Effects of maternal treatment with β‐hydroxy‐β‐metylbutyrate and 2‐oxoglutaric acid on femur development in offspring of minks of the standard dark brown type

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The existing mink farms are steadily increasing in the number of animals, and new farms are being established. High production results are achieved through proper nutrition, which involves appropriate selection of feed and properly arranged feed rations. Disturbances in reproduction, diseases in the perinatal period, but mostly metabolic diseases associated with the rearing period are the consequence of improper animal feeding. Deadlines of mating and pelt harvesting as well as the mean age of dams from outside the basic herd (ca. 6 months) and in the basic herd (ca. 3 years) are strictly defined in farms. Therefore, the nutrition schemes in large‐stock breeding do not allow individual treatment of animals. All these factors result in the lack of knowledge about problems associated with the skeletal system in fur animals. The only reports of movement disorders in mink concern discospondylitis. There are reports in the United States, Canada and Spain describing discospondylitis as a cause of hindlimb paresis/paralysis in farmed minks; however, this disease, to our knowledge, affecting juvenile minks, is a bacterial or fungal infection of the vertebrae and intervertebral discs (Martínez et al., 2003).
Physiological, neuroendocrine or metabolic adaptation of the foetus to suboptimal intrauterine conditions results in programming of the developmental pattern. Nutritional elements can operate in the regulation of the growth and homeostasis of bone mass in the adult (Śliwa, 2006; Śliwa & Dobrowolski, 2007). Knowledge about the mechanisms of permanent intrauterine programming of the phenotype in the offspring of farm animals is still limited, including studies on fur animals in this field. However, the number of studies showing a relationship between alterations induced by the impact of the mother during pregnancy in the foetal development with many consequences observed in their offspring is still rising. Maternal dietary protein feed is important for availability of amino acids to the foetus, which influences its growth (Vesterdorf, Blache, Harrison, Matthiesen, & Tauson, 2014). The restriction of maternal dietary protein decreases the foetal protein plasma concentration and decreases the level of many amino acids, including glutamine, proline, alanine and arginine, which results in foetal retardation of growth and development (Fowden, Giussani, & Forhead, 2005; Namgung & Tsang, 2003; Vesterdorf et al., 2014; Wu, Pond, Ott, & Bazer, 1998). Additionally, there is a close positive relationship between the size at birth and peak bone and muscle mass. The limitation of post‐natal growth relates not only to the skeleton but also to muscle mass. It is known that small newborns exhibit reduced muscle mass and altered some metabolic functions (Frost, 1997; Sayer & Cooper, 2005; Smith & Ozanne, 2006), which can have clinical consequences, for example a risk of pulmonary complications when respiratory muscles are involved (Hasselgren, 2014).
β‐Hydroxy‐β‐methylbutyrate (HMB) and 2‐oxoglutaric acid (2‐Ox) are among the interesting feed additives with potential health benefits. Their role in pre‐natal programming is still investigated in livestock (Śliwa, Kowalik, et al. 2005; Śliwa, Tatara, et al., 2005; Śliwa, Tatara, Nowakowski, Pierzynowski, & Studziński, 2006; Śliwa, 2006; Śliwa, Tatara, & Pierzynowski, 2006; Śliwa, Dobrowolski, Siwicki, & Pierzynowski, 2007; Śliwa et al., 2009; Śliwa, Adaszek, Tatara, & Dobrowolski, 2010; Tatara, Śliwa, & Krupski, 2007; Tomaszewska & Dobrowolski, 2011; Świetlicka et al., 2016). There is no knowledge about their effect on production results in fur animals. Therefore, there are no reports on their use and impact not only on the mink farm production results, but first of all on the skeletal system of minks.
2‐Ox is a precursor of glutamine, glutamate, proline, histidine, arginine and ornithine, which constitute the “glutamate family” of amino acids.
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