Open access publications in the SLU publication database

Abstract

Metabolic imbalance is a problem in the dairy industry because the metabolic
demands of increased milk production can lead to decreased fertility, and more
knowledge about improving the management and physical conditions of the cow
(the links between fertility, nutrition, milking, and dry period) is needed. Insulin
is an important hormone regulating the energy balance in the body, and insulin
concentrations change in situations of energy deficiency or excess, both of which
are known to decrease fertility in cows as well as in humans. Hyperinsulinemia
is associated with decreased fertility by impairing the developmental potential
of embryos, but the underlying reasons for this remain unclear. Our aim was to
investigate insulin-induced changes on development, morphology and molecular
signature in bovine blastocysts on Day 8 (BC8).

An in vitro model was used and morphology and gene expression were
analysed by combining confocal microscopy and microarray-based
transcriptome studies. Blastocysts were produced in vitro according to standard
methods using oocytes that were supplemented with three different insulin levels
(INS10 =10 µg/ml; INS0.1= 0.1 µg/ml; INS0=control) during maturation. The
transcriptome profile of BC8 was obtained and embryo quality grades,
developmental stages and morphologies were further assessed in terms of Factin,
DNA, and active mitochondria. Significant differences were observed in
developmental rates and morphology after insulin exposure. The observed
changes were reflected by increased expression of genes involved in cell division
and structure, mitochondrial activation, lipid metabolism, and oxidative stress.

Combining all of the results, it was shown that elevated insulin impairs the
developmental potential of the embryo. This work contributes to new knowledge
about the molecular background of embryos developing under metabolic stress
conditions such as hyperinsulinemia. Moreover, the studies are of comparative
value for humans where impaired fertility is often related to metabolic disorders.