title: Vitamin B-12 deficiency and hyperhomocysteinemia are partly ameliorated by cobalt and nickel supplementation in pigs.
abstract: Vitamin B-12 deficiency and hyperhomocysteinemia alter the metabolism of trace elements. This study tested the hypothesis that there is a reverse relationship in which diets high in iron, copper, nickel and cobalt would influence vitamin B-12 deficiency outcomes including hyperhomocysteinemia. Piglets (German Landrace x Pietrain) were assigned to six groups of 8 and fed one of the following diets for 166 d: a vitamin B-12-adequate and folate-fortified diet (30 microg/kg vitamin B-12 and 0.5 mg/kg folate) with normal trace element concentrations or one of five vitamin B-12-free, folate nonsupplemented diets (0.36 mg/kg), with either normal trace element concentrations or high concentrations of iron (300 mg/kg), copper (30 mg/kg), cobalt (1 mg/kg) or nickel (6 mg/kg). Feed intake and weight gain did not differ significantly among the groups. Vitamin B-12-deficient pigs developed diminished serum and liver concentrations of vitamin B-12 and folate, an accumulation of iron in the liver and hyperhomocysteinemia. The magnitude of changes differed among vitamin B-12-deficient groups. Vitamin B-12-deficient pigs fed 6 mg/kg nickel had distinctly higher vitamin B-12 concentrations in liver and serum and 45% lower serum concentration of homocysteine than the corresponding deficiency group fed 1 mg/kg nickel; iron concentration in liver was completely normalized. Vitamin B-12-deficient pigs fed 1 mg/kg cobalt had 47% lower homocysteine concentrations in serum than the vitamin B-12-deficient group fed 0.13 mg/kg cobalt, but the vitamin B-12 status was unaffected. Supplementation of iron and copper did not affect these variables. The dietary manipulations had no detrimental effects on variables symptomatic of oxidative stress. The findings indicate a collaborative relationship between vitamin B-12 metabolism and the trace elements nickel and cobalt.
authors: Institute of Nutritional Sciences, University of Technology of Munich, 85350 Freising-Weihenstephan, Germany.
authors: G I
authors: GI
authors: Stangl
authors: D A
authors: DA
authors: Roth-Maier
authors: M
authors: M
authors: Kirchgessner
mesh_terms: D000821:Animal Feed; D000818:Animals; D003035:Cobalt / Q000008:administration & dosage* / Q000494:pharmacology; D003300:Copper / Q000008:administration & dosage; D019587:Dietary Supplements; D004195:Disease Models, Animal; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage; D006710:Homocysteine / Q000032:analysis; D020138:Hyperhomocysteinemia / Q000178:diet therapy*; D007501:Iron / Q000008:administration & dosage; D008099:Liver / Q000502:physiology; D008297:Male; D009532:Nickel / Q000008:administration & dosage* / Q000494:pharmacology; D013552:Swine; D014131:Trace Elements / Q000378:metabolism; D014805:Vitamin B 12 / Q000008:administration & dosage / Q000032:analysis; D014806:Vitamin B 12 Deficiency / Q000178:diet therapy*
chemical_list: D014131:Trace Elements; D006710:Homocysteine; D003035:Cobalt; D003300:Copper; D009532:Nickel; D005492:Folic Acid; D007501:Iron; D014805:Vitamin B 12