Abstract
BackgroundPersistent lactation, as the result of mammary cellular anabolism and secreting function, is dependent on substantial mobilization or catabolism of body reserves under nutritional deficiency. However, little is known about the biochemical mechanisms for nutrition-restricted lactating animals to simultaneously maintain the anabolism of mammary cells while catabolism of body reserves. In present study, lactating sows with restricted feed allowance (RFA) (n = 6), 24% feed restriction compared with the control (CON) group (n = 6), were used as the nutrition-restricted model. Microdialysis and mammary venous cannulas methods were used to monitor postprandial dynamic changes of metabolites in adipose and mammary tissues.ResultsAt lactation d 28, the RFA group showed higher (P < 0.05) loss of body weight and backfat than the CON group. Compared with the CON group, the adipose tissue of the RFA group had higher (P < 0.05) extracellular glutamate and insulin levels, increased (P < 0.05) lipolysis related genes (HSL and ATGL) expression, and decreased (P < 0.05) glucose transport and metabolism related genes (VAMP8, PKLR and LDHB) expression. These results indicated that under nutritional restriction, reduced insulin-mediated glucose uptake and metabolism and increased lipolysis in adipose tissues was related to extracellular high glutamate concentration. As for mammary glands, compared with the CON group, the RFA group had up-regulated (P < 0.05) expression of Notch signaling ligand (DLL3) and receptors (NOTCH2 and NOTCH4), higher (P < 0.05) extracellular glutamate concentration, while expression of cell proliferation related genes and concentrations of most metabolites in mammary veins were not different (P > 0.05) between groups. Accordingly, piglet performance and milk yield did not differ (P > 0.05) between groups. It would appear that activation of Notch signaling and adequate supply of glutamate might assist mammogenesis.ConclusionsMammary cell proliferation and catabolism of adipose tissues in nutrition-restricted lactating sows were associated with extracellular high glutamate levels.
Highlights
Persistent lactation, as the result of mammary cellular anabolism and secreting function, is dependent on substantial mobilization or catabolism of body reserves under nutritional deficiency
Performance of sows and piglets The CON group sows had higher (P < 0.05) feed intake, lesser (P < 0.05) body weight and backfat loss than the restricted feed allowance (RFA) group sows at lactation d 28 (Table 2)
Extracellular glucose concentrations of adipocytes decreased, with the first significant (P < 0.05) decrease observed at 45 min postprandial in the CON group while 90 min postprandial in the RFA group
Summary
Persistent lactation, as the result of mammary cellular anabolism and secreting function, is dependent on substantial mobilization or catabolism of body reserves under nutritional deficiency. Little is known about the biochemical mechanisms for nutrition-restricted lactating animals to simultaneously maintain the anabolism of mammary cells while catabolism of body reserves. Maternal reserves, such as lipids from adipose tissues, is mobilized to offer energy and substrates to mammary glands to satisfy lactation [3]. Insulin resistance expedites the lipolytic rate of white adipose tissue [4]. It appears that insulin and HSL work together to regulate the catabolism and anabolism of adipose tissues
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