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5. Pernicious anemia is a disease in VITAMIN B12 which the intestine is unable to absorb vitamin INTRINSIC FACTOR 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"). DIETARY B12 ANTIBODIES PERNICIOUS ΑΝΑΕΜΙΑ HYDROXYCOBALAMIN ILEUM NUMBNESS In pernicious anemia, N5-methyltetrahydrofolate accumulates, and cells run out of (a) 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) . B12 and why? What would happen to the rate of conversion of serine to glycine in the absence of vitamin

5. Pernicious anemia is a disease in VITAMIN B12 which the intestine is unable to absorb vitamin INTRINSIC FACTOR 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"). DIETARY B12 ANTIBODIES PERNICIOUS ΑΝΑΕΜΙΑ HYDROXYCOBALAMIN ILEUM NUMBNESS In pernicious anemia, N5-methyltetrahydrofolate accumulates, and cells run out of (a) 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) . B12 and why? What would happen to the rate of conversion of serine to glycine in the absence of vitamin

Biology: The Dynamic Science (MindTap Course List)
Biology: The Dynamic Science (MindTap Course List)
4th Edition
ISBN:9781305389892
Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan
Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan
Chapter47: Animal Nutrition
Section: Chapter Questions
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5. Pernicious anemia is a disease in VITAMIN B12 which the intestine is unable to absorb vitamin INTRINSIC FACTOR 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"). DIETARY B12 ANTIBODIES PERNICIOUS ANAEMIA" HYDROXYCOBALAMIN ILEUM NUMBNESS In pernicious anemia, N5-methyltetrahydrofolate accumulates, and cells run out of (a) 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) . B12 and why? What would happen to the rate of conversion of serine to glycine in the absence of vitamin
Transcribed Image Text:5. Pernicious anemia is a disease in VITAMIN B12 which the intestine is unable to absorb vitamin INTRINSIC FACTOR 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"). DIETARY B12 ANTIBODIES PERNICIOUS ANAEMIA" HYDROXYCOBALAMIN ILEUM NUMBNESS In pernicious anemia, N5-methyltetrahydrofolate accumulates, and cells run out of (a) 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) . B12 and why? What would happen to the rate of conversion of serine to glycine in the absence of vitamin
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