Fed State Metabolism Flashcards
1
Q
Why can’t we digest cellulose?
A
- lots of linear beta linkages
- structure allows for cellulose molecules to stack, not very hydrated
- our enzymes cannot access the cellulose molecules very well when they are stacked
2
Q
What does amylase in our saliva break starches into?
A
- maltoses
- dextrins
3
Q
Which bonds does amylase hydrolyze?
A
-1-4 glycosidic bonds
4
Q
What transporter transports glucose into intestinal epithelial cells?
A
-SGLT1
5
Q
Where are GLUT 4 transporters present?
A
- Adipose tissue
- Muscle Tissue
6
Q
Where are SGLT 1 transporters present?
A
- Duodenum
- Jejunum
- Renal Tubules
7
Q
Where are GLUT 5 receptors present?
A
the jejunum
8
Q
What happens when insulin binds its receptor on adipose and muscle cells?
A
-GLUT4 is upregulated and inserted into the membrane so more glucose can be uptaken
9
Q
What will happen to extra glucose in the liver?
A
- protein synthesis
- glycogen synthesis
- VLDL synthesis
10
Q
Where does most fat synthesis occur?
A
- liver
- then transported to adipose tissue
11
Q
What will happen to extra glucose in the muscle?
A
- protein synthesis
- a little bit of glycogen synthesis
12
Q
What are the three regulated steps in glycolysis?
A
- Glucose –> glucose 6-phosphate
- Fructose 6-phosphate –> fructose 1,6-bisphosphate
- Phosphoenol Pyruvate –> Pyruvate
13
Q
What are the only tissues that undergo anaerobic metabolism? Why?
A
- blood: no mitochondria
- Muscle: sometimes needs ATP very quickly, no time for oxidative phosphorylation
14
Q
What is the first step of glycogen synthesis? Enzyme?
A
- conversion of glucose 6-phosphate into glucose 1-phosphate
- phosphoglucomutase
15
Q
What type of bonds are formed by the elongation of glycogen molecules?
A
-alpha 1-4 bonds
16
Q
What type of bonds are formed by branching of glycogen molecules?
A
-alpha 1-6 bonds
17
Q
What activates/inhibits glycogen synthase?
A
- Activate: glucose 6 phosphate (high energy state)
- Inhibits: AMP, Ca, PKA (cAMP)
18
Q
What is von Gierke disease?
A
- a defect in glucose 6-phosphatase or the glucose transport system that prevents effective gluconeogenesis
- results in glycogen accumulation and massive liver enlargement
19
Q
What is Andersen Disease?
A
- defect in the branching enzyme of glycogen synthesis resulting in abnormally long chains with fewer branches
- generally fatal by age 2
20
Q
What is McArdle/Hers Disease?
A
- defects in muscle and liver phosphorylase activity, respectively
- retards the ability of glycogen to be utilized as an energy source
21
Q
What protease cleaves proteins in the stomach?
A
-pepsin
22
Q
What activates pepsin (from pepsinogen)?
A
-low pH
23
Q
Where does pepsin cleave proteins?
A
at aromatic residues
24
Q
Why is having a low pH in the stomach good for digestion?
A
- it denatures the proteins we eat
- makes them more accessible to pepsin
25
Why are proteases released as inactive zymogens instead of active enzymes?
-to prevent self-digestion of the secretory tissue and proteases
26
What are the two ways in which amino acids are absorbed into intestinal epithelial cells?
- sodium-amino cotransporter
| - proton-peptide cotransporter
27
What happens to peptides when they enter the intestinal epithelial cell?
-they are cleaved by peptidases into single amino acids then excreted through the basolateral membrane
28
What are the essential amino acids according to Steen?
- Histidine
- Methionine
- Threonine
- Valine
- isoleucine
- Phenylalanine
- Leusine
- Lysine
- Tryptophan
29
What enzyme converts glutamate to glutamine in most tissues?
-glutamine synthetase
30
What enzyme converts glutamine to glutamate in the liver?
glutaminase
31
Which organ creates most of the urea we excrete?
-liver
32
What do most tissues use as a nitrogen carrier to the liver?
-glutamine
33
What does muscle tissue use as a nitrogen carrier to the liver?
-alanine
34
What is the net reaction of the urea cycle?
2 R-NH2 + HCO3 --> H2N-CO-NH2 (Urea)
35
What amino acid delivers nitrogen to the urea cycle?
-aspartate
36
Where do the nitrogens in urea come from?
- one from ammonium from oxidative deamination (or from kidneys)
- one from aspartate
37
What vitamin is required for amino transferases?
-vitamin B6
38
What doe glutamate dehydrogenase use as a reducing agent when synthasizing alpha-ketoglutarate from glutamate, and vice versa?
- NAD+
| - NADP+
39
Why isn't arginine an essential amino acid?
-it is synthesized as an intermediate in the urea cycle
40
Where does the urea cycle take place?
-split between both the mitochondria and cytosol of liver cells
41
What results from arginosuccinate lyase defficincy?
-the inability to synthesize arginine
42
What is the treatment for arginosuccinate lyase defficiency?
- low protein diet
| - must be high in arginine though
43
What breaks down triglycerides into diglycerides, monoglycerides, and fatty acids?
-lipases
44
How are fatty acids absorbed into the intestine and beyond?
- fatty acids are absorbed via diffusion into intestinal epithelial cells
- there they are reconverted back into triglycerides
- These triglycerides are then packaged into micelles called chylomicrons, and secreted into the lymph
45
What are chylomicrons?
- lipoproteins that are very triglyceride rich
| - they contain specific apolipoprtoteins that mediate the uptake of chylomicrons by adipose and liver
46
What happens to chylomicrons once they reach the blood stream?
- travel to adipose tissue and muscle where they unload TAGs for storage of energy
- Travel to the liver where they are broken down and repackaged as VLDLs, which are then sent to the adipose tissue or muscle
47
Where does the lymphatic system dump into the blood stream?
Left Subclavian vein
48
What's the difference between chylomicrons and VLDLs?
- they have same function of delivering fat to the rest of the body, they just have a different origin
- also, VLDL's are smaller than chylomicrons
49
What does lipoprotein lipase do?
- breaks down TAGs from chylomicrons and VLDL's so that they can be absorbed into tissues
- the entire chylomicron or VLDL is not eaten by the cell, there is a progressive decrease in TAGs
50
What is the main substrate of Fatty Acid synthesis?
-malonyl CoA
51
What enzyme catalyzes the entire process of fatty acid synthesis?
-fatty acid synthase
52
How is Acetyl CoA transported out of the mitochondria?
The citrate/pyruvate shuttle
- citrate is exported out of the mitochondria and converted to acetyl CoA and oxaloacetate
- Oxaloacetate is then converted to pyruvate using ATP and transported back into the mitochondria
53
What enzyme converts Acetyl CoA into Malonyl CoA?
-Acetyl CoA carboxylase
54
How is acetyl CoA carboxylase present normally in the cell? How is it activated?
- it is in an inactive dimer
| - converted to active polymer form in the presence of citrate and other high energy signals like insulin
55
What cofactor serves as a flexible arm to carry the synthetic intermediates of fatty acid synthesis between various active sites of fatty acid synthase?
-phosphopantatheine
56
When is the process of fatty acid synthesis complete?
- when it gets to palmitate
| - a 16 carbon fatty acid
57
What is the purpose of the pentose phosphate pathway?
- For FA synthesis: generates NADPH
- Source of 5-C sugars for ribonucleotides
- provides for the breakdown or interconversion of 5-C sugars to glycolytic intermediates, and vice versa
58
How many NADPH's are produced per glucose 6-phosphate that enters the pentose phosphate pathway?
-2 NADPH
59
Where are the only locations along a fatty acid that post-synthetic desaturation can occur? What are the implications of this restriction?
- C4, 5, 6, and 9 counting from the carboxylate carbon
- this means that some fatty acids that we require for other pathways cannot be synthesized, and must be acquired from our diet
60
Describe how glucose stimulates insulin release.
- Increased glucose concentration stimulates insulin release by B-cells of the pancreas.
- Glucose enters the B-cells via GLUT 2 receptors, which leads to an increase in intracellular ATP. The increase in ATP inhibits the Sulfonylurea/Potassium channel, which decreases potassium flux, thus depolarizing the cell. Depolarization leads to influx of calcium ions (via V-Ca channels) which triggers vesicular release of insulin.
61
What are the two main signaling metabolites who's levels are affected by insulin?
- Fructose 2,6-bisphosphate
| - Malonyl CoA
62
Which tissue(s) utilize Gln from protein degradation for energy?
A. Brain
B. Brain and blood
C. Kidney and intestine
D. Blood
E. Muscle
C. Kidney and Intestine
63
Intestine can utilize which of the following nutrients:
A. Glucose
B. FAs
C. Glucose and FAs
D. Glucose, FAs, and Gln
E. Glucose, FAs, Gln, and ketone bodies
E. Glucose, FAs, Gln, and ketone bodies
64
Resting muscle prefers which energy store during fasting?
A. Glucose
B. FAs
C. Glucose and FAs
D. ketone bodies and glucose
E. Triglycerides
B. Fatty acids
65
In the fed state, adipose tissue uses which nutrient for energy?
A. Glucose
B. FAs
C. Ketone bodies
D. Ala and Gln
E. Both Glucose and FAs
A. Glucose
66
In which of the following states is liver gluconeogenesis inactive?
A. Fed
B. Fasted
C. Starved
D. Stressed
E. Exercised
A. Fed
67
Insulin drops when:
A. you eat a big meal
B. you enter a fasting state
C. you exercise
D. A and C
E. B And C
E. When you enter a fasting state and when you exercise.
68
Lipolysis is increased in response to all but which of the following hormones:
A. Glucagon
B. Insulin
C. Norepinephrine
D. Cortisol
E. Growth Hormone
B. Insulin
69
When digesting a substantial meal, fat is transported as:
A. Free fatty acids on serum albumin (NEFA)
B. VLDL
C. Free triglycerides
D. Chylomicrons
E. B And D
E. VLDL and Chylomicrons
70
In the post-absorptive states 3-5 hours after feeding, the main source of blood glucose is:
A. Muscle
B. Liver glycogen
C. Liver Gluconeogenesis
D. Kidney Gluconeogenesis
E. Intestinal breakdown of food
B. Liver Glycogen
71
All but which of the following are gluconeogenic precursors?
A. Glutamine (Gln)
B. Alanine (Ala)
C. Glycerol (GOL)
D. Lactate (Lac)
E. Fatty acids (FA)
E. Fatty Acids (FA)
72
Which of the following are circulating energy sources during starvation:
A. Glucose
B. Fatty Acids
C. Acetoacetate
D. 3-hydroxybutyrate
E. All of the above
E. All
