Showing papers on "White Muscle Disease published in 2006"

Microarray analysis of selenium-depleted and selenium-supplemented mice.

Abstract: Nutritional selenium deficiency is associated with Keshan disease in humans and white muscle disease in ruminant livestock. In this study, mice were fed a selenium-deficient diet for three generations. Female mice from the third depleted generation of these mice were given water containing either no added selenium or 0.1 or 1.0 ppm selenium as sodium selenate; DNA microarrays were used to compare gene expression in the muscle from mice fed the selenium diets to that from mice remaining on the depleted diet. The most prominent expression increases were observed with Ptger2 (a prostaglandin E receptor), Tcrb-V13 (a T-cell receptor beta), Tcf-7 (a T-cell transcription factor), and Lck (lymphocyte protein tyrosine kinase), and the major consistent decrease was Vav2, an oncogene in mice consuming the selenium containing diets.

New Zealand Nutrition Society: Muriel Bell Lecture

Abstract: Department of Human Nutrition, University of Otago, Dunedin, New Zealand Introduction New Zealand was once known as one of the lowest selenium (Se) environments in the world, but the implications in terms of human health were not clear. In 1988 Ray Burk described the situation as “selenium deficiency in search of a disease” (1), which reflected the uncertainties at that time. Clearly there were many ‘selenophiles’ who believed that Se was a cure for all ills, including cancer, cardiovascular disease (CVD), rheumatoid arthritis, male infertility and many others, while other researchers were more cautious because of the lack of clear evidence for these associations. We now know much more about Se deficiency and function, which helps to clarify the role of Se in health and disease, but there are many questions remaining. This paper will review briefly what we currently know about Se’s role in health in disease, with particular reference to those conditions of interest for the New Zealand population. Se exerts its functions through the selenoproteins, which contain selenocysteine residues, usually at their active sites (2). There are 25 mammalian selenoproteins, not all of which we know the function. When Se intake is limited, there is a clear priority for Se supply, both to certain tissues and to certain selenoproteins, resulting in a “hierarchy” of importance of selenoproteins (3). Many of the effects of Se deficiency or health effects can be attributed to these proteins, but some actions of Se, such as proposed anti-cancer properties, may operate independently of the selenoproteins. Selenium deficiency Muscular syndrome in New Zealand One of the first indications of a possible role for Se in human health in New Zealand was a mysterious fibromyalgia widespread amongst residents of Southland (4), which sparked our interest in Se in the late 1960s. The late Dr Peter Snow, a Tapanui GP, referred to Southland residents, who seemed to be prone to an epidemic form of muscular rheumatism (personal communication). These patients sought help from their veterinary surgeons who advised the use of Se in the form of ‘Selovet’ – a veterinary preparation for treatment and prevention of white muscle disease and other Se-responsive conditions in sheep and cattle. Se appeared to help the condition and Peter Snow believed that there was sufficient evidence to correlate the Se responsive conditions in livestock with the endemic rheumatism in humans. A double blind trial was undertaken to determine the effectiveness of Se supplementation in preventing these muscular symptoms in humans. Symptoms improved in approximately half of the subjects in both placebo and supplemented groups, suggesting that beneficial effects ascribed to Se may have been due to a placebo effect (5). The usual dose taken by farmers at that time was 5 mg Se as sodium selenate, nearly 100 times the current recommended intake of 60-70 µg/day (6), and there was concern about the effects of such large intakes on the human population. Selenium deficiency in total parenteral nutrition patients This muscular syndrome was mirrored in a surgical patient in New Zealand, who had been on total parenteral nutrition (TPN) for some time, and presented with a severe muscular syndrome that prevented her from walking (7). At that time alimentation fluids did not contain trace elements and Se deficiency was suspected. Supplementation dramatically reversed the symptoms (8). Se deficiency in TPN was subsequently reported in other parts of the world with patients presenting with varying symptoms of cardiomyopathy and muscle syndromes including muscle pain, fatigue and proximal weakness (9). But this was not a natural deficiency, and inclusion of trace elements in fluids has now eliminated this problem. The mechanism behind this muscular involvement is unknown. It is tempting to speculate that selenoprotein W, which is abundant in skeletal and cardiac muscle, but is eliminated from tissues in Se deficiency, or selenoprotein N may be involved (10). The reason that only a small number of Se-deficient patients present with skeletal muscle disorders is unclear and possibly related to cofactors, such as viral infections and drugs (9). Keshan Disease and Kaschin-Beck Disease The only known natural deficiency diseases are Keshan Disease, an endemic cardiomyopathy that occurs during preadolescent and adolescent years and Kaschin Beck disease, an endemic osteoarthritis, both of which occur in low Se areas of China (11). Intakes in areas where Keshan Disease was endemic were around 7 µg/day. Because of the seasonal nature of the disease, other factors are thought to be involved. The most likely candidate is a virus. Co-existing iodine and Se deficiency may be involved in the aetiology of Kaschin-Beck disease (12). These intakes are much lower than in New Zealand and most other countries. Severe Se deficiency such as in these conditions is not a