Adiponectin deficit during the precarious glucose economy of early lactation in dairy cows.

In rodents and primates, insulin resistance develops during pregnancy and fades after parturition. In contrast, dairy cows and other ruminants maintain insulin resistance in early lactation (EL). This adaptation favors mammary glucose uptake, an insulin-independent process, at a time when the glucose supply is scarce. Reduction in circulating levels of the insulin-sensitizing hormone adiponectin promotes insulin resistance in other species, but whether it contributes to insulin resistance in EL dairy cows is unknown. To address this question, plasma adiponectin was measured in high-yielding dairy cows during the transition from late pregnancy (LP) to EL. Plasma adiponectin varied in quadratic fashion with the highest levels in LP, a maximal reduction of 45% on the day after parturition and a progressive return to LP values over the next 8 wk. Adiponectin circulated nearly exclusively in high molecular weight complexes in LP, and this distribution remained unaffected in EL. The reduction of plasma adiponectin in EL occurred without changes in adiponectin mRNA in adipose tissue but was associated with repression of the expression of proteins associated with the endoplasmic reticulum and involved in assembly of adiponectin oligomers. Finally, EL increased the expression of the adiponectin receptor 1 in muscle and adiponectin receptor 2 in liver but had no effect on the expression of these receptors in adipose tissue and in the mammary gland. These data suggest that reduced plasma adiponectin belongs to the subset of hormonal adaptations in EL dairy cows facilitating mammary glucose uptake via promotion of insulin resistance.

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