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Cardiac structure and function in vitamin B-12-deprived rats
The Journal of Nutrition
|December 1, 1975
Summary
Prolonged vitamin B-12 deficiency in rats causes heart fibrosis and enlarged mitochondria. Cardiac propionic acid metabolism is impaired, while linoleic acid oxidation increases, impacting heart function.
Area of Science:
- Biochemistry
- Cardiology
- Nutritional Science
Background:
- Vitamin B-12 is crucial for cellular metabolism.
- Deficiency can lead to neurological and hematological issues.
- Its specific impact on cardiac structure and function requires further elucidation.
Purpose of the Study:
- To investigate the effects of long-term vitamin B-12 deprivation on rat heart histology.
- To examine alterations in cardiac linoleic acid oxidation.
- To identify metabolic defects in B-12 deficient rat hearts.
Main Methods:
- Rats were fed vitamin B-12-deficient diets for up to 16 months.
- Urinary methylmalonic acid levels monitored B-12 deficiency.
- Histological and electron microscopy analyses of heart tissue.
- Isolated heart perfusion studies with labeled propionic acid and linoleic acid.
Main Results:
- Vitamin B-12 deficiency led to extensive cardiac fibrosis and enlarged, distorted mitochondria.
- Hearts from deficient rats showed significantly reduced uptake and oxidation of propionic acid, with methylmalonate accumulation.
- Linoleic acid extraction was unaffected, but its oxidation was markedly increased.
- Reduced succinate levels were observed in perfusion media from deficient hearts.
Conclusions:
- Prolonged vitamin B-12 deficiency severely impacts cardiac structure and metabolism in rats.
- A metabolic block in propionic acid processing contributes to cardiac dysfunction.
- Altered fatty acid oxidation pathways may represent a compensatory mechanism or contribute to pathology.