Adiponectin and resistin are two hormones mainly produced by adipose tissue. These hormones, also called adipokines, play a key role in lipid metabolism and glucose homeostasis. Moreover, they have recently been shown to be involved in the control of female reproduction in different species. Nevertheless, few data are available about the involvement of these adipokines in bovine fertility, which is known to be decreased since several decades, especially for dairy cows. Thus, the objectives of this work were to study in cow: 1) the protein expression of adiponectin, its receptors (AdipoR1, AdipoR2) and resistin in the reproductive axis, and 2) the effects of these adipokines on the oocyte maturation, early embryo development and/or granulosa cell (GC) proliferation and steroidogenesis.

In vitro maturation (22h) of bovine cumulus-oocyte complexes (COCs) (from 3-6mm follicles) was performed with or without human recombinant adiponectin (10mg/mL). Nuclear maturation of oocytes was determined by chromatin DAPI-staining. Cleavage and blastocyst rates were assessed 48h and 8 days after in vitro fertilization of COCs, respectively. Bovine GC were incubated with or without human recombinant resistin (667ng/mL) or adiponectin (10mg/mL) in presence or absence of IGF1 (10^-8M) and insulin (10^-8M). Cell proliferation (24h) and progesterone secretion in the culture medium (48h) were measured by [3H] thymidine incorporation and RIA assay, respectively. The protein detection of adiponectin, its receptors and resistin and the phosphorylation of ERK1/2, p38, AMPKa and AKT1/2/3 were performed by immunohistochemistry and/or Western Blotting.

Adiponectin, its receptors and resistin were detected in ovary (small and large follicles, corpus luteum, oocytes), pituitary and hypothalamus.

Nuclear maturation, cleavage and blastocyst rates were unchanged by adiponectin.

In GC, basal or insulin-stimulated cell proliferation was not modified by adiponectin or resistin. Conversely, IGF-1- induced cell proliferation was increased by adiponectin treatment only (+18%, P<0.05). Resistin has decreased IGF-1-stimulated progesterone secretion (-24%, P<0.05), whereas it did not affect basal or insulin-induced secretion (in progress for adiponectin). A transient increase of ERK1/2 phosphorylation was observed after 1min of adiponectin or resistin stimulation (+54% and +36%, respectively, P<0.05). The other cell signalling pathways studied did not seem to be modified.

In conclusion, the results of our study suggest a role of adiponectin and resistin in bovine ovarian functions and especially on cell proliferation or progesterone secretion of GC. The role of these hormones on the whole reproductive axis has to be investigated, in the presence or in the absence of various adipokines or growth factors.