FED state
9
Q
What state does glycogenolysis occur?
A
FASTED state
10
Q
What is the enzyme involved in step 2 of glycogenolysis?
A
Glycogen de-branching enzyme
11
Q
What two types of reactions does glycogen de-branching enzyme do?
A
First it does a transferase reaction and then it does a hydrolysis reaction
12
Q
What enzyme converts glucose-1-phosphate to glucose-6-phosphate in the last step of glycogenolysis?
A
Phosphoglucomutase
13
Q
What enzyme further dephosphorylates glucose-6-phosphate to eventually become glucose that the liver will dump into blood serum?
A
Glucose-6-Phospatase
14
Q
How often are branches formed in glycogen molecules being formed?
A
Every 8-10 glucosyl residue
15
Q
What is the role of glycogenin?
A
The role of glycogenin is to serve as the core for the glycogen granule and to link glucose to itself to form a primer for glycogen formation.
16
Q
What hormone inhibits glycogenolysis and activates glycogenesis?
A
Insulin
17
Q
What hormone activates glycogenolysis and inhibits glycogenesis?
A
Glucagon
18
Q
In the fasted state, glucagon binds to the g-protein-coupled receptor which activates what?
A
Protein Kinase A
19
Q
What enzyme phosphorylates glycogen phosphorylase to make it active?
A
Phosphorylase kinase
20
Q
What enzymes phosphorylates glycogen synthase to make it inactive?
A
Protein Kinase A
21
Q
When insulin binds to its g-protein-coupled receptor, what does it activate?
A
Protein Phosphatase-1
22
Q
In the liver and muscle, what activates glycogen synthase?
A
Glucose-6-phosphate
23
Q
In the liver and muscle, what inhibits glycogen phosphorylase?
A
Glucose-6-phosphate and ATP
24
Q
In just muscle, what activates glycogen phosphorylase?
A
AMP
25
In the liver, what inhibits glycogen phosphorylase?
Glucose
26
What is the rate-limiting step of glycogenesis (glycogen synthesis)
Glycogen Synthase
27
What is the rate-limiting step of glycogenolysis (glycogen breakdown)?
Glycogen Phosphorylase
28
What is the main product of glycogen breakdown (glycogenolysis)?
Main product is glucose-1-phosphate with minor products being free glucose
29
Where does the synthesis and degradation of cholesterol occur?
Cytosol and endoplasmic reticulum
30
What is the regulatory enzyme of cholesterol synthesis?
HMG-CoA reductase
31
What are hormone levels when glycogenolysis is occurring?
Occurs in the FASTED state. Decreased levels of blood glucose and, therefore, decreased levels of insulin. Increased levels of glucagon and epinephrine
32
What are hormone levels when glycogenesis is occurring?
Occurs in the FED state. Decreased levels of glucagon and epinephrine. Increased levels of blood glucose, therefore, increased level of insulin
33
What is the rate-limiting enzyme of glycogenesis?
Glycogen Synthase
34
What is the rate-limiting enzyme of glycogenolysis?
Glycogen Phosphorylase
35
Insulin binding to the g-protein-coupled receptor activates what enzyme?
Protein Phosphatase-1
36
What are the 3 sources of blood glucose in the body?
Diet, gluconeogenesis, and glycogenolysis
37
What are the 2 ways to the body gets cholesterol?
Diet and De Novo Synthesis
38
Where does cholesterol synthesis occur?
Cytosol and Endoplasmic reticulum
39
What is the regulatory enzyme of cholesterol synthesis?
HMG-CoA Reductase
40
Cholesterol is a very ________ molecule.
Hydrophobic
41
The process of making cholesterol is an _____ process and requires ______.
Anabolic; energy
42
What hormone increases the activity of HMG-CoA Reductase?
Insulin
43
What hormone decreases the activity of HMG-CoA Reductase?
Glucagon
44
Where does feedback inhibition (negative feedback) on cholesterol synthesis by cholesterol occur?
Only the liver
45
What are steroid hormones' primary functions regarding gene expression?
They bind to intracellular receptors, where they act as transcription factors to alter protein synthesis
46
Can cholesterol be oxidized like fatty acids to provide energy?
No, cholesterol is not oxidized to make energy. The steroid nucleus of cholesterol is eliminated from the body in the form of bile salts.
47
What is the starting molecule for cholesterol synthesis?
Acetyl CoA
48
Cholesterol is almost made in every tissue of the body. However, 20% of endogenous cholesterol comes from this organ?
Liver
49
What is the reducing agent in cholesterol synthesis?
NaDPH
50
Cholesterol esters have ______ attached to the third carbon of ring A. This makes the cholesterol ester more hydrophobic than non-esterified cholesterol.
Fatty Acid
51
What are the three groups of steroid hormones discussed in class?
Glucocorticoids, Mineralcorticoids, and sex hormones
52
What is an example of a glucocorticoid?
Cortisol
53
What is an example of a mineralocorticoid?
Aldosterone
54
What are three examples of sex hormones?
Testosterone, estrogen, and progesterone
55
Where does de novo fatty acid synthesis occur?
Mainly in the liver and mammary glands. Lesser extent in adipose tissue
56
De novo fatty acid synthesis occurs in the ______ state when ______ hormone levels are high. This process is also an __________ process.
FED; insulin; anabolic
57
What is step 1 of de novo fatty acid synthesis?
Converting Acetyl CoA to citrate so it can cross inner mitochondrial matrix to enter cytosol to be used in fatty acid synthesis.
58
What enzyme catalyzes the condensation reaction between acetyl CoA and oxaloacetate to form citrate in fatty acid synthesis?
Citrate Synthase
59
What enzyme catalyzes the conversion of citrate to Acetyl CoA once in the cytosol for fatty acid synthesis?
ATP citrate lyase
60
What enzyme is the rate-limiting step of fatty acid synthesis?
Acetyl CoA carboxylase (ACC)
61
What reaction does acetyl CoA carboxylase catalyze?
It catalyzes the carboxylation reaction converting Acetyl CoA to Malonyl CoA
62
What activates Acetyl CoA Carboxylase?
Increased insulin levels due to excess calories from carbohydrates and/or protein
63
What are the two molecules needed to start the fatty acid synthase system?
Acetyl CoA and Malonyl CoA
64
What are the 4 types of reactions that occur in 1 cycle of the fatty acid synthase system?
Condensation, reduction, dehydration, and reduction
65
What is the end product of cycle 1 in the fatty acid synthesis of the fatty acid synthase system?
Butyryl ACP
66
When is the fatty acid synthase system terminated?
When it reaches the 16 carbon molecule of palmitic acid
67
What general term is used for enzymes that elongate a fatty acid after it is synthesized?
Elongases
68
What general term is used for enzymes that desaturate a fatty acid after it is synthesized?
Desaturases
69
What state is Acetyl CoA Carboxylase in when it is active?
Dephosphorylated
70
What state is Acetyl CoA Carboxylase in when it is deactivated?
Phosphorylated
71
What enzyme phosphorylated Acetyl CoA Carboxylase to make it inactive?
AMP-Dependent Kinase
72
What hormone increases the express of ACC?
Insulin
73
What hormone decreases the expression of ACC?
Glucagon
74
What substrate activates Acetyl CoA carboxylase and why?
Citrate activates ACC because high levels of citrate inhibit TCA cycle allowing the fate of acetyl CoA to be pushed towards storage.
75
What substrate inhibits Acetyl CoA carboxylase and why?
Long-chain fatty acyl CoA inhibits ACC because these re generated from lipolysis, and we do not want to be building and breaking down fatty acids at the same time.
76
What is the general fate of fatty acids from de novo synthesis?
Since fatty acid synthesis mainly occurs in the liver, the fatty acid will enter circulation and go to tissues that need them to build fatty acid-based molecules or 3 fatty acids that will attach to glycerol to form a triglyceride (triacylglycerol)
77
What state are fatty acids stored in?
Triglyceride form
78
Fat eaten in a meal is stored as fat in ________ tissue.
Adipose
79
The acetyl CoA that combines with oxaloacetate to generate citrate in the mitochondria of the liver then travels to the cytosol is derived from_______.
Glucose
80
Once the acetyl CoA is in the cytosol and available for fatty acid synthesis, it then participates in a reaction with the enzyme ______ and forms malonyl CoA.
Acetyl CoA Carboxylase
81
Fatty acid synthesis begins with two units of acetyl CoA. One of the acetyl CoA is converted to malonyl CoA. The second acetyl CoA (Acetyl ACP) is attached to malonyl ACP due to a condensation reaction. Following the condensation reaction, there is a reduction, ____, and then a reduction.
Dehydration
82
At the end of the first pass of this cycle, a 4-carbon butyryl ACP is generated. The butyryl ACP then participates in a condensation reaction with malonyl CoA and then goes through a reduction, dehydration, and reduction reaction to form a 6-carbon molecule. The 6-carbon molecule then participates in a condensation reaction with _____. The malonyl CoA is generated from the supply of acetyl CoA that was made from excess carbs and proteins. Don’t forget that the mitochondrial-derived acetyl coA has to be transferred to the cytosol via citrate.
Malonyl CoA
83
The fatty acid will continue through the fatty acid synthase complex until the fatty acid is ___ carbons long. This 16-carbon fatty acid is called ____.
16; palmitic acid
84
_________ is the end product of fatty acid synthesis, not butyryl ACP.
Palmitic acid
85
Once the 16-carbon fatty acid is formed, it can then be ____ and/or desaturated. Elongases are the enzymes that elongate or lengthen the fatty acid. The fatty acid does not go through the Fatty Acid Synthase Enzyme Complex (the condensation, reduction, dehydration and reduction reactions) to be elongated. Instead, the enzyme elongases are used to add _______ as the two-carbon donor.
Elongated; Malonyl CoA
86
The ____ enzymes present in the smooth endoplasmic reticulum (SER) are responsible for desaturating long-chain fatty acids by adding cis double bonds.
Desaturases
87
Once fatty acids are made in the liver, they will be transported into circulation and delivered to tissues that need the fatty acids to build fatty acid-containing molecules, or the fatty acid will attach to a ______ to be stored as a triacylglycerol/triglyceride in fat tissue.
Glycerol
88
The enzyme, ACC, is a key regulatory step in fatty acid synthesis (FAS). Allosterically, ACC is activated by ____. This makes sense since FAS takes place in the cytosol, and the only reason citrate would be in the cytosol is to provide the 2-carbon acetyl group to make malonyl CoA. The citrate is initially generated in the mitochondria in the Krebs cycle. The excess acetyl CoA is derived from protein and carbohydrate metabolism. The acetyl group combines with OAA to form _____, which can then cross the mitochondrial membrane into the cytosol to be ligated, leaving 2-carbon acetyl and OAA.
Citrate; citrate
89
A negative allosteric regulator of Acetyl CoA Carboxylase is _________.
Long Chain Fatty Acyl CoA
90
ACC is also regulated by _____ modification. The covalent modification indicates phosphorylation/de-phosphorylation. _____ stimulates the activity of ACC while glucagon inactivates it.
Covalent; Insulin
91
Where does Beta oxidation occur?
Mitochondrial Matrix
92
What enzyme cleaves fatty acids and glycerol from adipose tissue during lipolysis?
Hormone Sensitive Lipase (HSL)
93
Active hormone-sensitive lipase has a _______ attached.
Phosphate
94
What is the fate of glycerol of lipolysis?
Brought to liver to be converted to DHAP by enzyme Glycerol-P-Dehydrogenase where it can enter gluconeogenesis
95
What enzyme catalyzes the conversion of fatty acid to fatty acyl CoA?
Long-chained fatty acyl CoA synthase
96
What enzyme adds an acyl to carnitine to form acyl carnitine?
CPT1
97
What enzyme removes and acyl group from acyl carnitine to create free carnitine?
CPT2
98
What are the four reaction steps in beta-oxidation?
Oxidation, hydration, oxidation, thiolysis
99
What does each cycle of beta-oxidation produce?
1 NaDH, 1 FaDH2, and 1 acetyl CoA
100
Beta oxidation is allosterically inhibited by what two things?
Malonyl CoA and Acetyl CoA
101
What else inhibits beta-oxidation?
Increased ratio difference between Acetyl CoA and free CoA decreases beta-oxidation
102
In response to glucagon or ____, the beta-oxidation pathway is stimulated.
Epinephrine
103
The oxidation of ______ generates more ATP than glucose.
fatty acids
104
It is through beta-oxidation that _____ are degraded to acetyl CoA.
Fatty Acyl CoA/ fatty acids
105
To make fatty acids available for oxidation in tissues, the fatty acid first needs to be released from fat stores. ____ is the process which releases fatty acids from fat tissue. The enzyme hormone-sensitive lipase (HSL) is activated in response to the hormone ____.
Lipolysis; epinephrine
106
To be transported through circulation, the fatty acid must attach to _____ once it leaves adipose tissue. This protein is water soluble and can transport the fatty acid in the circulation.
Albumin
107
To get a long-chain fatty acid into the mitochondria of a cell to be oxidized through beta-oxidation, it needs the help of several enzymes to get there. The cytosolic enzyme _____ activates the fatty acid to fatty acyl CoA by adding a CoA to it. Then the outer mitochondrial membrane enzyme ____ acts on the fatty acyl CoA. This enzyme swaps out the CoA for carnitine making fatty acyl ______. The fatty acyl carnitine can cross the inner mitochondrial membrane. At this time, the enzyme _____ acts on the fatty acyl carnitine to remove the carnitine and add a CoA. Together, the action of those enzymes results in the fatty acyl CoA being available in the mitochondrial matrix of the cell for beta-oxidation.
Long-chain fatty acyl CoA synthase; CPT1; carnitine; CPT2
108
Lipolysis is regulated at the level of the enzyme, ______, which is regulated by covalent modification. More specifically, HSL is activated when it is phosphorylated by a phosphorylation cascade that is turned on in response to epinephrine.
Hormone-sensitive Lipase (HSL)
109
Beta oxidation is allosterically regulated at the ____ enzyme. CPT I is inhibited by _____ and acetyl CoA. A high level of malonyl CoA indicates FAS pathways are turned on as malonyl CoA is generated from acetyl CoA during the initial steps of fatty acid synthesis. Therefore, excess acetyl CoA also indicates a cell is in a high energy state and decreases fatty acid oxidation.
CPT1; Malonyl CoA
110
The reactions of beta-oxidation (a.k.a. fatty acid oxidation) is oxidation, _______, oxidation, and thiolysis. The first enzyme of beta-oxidation that catalyzes the first step of the pathway is ______. There are several isoforms of Acyl CoA dehydrogenase. The length of the fatty acid will determine which acyl CoA dehydrogenase will act on it.
Hydration; Acyl CoA dehydrogenase
111
Some difference between beta-oxidation and fatty acid synthesis is that the series of reactions involve ______ reactions rather than reductions. _______ and NADH are generated rather than NADP and FAD. And after each cycle turn, the fatty acid chain shortens by 2 carbons rather than lengthens by 2 carbons as seen in fatty acid synthesis.
Oxidations; FaDH2
112
The fatty acid chain will continue through the series of beta-oxidation enzymes until there is a 2-carbon acetyl CoA remaining or a 3-carbon ______ in the event of oxidation of an odd-numbered fatty acid. The propionyl CoA will ultimately be converted to OAA, and it will enter the gluconeogenesis pathway.
Propinyl
113
Oxidation of ______ fatty acids provides less energy compared to saturated fatty acids. This is because unsaturated fatty acids are less _______, and therefore, fewer _______ are made that can enter into the ETC.
Unsaturated; highly reduced; reducing equivalents
114
The ATP generated from the oxidation of a fatty acid comes from each unit of acetyl CoA entering the _____ to generate reducing equivalents to go to the ETC, and the FADH2 and ____ generated from the oxidation steps of beta-oxidation each time the fatty acid is cleaved by 2 carbons. The FADH2 and NADH that are generated go to the _____ to make ATP.
Kreb's cycle; NaDH; ETC
115
How much ATP energy do we make from the beta-oxidation of one palmitic acid?
131 ATP total minus the 2 ATP to make a palmitic acid making a net energy income of 129 ATP. (Totally 8 Acetyl CoA, 7 FaDH and 7 NaDH2)
116
Where does ketogenesis occur?
Only in the cytosol of hepatocytes
117
What are the three types of ketone bodies?
Acetoacetate, Beta-hydroxybutyrate, and acetone
118
Under what states does ketogenesis occur?
Fasted state or fed state with total carbohydrate starvation
119
The process of ketogenesis is ___________.
Catabolic
120
What two processes are always turned on at the same time?
Ketogenesis and gluconeogenesis
121
In peripheal tissues, how is B-hydroxybutyrate used for energy?
It is oxidized back to acetoacetate, where succinyl CoA gives it is CoA. It is now acetoacetyl CoA which us cleaved ti produce 2 acetyl CoA for energy that can enter Kreb's and then TCA
122
What is the metabolic fate is acetone?
Breathed out
123
Ketolysis occurs in what state?
?
124
Why is the formation of ketone bodies important?
Ketones are water-soluble, meaning they can be transported in blood without a carrier. Ketone bodies allow for an alternate route of extra Acetyl CoA in the liver. It allows for more energy to go to non-hepatic tissues including the brain.
125
The first couple of steps of ketone synthesis is the same as which process?
Last step of beta-oxidation is the first step in ketogenesis
126
Why are fatty acids used to form ketones in the liver rather than entering the Kreb's cycle?
If ketogenesis is on, that means gluconeogenesis is also in the liver. This means that oxaloacetate is being used to go back up the chain and form glucose and is not available to combine with Acetyl CoA to form citrate and enter into Krebs' cycle. THis is why the extra acetyl CoA is being used to form ketone bodies.
127
Ketogenesis is a process that occurs during a(n) _______ state. It generates ketone bodies which are another fuel source of acetyl CoA.
Catabolic
128
What happens to ketones once they leave the liver?
B-hydroxybutyrate is oxidized back to acetoacetate in peripheral tissues. The acetoacetate is given a CoA from succinyl CoA, which generates acetoacetyl CoA. That molecule is then cleaved to produce 2 acetyl CoA, which can enter into Krebs and then TCA.
129
Ketones are generated during fasting, starvation or _____. The formation of ketone bodies occurs in the mitochondria of ____. Ketone bodies are formed from the oxidation of _____ or de-aminated amino acids. Therefore, beta-oxidation has to take place to provide acetyl CoA from oxidized fatty acids.
Carb starvation; liver cells; fatty acids
130
Ketogenesis and gluconeogenesis are turned on simultaneously in the liver tissue. Because these two pathways are turned on simultaneously, it affects the fate of oxaloacetate. The oxaloacetate that is generated from amino acids, pyruvate and citric acid intermediates is being shunted into the ______ pathway to ultimately generate glucose. The oxaloacetate enters gluconeogenesis as PEP. This action of oxaloacetate being used in gluconeogenesis has essential implications for forming ketone bodies.
Gluconeogenic
131
This shunting of OAA into gluconeogenesis allows for ketone bodies to be formed because the acetyl CoA generated from _____ is being used to form ketones rather than combined with OAA to form citrate. The gluconeogenic amino acids will continue to feed into the Krebs cycle to form _________, which will then enter the gluconeogenesis pathway.
Beta oxidation; oxaloacetate
132
The acetyl CoA generated from fatty acid oxidation has different fates in the liver and muscle tissues. In the liver, the acetyl CoA derived from the oxidation of fatty acids is used to make _______. The ketones leave the liver and are used to feed the rest of the body. In the muscle, the fatty acids that are oxidized to acetyl CoA enter the ________ to generate energy for muscle tissue.
Ketones; TCA cycle
133
The ketone that is considered a metabolic dead end because it is breathed off rather than being broken down to acetyl CoA to be used for energy is ______.
Acetone
134
The enzyme _____ is the last enzyme of beta-oxidation and is the enzyme that catalyzes the first reaction of ketogenesis.
Thiolase enzyme
135
Ketogenesis and _____ synthesis share the first two to steps of synthesis.
Cholesterol
136
Once the ketone, acetoacetate is formed it can form the ketones _____ or _____.
Beta-hydroxybutyrate; acetone
137
Once in peripheral tissues, the acetoacetate obtains ______ from succinyl CoA to form acetoacetyl CoA. The acetoacetyl CoA is converted to 2 _____ which can then enter the Krebs cycle.
CoA; acetyl CoA
138
What are the three ways the body gets amino acids?
Diet, de novo synthesis, and normal protein degradation
139
What depletes the amino acid pool in the body?
Protein synthesis, forming nitrogen-containing compounds, storing them as fat or to make ketone bodies (ketogenic amino acids), gluconeogenesis (glucogenic amino acids), had oxidizing amino acids for energy
140
What is the primary location for amino acid metabolism?
Liver
141
What happens to the alpha-ketoacid in the FED state?
In FED state, these are stored back as fatty acids.
142
What happens to the alpha-ketoacid in the FASTED state?
In FASTED state, they are used to create glucose or ketone bodies or are oxidized for energy and carbon dioxide.
143
What are the two ways to remove an amino group from an amino acid?
Transamination and deamination
144
What is transamination?
The process of transferring an amino group for one amino acid to an alpha-ketoacid to form a new alpha-ketoacid and non-essential amino acid.
145
What is deamination?
This is the process of removing an amino group that is excreted in urea
146
What is the enzyme that does deamination?
Glutamate dehydrogenase
147
How do amino acids end up in the lipogenesis (fatty acid synthesis) pathways?
In a fed state, excess amino acids enter Krebs' cycle to generate a carbon skeleton, but instead of OAA being used to make glucose, it is used to form citrate, which allosterically activates acetyl CoA carboxylase to promote fatty acid synthesis.
148
How can amino acids end up in the gluconeogenic pathway?
In the fasted state, alpha-ketoacids serve as intermediates in the TCA cycle that will generate OAA to enter the gluconeogenic pathway as PEP to generate glucose.
149
How are non-essential amino acids generated from transamination reactions?
The amino acid has its amino group removed and placed onto an alpha-ketoacid. That makes the old amino acid an new alpha-ketoacid and formed a new non-essential amino acid
150
Which vitamin serves as a coenzyme for transamination reactions?
Vitamin B6
151
What determines the coenzyme (NADH+H or NADPH+H) for the reaction catalyzed by glutamate dehydrogenase?
Deamination requires NAD+ while amination requires NADPH.
152
What kind of reaction does glutamate dehydrogenase catalyze?
Redox reaction
153
How is ammonia excreted from most tissues?
Through the glutamine synthesis pathway
154
What enzyme combines ammonia with glutamate to form glutamine?
Glutamine Synthetase
155
What enzyme hydrolyzed glutamine once in the liver to remove the first amino group?
Glutaminase
156
Which tissues are involved in the Glucose-Alanine cycle?
Liver and muscle
157
What is the purpose of the glucose-alanine cycle?
This cycle is a mechanism for getting ammonia out of the muscle and glucose from the liver to the muscle to sustain energy needs.
158
Uses of the amino acid pool include body protein, synthesis of nitrogen-containing molecules, ketones, _____ or oxidized to energy.
glucose
159
Amino acids must be obtained from ______, synthesized de novo, or produced from normal protein degradation.
Diet
160
In the _______ (fasting or fed) state the amino acids are critical to forming glucogenic precursors or ketone bodies in the liver. In order for amino acids to be used in energy metabolism the _____ group must be removed, which leaves a carbon skeleton. The carbon skeleton can serve as intermediates in the ______.
FASTING; amino; TCA cycle
161
In the fed state, the ____ is the primary site for the uptake of most amino acids following ingestion of a protein-containing meal. The hormone ___ increases protein synthesis. Once body proteins are made as directed by the genetic code, the proteins are then converted to ____.
Liver; insulin; fat
162
To be converted to fat, the excess amino acids have their _____ removed, which leaves a carbon skeleton. The carbon skeleton can enter at different points of the Krebs cycle. They will eventually be converted to _____. Once they are converted to OAA, the OAA is used to form citrate rather than being used to make glucose. Citrate is generated instead of glucose because this situation is in the fed state. Citrate is a positive allosteric regulator of the fatty acid synthesis enzyme, _____.
Amino; Oxaloacetate; Acetyl CoA Carboxylase
163
Amino acids can be classified as ______, ketogenic or both. Their classification is based on which intermediate is produced that will eventually lead to the formation of glucose or ketones.
Glucogenic
164
One fate of the amino group that is removed from the amino acids is the _____ cycle. Once the amino group is removed, the carbon skeleton remains.
?
165
The fate of the carbon skeleton depends on whether the body is in a fasted or fed state. In the fasted state, it can be oxidized to energy and form glucose or ketone bodies. In the fed state, the carbon skeleton will be converted to ____.
fatty acids
166
Transferring an amino group to a different carbon skeleton (or alpha-keto acid) is known as _____. The result of a transamination reaction is a new amino acid, and carbon skeleton is generated. The enzyme ______ catalyzes these reactions.
Transamination; amino transferases
167
The aminotransferases are found in the _____ and mitochondria of cells throughout the body, but especially in the liver, kidney, intestine and muscle. This means that cells all over the body can use amino acids for energy and to make _________ amino acids. These non-essential amino acids can be used to make proteins in cells. However, only the liver can convert it to glucose.
cytosol; non-essential
168
The enzyme, _______, catalyzes deamination reactions. This involves removing the amino group from an amino acid without transferring the amino group to another amino acid. Instead, the amino group (free ammonia) can be used as a source of ______ for synthesising urea. The coenzymes NAD and _____ are used depending on whether an amino group is being added or removed. When ammonia levels are high in a cell, glutamate dehydrogenase will favour the reduction of alpha-ketoglutarate to form glutamate and the ______ of NADPH to form _____. This is done to eliminate the ammonia building up in a cell.
Glutamine dehydrogenase; urea cycle; NADPH; oxidation; NADP+
169
The purpose of the glucose alanine cycle is to get ______ out of the tissue and provide a source of glucose for the muscle. Removing ammonia from the tissue and bringing it to the liver will prevent the pH from going too high. The enzyme glutamine synthetase will assist in ridding peripheral tissue of ammonia by combining the NH3 with alpha-ketoglutarate to make ______. Glutamine now has two amino groups. It then goes to the ____ tissue.
Ammonia; Glutamate; liver
170
In the liver, the enzyme _______ removes NH3 to regenerate glutamate. The NH3 that was removed goes to the urea cycle. The glutamate is then acted on by the enzyme, _______, to deaminate glutamate to alpha-KG. The alpha-KG is now available to participate in a _______ reaction with alanine and pyruvate. Alanine amino-transferase catalyzes the transfer of the amino group from alanine to alpha-KG. This transamination generates pyruvate and glutamate. The amino group that is now attached to glutamate can be deaminated by glutamate dehydrogenase, which will send the ammonia to the _______. The pyruvate that was generated will go through _____ to make glucose.
Alanine-amino transferase; Glutamine dehydrogenase; ?; urea cycle; gluconeogenesis
171
The glucose will then leave the liver and go to muscle tissue. Once in the muscle, the glucose will enter _____ to generate pyruvate. Once pyruvate is generated, it is available to participate in a ________ reaction with alanine, alpha-KG and glutamine. The glutamate was generated from amino acid metabolism in the muscle, which resulted in amino groups being added to alpha-KG by the enzyme ______ to make glutamate. Glutamate then transfers its amino group to pyruvate via a transferase enzyme which generates alanine and alpha-KG. The alanine can leave the muscle and enter the liver tissue hence safely removing ammonia from muscle tissue while providing a source of glucose for the muscle.
Glycolysis; ?; ?;
172
The urea cycle occurs in the ______?
Liver
173
Urea production begins in the ______ of the liver and is completed in the ______. The urea is transported into the blood to the _______ for excretion in the urine.
Mitochondria; cytosol; kidneys
