5. Pernicious anemia is a disease in which the intestine is unable to absorb vitamin B12, frequently due to the loss of the generically named "intrinsic factor" produced by the parietal cells of the stomach lining. Intrinsic factor is a glycoprotein that binds to vitamin B12 and is required for its uptake in the ilium. Vitamin B12 is synthesized only by microbes, and we get it either from digesting animal protein or from our commensal microbiome. Vitamin B12 is unique among metabolic cofactors in that it contains the trace element cobalt, coordinated in a corrin ring structure that is similar to the porphyrin ring system in heme. Loss of intrinsic factor, often through autoimmunity, results in the inability to absorb B12 and ultimately a loss of red blood cells that results in anemia and can be deadly (“pernicious"). VITAMIN BI2 INTRINSIC FACTOR DIETARY B12 ANTIBODIES PERNICIOUS ΑΝΑΕΜΙΑ HYDROXYCOBALAMIN ILEUM NUMBNESS (a) In pernicious anemia, N5-methyltetrahydrofolate accumulates, and cells run out of tetrahydrofolate. This results in an inability to synthesize nucleotides, preventing DNA replication and the production of red blood cells. Why does N5-methyltetrahydrofolate accumulate in the absence of vitamin B12? What other metabolites accumulate and are depleted in this pathway due to the loss of vitamin B12? (b) How might loss of vitamin B12 alter gene expression? (c) What would happen to the rate of conversion of serine to glycine in the absence of vitamin B12 and why?

Human Physiology: From Cells to Systems (MindTap Course List)
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Chapter19: The Peripheral Endocrine Glands
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Y
ANTIBODIES
DIETARY
B12
PERNICIOUS
ANAEMIA
HYDROXYCOBALAMIN
5. Pernicious anemia is a disease in which the
intestine is unable to absorb vitamin B12,
frequently due to the loss of the generically
named "intrinsic factor" produced by the parietal
cells of the stomach lining. Intrinsic factor is a
glycoprotein that binds to vitamin B₁2 and is
required for its uptake in the ilium. Vitamin B12 is
synthesized only by microbes, and we get it
either from digesting animal protein or from our
commensal microbiome. Vitamin B₁ is unique
among metabolic cofactors in that it contains the trace element cobalt, coordinated in a corrin ring
structure that is similar to the porphyrin ring system in heme. Loss of intrinsic factor, often through
autoimmunity, results in the inability to absorb B12 and ultimately a loss of red blood cells that results in
anemia and can be deadly ("pernicious").
ILEUM
NUMBNESS
(a) In pernicious anemia, N 5-methyltetrahydrofolate accumulates, and cells run out of tetrahydrofolate.
This results in an inability to synthesize nucleotides, preventing DNA replication and the production of
red blood cells. Why does N5-methyltetrahydrofolate accumulate in the absence of vitamin B12? What
other metabolites accumulate and are depleted in this pathway due to the loss of vitamin B12?
(b) How might loss of vitamin B₁2 alter gene expression?
(c) What would happen to the rate of conversion of serine to glycine in the absence of vitamin B12 and
why?
VITAMIN B12
INTRINSIC
FACTOR
Transcribed Image Text:Y ANTIBODIES DIETARY B12 PERNICIOUS ANAEMIA HYDROXYCOBALAMIN 5. Pernicious anemia is a disease in which the intestine is unable to absorb vitamin B12, frequently due to the loss of the generically named "intrinsic factor" produced by the parietal cells of the stomach lining. Intrinsic factor is a glycoprotein that binds to vitamin B₁2 and is required for its uptake in the ilium. Vitamin B12 is synthesized only by microbes, and we get it either from digesting animal protein or from our commensal microbiome. Vitamin B₁ is unique among metabolic cofactors in that it contains the trace element cobalt, coordinated in a corrin ring structure that is similar to the porphyrin ring system in heme. Loss of intrinsic factor, often through autoimmunity, results in the inability to absorb B12 and ultimately a loss of red blood cells that results in anemia and can be deadly ("pernicious"). ILEUM NUMBNESS (a) In pernicious anemia, N 5-methyltetrahydrofolate accumulates, and cells run out of tetrahydrofolate. This results in an inability to synthesize nucleotides, preventing DNA replication and the production of red blood cells. Why does N5-methyltetrahydrofolate accumulate in the absence of vitamin B12? What other metabolites accumulate and are depleted in this pathway due to the loss of vitamin B12? (b) How might loss of vitamin B₁2 alter gene expression? (c) What would happen to the rate of conversion of serine to glycine in the absence of vitamin B12 and why? VITAMIN B12 INTRINSIC FACTOR
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