Agriculture Reference
In-Depth Information
because of its high content of secoisolariciresinol diglycoside, which is a precursor for
lignin formation, which in turn exhibits estrogenic activities (Adlercreutz
et al.
, 1987).
Yet, dietary supplementation with 10% flaxseed from 88 days until 212 days of age did not
lead to significant changes in mammary development on day 212 (Farmer
et al.
, 2007b).
Nutrition of growing gilts can also affect their mammary development at the end of
gestation. Lyvers-Peffer and Rozeboom (2001) studied the effects of a growth-altering
feeding regimen before puberty on mammary development at the end of gestation. They
used dietary fiber (35% ground sunflower hulls) to achieve phases of moderate growth
which alternated with phases of maximum growth. They reported that gilts on the
moderate feeding regimen from 9 to 12 weeks and 15 to 20 weeks of age had less mammary
parenchyma on day 110 of gestation than control gilts. In a later experiment using a similar
approach, specific periods of diet deprivation (providing 70% of the protein and DE
contents from the control diet) followed by over-allowance (providing 115% of the protein
and DE contents from the control diet) in growing gilts did not have any beneficial effect
on mammary development after puberty. In fact, this feeding regime led to a decrease in
parenchymal tissue mass at puberty (Farmer
et al.
, 2012a). The same nutritional treatment
also did not affect parenchymal mass at the end of gestation but led to a tendency for
reduced percent protein in mammary parenchyma (Farmer
et al.
, 2012b).
Nutrition during pregnancy undoubtedly affects mammary development at the end of
gestation. An early study where body composition of sows was altered by manipulating
protein and energy intakes during gestation demonstrated that overly fat (36 mm backfat)
and leaner gilts (24 mm backfat) had similar mammary weights at the end of gestation but
there was a drastic reduction (approximately threefold) in mammary DNA concentration
(i.e. cell number) in overly fat gilts compared with leaner gilts (Head and Williams, 1991).
Yet, these body conditions are not representative of what is seen commercially and it is
not known if such a difference in mammary DNA would be seen when comparing fat,
average and lean gilts according to current standards. This is something which needs to be
looked at in order to determine the ideal body condition required for optimal mammary
development at the end of gestation. Increasing dietary energy (5.76 vs. 10.5 Mcal/ME)
from day 75 of gestation until the end of gestation decreased mammary parenchymal
weight and parenchymal DNA on day 105 of gestation (Weldon
et al.
, 1991). On the other
hand, increasing protein intake (330 vs. 216 g CP/d) had no effects on mammogenesis
(Weldon
et al.
, 1991). This finding was later corroborated by Kusina
et al.
(1999) who
showed that lysine intakes of 4, 8 or 16 g/d from days 25 to 105 of gestation did not alter
mammary development at the end of gestation. When using a period of diet deprivation
(providing 70% of the protein and DE contents from the control diet) for the first 10 weeks
of gestation, followed by a period of over-allowance (providing 115% of the protein and
DE contents from the control diet) until the end of gestation, there was less parenchymal
tissue at the end of gestation with no changes in parenchymal tissue composition (Farmer
et al.
, 2014b). The goal of that project was to look at the effect of compensatory feeding
on mammary development yet, even though growth rate was increased in the over-
feeding period, this increase was not large enough to compensate for the body weight
loss in the restriction period during early gestation. A better adapted feeding regime
needs to be developed to be able to truly assess the impact of compensatory feeding on
