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| ==Why is it Important?== | | ==Why is it Important?== |
− | Cobalamin in the form of methylcobalamin and adenosylcobalamin are [[Nutrition Glossary#Cofactor|cofactors]] required for reactions involved in single-carbon transfer and fatty acid metabolism. | + | Cobalamin in the form of methylcobalamin and adenosylcobalamin are [[Nutrition Glossary#Cofactor|cofactors]] required for reactions involved in single-carbon transfer and [[Fatty Acids Overview - Nutrition|fatty acid]] metabolism. |
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| ==Roles in the Body== | | ==Roles in the Body== |
| #'''Carbon Transfer''': Cobalamin is a cofactor for methionine synthase, used to transfer a methyl group to homocysteine and regenerate [[Methionine and Cysteine - Nutrition|methionine]] and tetrahydrofolate.<ref name="NRC"/><ref name="Shane">Shane B. Folic Acid, Vitamin B12, and Vitamin B6. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p. 500-511.</ref>. | | #'''Carbon Transfer''': Cobalamin is a cofactor for methionine synthase, used to transfer a methyl group to homocysteine and regenerate [[Methionine and Cysteine - Nutrition|methionine]] and tetrahydrofolate.<ref name="NRC"/><ref name="Shane">Shane B. Folic Acid, Vitamin B12, and Vitamin B6. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p. 500-511.</ref>. |
− | #'''Propionate Metabolism''': Propionyl-CoA is created during catabolism of specific amino acids (i.e., isoleucine, valine, methionine and [[Threonine - Nutrition|threonine]]) as well as mitochondrial β-oxidation of odd-chain fatty acids<ref name="Shane"/>. Propionyl-CoA is then converted to methylmalonyl-CoA via the biotin-containing enzyme proprionyl-CoA carboxylase. The cobalamin-dependant enzyme, methylmalonyl-CoA mutase, then converts methylmalonyl-CoA to succinyl-CoA, which can feed into the tricarboxylic acid (TCA) cycle, be used for heme synthesis, or as a carbon skeleton for gluconeogenesis. | + | #'''Propionate Metabolism''': Propionyl-CoA is created during catabolism of specific [[Amino Acids Overview - Nutrition|amino acids]] (i.e. [[Branched-Chain Amino Acids - Nutrition|isoleucine, valine,]] [[Methionine and Cysteine - Nutrition|methionine]] and [[Threonine - Nutrition|threonine]]) as well as mitochondrial β-oxidation of odd-chain fatty acids<ref name="Shane"/>. Propionyl-CoA is then converted to methylmalonyl-CoA via the biotin-containing enzyme proprionyl-CoA carboxylase. The cobalamin-dependant enzyme, methylmalonyl-CoA mutase, then converts methylmalonyl-CoA to succinyl-CoA, which can feed into the tricarboxylic acid (TCA) cycle, be used for [[Erythrocytes#Function|heme]] synthesis, or as a carbon skeleton for gluconeogenesis. |
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| ==Consequences of Cobalamin Deficiency== | | ==Consequences of Cobalamin Deficiency== |
| ====Dogs:==== | | ====Dogs:==== |
− | Puppies affected by an inherited defect in cobalamin absorption develop inappetance and lethargy; hyperammonaemia and associate neurological signs<ref>Battersby IA, et al. Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border collie. JSAP 2005;46:339-344.</ref>; [[neutropenia]] with hypersegmentation and megablastic anaemia<ref>Fyfe JC, et al. Inherited selective intestinal cobalamin malabsorption and cobalamin deficiency on the dog. Pediatr Res 1991;29:24-31.</ref>. Adult dogs with chronic intestinal disease can develop impaired cobalamin absorption either due to the primary intestinal disease or [[Nutrition Glossary#Bacterial Dysbiosis|bacterial dysbiosis]]<ref>Berghoff N, et al. Serum cobalamin and methylmalonic acid concentrations in dogs with chronic gastrointestinal disease. AJVR 2013;74:84-89.</ref>. Clinical signs of hypocobalaminaemia in adult dogs are similar to that of the underlying intestinal disorder (e.g., [[diarrhoea]] and weight loss); the presence of hypocobalaminaemia in dogs with chronic enteropathies is a negative prognostic indicator<ref>Allenspach K, et al. Chronic enteropathies in dogs: evaluation of risk factors for negative outcome. JVIM 2007;21:700-708.</ref>. | + | Puppies affected by an inherited defect in cobalamin absorption develop inappetance and lethargy; hyperammonaemia and associate neurological signs<ref>Battersby IA, et al. Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border collie. JSAP 2005;46:339-344.</ref>; [[neutropenia]] with hypersegmentation and [[Nutrition Glossary#Megaloblastic Anaemia|megaloblastic anaemia]]<ref>Fyfe JC, et al. Inherited selective intestinal cobalamin malabsorption and cobalamin deficiency on the dog. Pediatr Res 1991;29:24-31.</ref>. Adult dogs with chronic intestinal disease can develop impaired cobalamin absorption either due to the primary intestinal disease or [[Nutrition Glossary#Bacterial Dysbiosis|bacterial dysbiosis]]<ref>Berghoff N, et al. Serum cobalamin and methylmalonic acid concentrations in dogs with chronic gastrointestinal disease. AJVR 2013;74:84-89.</ref>. Clinical signs of hypocobalaminaemia in adult dogs are similar to that of the underlying intestinal disorder (e.g. [[diarrhoea]] and weight loss); the presence of hypocobalaminaemia in dogs with chronic enteropathies is a negative prognostic indicator<ref>Allenspach K, et al. Chronic enteropathies in dogs: evaluation of risk factors for negative outcome. JVIM 2007;21:700-708.</ref>. |
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| ====Cats:==== | | ====Cats:==== |
| Kittens weaned onto a cobalamin deficient diet will initially grow normally, then will cease growing and begin lose weight after 3-4 weeks<ref>Morris, J.G. Idiosyncratic nutrient requirements of cats appear to be diet-induced evolutionary adaptations. Nutr Res Rev 2002;15; 153-168.</ref>. Similar to dogs, adult cats with chronic intestinal disease can develop cobalamin deficiency resulting in worsening [[vomiting]], diarrhoea, and weight loss<ref>Vaden SL, et al. Cobalamin deficiency associated with methymalonic aciduria in a cat. JAVMA 1992;200:1101-1103.</ref><ref>Simpson KW, et al. Subnormal concentrations of serum cobalamin (vitamin B<sub>12</sub>) in cats with gastrointestinal disease. JVIM 2001;15:26-32.</ref><ref>Ruaux CG, et al. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. JVIM 2005;19:155-160.</ref>. | | Kittens weaned onto a cobalamin deficient diet will initially grow normally, then will cease growing and begin lose weight after 3-4 weeks<ref>Morris, J.G. Idiosyncratic nutrient requirements of cats appear to be diet-induced evolutionary adaptations. Nutr Res Rev 2002;15; 153-168.</ref>. Similar to dogs, adult cats with chronic intestinal disease can develop cobalamin deficiency resulting in worsening [[vomiting]], diarrhoea, and weight loss<ref>Vaden SL, et al. Cobalamin deficiency associated with methymalonic aciduria in a cat. JAVMA 1992;200:1101-1103.</ref><ref>Simpson KW, et al. Subnormal concentrations of serum cobalamin (vitamin B<sub>12</sub>) in cats with gastrointestinal disease. JVIM 2001;15:26-32.</ref><ref>Ruaux CG, et al. Early biochemical and clinical responses to cobalamin supplementation in cats with signs of gastrointestinal disease and severe hypocobalaminemia. JVIM 2005;19:155-160.</ref>. |
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| ==Diagnosing Cobalamin Deficiency== | | ==Diagnosing Cobalamin Deficiency== |
− | Diagnosis of cobalamin deficiency is based on presence of low fasted serum cobalamin level. If the patient is not fasted prior to testing, falsely increased cobalamin concentrations may be noted. [[Nutrition Glossary#Megaloblastic Anaemia|Megaloblastic anaemia]] and [[neutropenia]] with hypersegmentation may be seen on haematology profile. | + | Diagnosis of cobalamin deficiency is based on presence of low fasted serum cobalamin level. If the patient is not fasted prior to testing, falsely increased cobalamin concentrations may be noted. [[Nutrition Glossary#Megaloblastic Anaemia|Megaloblastic anaemia]] and [[neutropenia]] with hypersegmentation may be seen on haematology profile. Diagnosis is also made on clinical signs consistent with deficiency and evaluation of diet. |
− | Diagnosis is also made on clinical signs consistent with deficiency and evaluation of diet. | |
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| ==References== | | ==References== |
| <references/> | | <references/> |
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− | | + | {{Reviewed Nutrition 1 |
| + | |date = 22 May 2015}} |
| + | {{Waltham}} |
| + | {{OpenPages}} |
| [[Category:Vitamins]] | | [[Category:Vitamins]] |
− | [[Category:To Do - Nutrition]]
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− | [[Category:To Do - Nutrition preMars]]
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