Effects of realimentation after nutrient restriction during mid‐ to late gestation on pancreatic digestive enzymes, serum insulin and glucose levels, and insulin‐containing cell cluster morphology

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The nutrient requirements of gestating cattle, along with nutrient availability in feedstuffs, fluctuate throughout the year and meeting dietary needs can be challenging (Freetly et al., 2005, 2008). Dietary variations, such as changes in feed intake and composition, influence the production and secretion of pancreatic digestive enzymes important for the breakdown and absorption of feed in the small intestine (Swanson and Harmon, 2002a; Mader et al., 2009). Studies have also shown significant nutritional impacts on pancreatic endocrine function (Fowden et al., 1989; Sano et al., 1999). The majority of experiments evaluating nutritional effects on pancreatic function in cattle have been conducted in growing animals and less is known about the impacts of nutrition and gestational stage on pancreatic function and development in mature cows and their foetuses respectively.
Maternal nutrition is responsible for both direct and indirect effects on foetal growth. Fowden and Hill (2001) have shown in ovine species that the pancreatic content of insulin increases in the foetus during gestation as long as the dam is provided with adequate nutrition. Restricted diets, however, may lead to reduced pancreatic endocrine cell number (Bertram and Hanson, 2001) as well as permanent deficiencies of insulin secretion and β‐cell proliferation (Weinkove et al., 1974; Snoeck et al.,1990; Dahri et al., 1995; Winick and Noble, 1996). The proportion of insulin‐containing tissue within the pancreas of sheep may also be decreased in nutrient‐restricted foetuses (Limesand et al., 2005). This effect is thought to be caused by diminished mitotic cell division; however, the impact on the pancreas of bovine tissue is unknown.
Responses of the gastrointestinal tract and associated tissues to pregnancy and time of gestation have been evaluated and some authors suggest that, in times of nutritional stress, the maternal body compensates for the loss of nutrients to the developing foetus by sacrificing maternal metabolic needs (Molle et al., 2004; Reed et al., 2007). The foetus is also able to adapt to periods of restriction by decreasing the rate of cell division, which could induce lifelong changes in the organ and whole‐animal functionality (Barker and Clark, 1997). Such an effect is termed developmental programming (Reynolds et al., 2010; Zhang, 2010).
In many species, realimentation has been able to increase the body weight of restricted animals to a level that matches non‐restricted contemporaries (Funston et al., 2010; Meyer et al., 2010). Realimentation of nutrient‐restricted animals was also successful in returning the weights of internal organs to those of their control counterparts (Zubair and Leeson, 1994). Although the growth of the conceptus is minimal during early gestation, changes in cell proliferation can still occur (Schoonmaker, 2013). Carlsson et al. (2010) reported noticeable pancreatic glucagon staining at day 25 with insulin apparent at day 26. Also, between day 89 and day 105, small sections of insulin clusters were beginning to assemble into larger groups. Changes in these developmental patterns have the potential to alter pancreatic function after conception. Although current knowledge of bovine pancreatic growth is minimal, numerous studies conducted in ewes undergoing nutrient restriction from early to mid‐gestation followed by realimentation until parturition indicate significant compensatory growth of other areas of the body such as in placentomes (Foote et al., 1958; Robinson et al., 1995; McMullen et al., 2005) and foetal musculature (Gonzalez et al., 2013). While the majority of foetal growth has been shown to occur during late gestation, it is important to determine the most effective timing of realimentation during gestation to avoid adverse physiological effects such as impaired growth or organ function postnatally.
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