Abstract
At the onset of lactation, dairy cows suffer from insulin resistance, insulin deficiency or both, similar to human diabetes, resulting in lipolysis, ketosis and fatty liver. This work explored the combined effects of different levels of magnesium (0.1, 0.3, 1 and 3 mM) and insulin (25, 250 and 25,000 pM) on metabolic pathways and the expression of magnesium-responsive genes in a bovine adipocyte model. Magnesium starvation (0.1 mM) and low insulin (25 pM) independently decreased or tended to decrease the accumulation of non-polar lipids and uptake of the glucose analog 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-6-deoxyglucose (6-NBDG). Activity of glycerol 3-phosphate dehydrogenase (GPDH) was highest at 25 pM insulin and 3 mM magnesium. Expression of SLC41A1 and SLC41A3 was reduced at 0.1 mM magnesium either across insulin concentrations (SLC41A1) or at 250 pM insulin (SLC41A3). MAGT1 expression was reduced at 3 mM magnesium. NIPA1 expression was reduced at 3 mM and 0.1 mM magnesium at 25 and 250 pM insulin, respectively. Expression of SLC41A2, CNNM2, TRPM6 and TRPM7 was not affected. We conclude that magnesium promotes lipogenesis in adipocytes and inversely regulates the transcription of genes that increase vs. decrease cytosolic magnesium concentration. The induction of GAPDH activity by surplus magnesium at low insulin concentration can counteract excessive lipomobilization.
Highlights
During the transition period, i.e., three weeks prepartum to three weeks postpartum, dairy cows undergo a dramatic change in their physiological state due to the onset of lactation
To assess the combined influence of insulin and magnesium on cellular lipid content, the accumulation of intracellular non-polar lipids was measured by Nile-Red staining of adipocytes from six animals after 14 and 21 days in differentiation medium
A significantly lower accumulation of non-polar lipids was observed at the lowest Mg concentration of 0.1 mM (LSM = 1.43 ± 0.056) in comparison to 0.3 mM (LSM = 1.67 ± 0.056), 1 mM
Summary
I.e., three weeks prepartum to three weeks postpartum, dairy cows undergo a dramatic change in their physiological state due to the onset of lactation. At the onset of lactation, the energy demand increases abruptly and cannot be met by adequate intake of feed dry matter [1]. The consequence is a negative energy balance. To compensate the inadequate energy intake, the balance between lipogenesis and lipolysis in adipose tissue is shifted towards dominant lipolysis. This state of lipomobilization is linked to very low serum insulin concentrations, insulin resistance or both [2]. The decreased insulin sensitivity of adipose tissue and skeletal muscles [3] reduces glucose uptake by these tissues and more energy metabolites, glucose, are available for the mammary gland [4]. The reduction of insulin signals is physiological and necessary; any exaggeration predisposes the animals to metabolic diseases such as ketosis, fatty liver, milk fever, metritis, retained placenta or displaced abomasum [5,6]
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