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Mitochondrial dysfunction may be a principal underlying event in aging, including the degenerative diseases of aging such as brain degeneration. Mitochondria provide energy for basic metabolic processes, and their decay with age impairs cellular metabolism and leads to cellular decline. Progress over the last decade in delaying the mitochondrial decay of aging is reviewed. [ABSTRACT FROM AUTHOR]

For many years, it was believed that supplemental biotin was not needed in swine diets because of the wide distribution of biotin in feedstuffs used in the formulation of swine diets, and because of the known synthesis of biotin by the animal's intestinal microflora. However, interest in biotin nutrition for swine was rekindled in the mid-1970s when several field reports indicated a biotin deficiency in swine that was responsive to biotin supplementation in many cases. Results from university research are accumulating, especially from long-term sow studies (three to four parities), which suggest that supplemental biotin will improve litter size, conception rate, weaning-to-estrus interval, toe lesions, and haircoat condition. Milk biotin concentration and plasma biotin concentration of sows and piglets were also elevated when supplemental biotin was fed. Using presently available feedstuffs and under modern swine production conditions, a marginal biotin deficiency is possible. Swine producers experiencing poor reproductive performance in their sow herds, associated with excessive loss of hair and severe foot lesions, should evaluate the biotin content of their sow diet and consider supplemental biotin.

Biotin deficiency can be induced readily in monogastric animals and is accompanied by characteristic abnormalities. These include dermal lesions involving hyper- and parakeratosis and, in fur-bearing animals, alopecia and achromatricia. Biochemical changes include depressions in the activities of biotin-dependent enzymes and the metabolic pathways in which they are involved. However, it has been shown in chickens that the relative changes in the activities of these enzymes and the resultant manifestations of the deficiency can be markedly influenced by the dietary content of other nutrients such as protein or fat. Biochemical criteria are required for the diagnosis of subclinical deficiency and these are best-established for poultry. Blood pyruvate carboxylase activity is a good criterion in young birds. Biotin-responsive disorders have been identified in several species. The etiology of fatty liver and kidney syndrome in chickens is now largely understood and is an interesting example of how a combination of nutritional and environmental factors can result in sudden death in, until then, apparently healthy animals.

Data are summarized from several papers on the effects of biotin deficiency on lipid metabolism, especially fatty acid synthesis, in chicks. Biotin deficiency inhibits in vivo lipogenesis and hepatic acetyl-CoA carboxylase (ACC) activity. Although acetate incorporation into fatty acids is inhibited in biotin-deficient chicks, malonate incorporation is not inhibited. In fact, dietary malonic acid stimulates lipogenesis during biotin deficiency as measured by total carcass fatty acid content. Biotin-deficient chicks exhibit altered hepatic and whole body fatty acid composition in comparison with control chicks. The deficiency results in an increased proportion of the 16-carbon to 18-carbon fatty acids, and the most striking increase is for palmitoleic (16:1) acid. Biotin deficiency increases the relative incorporation of palmitate and stearate into phospholipids and decreases the relative incorporation of these fatty acids into triglycerides. Finally, mercury stimulates lipogenesis in biotin-deficient, but not in control, chicks by an unknown mechanism.