Adipose tissue expression and circulating concentrations of monocyte chemoattractant protein-1 (MCP-1) correlate positively with adiposity. To ascertain the roles of MCP-1 overexpression in adipose, we generated transgenic mice by utilizing the adipocyte P2 (aP2) promoter (aP2-MCP-1 mice). These mice had higher plasma MCP-1 concentrations and increased macrophage accumulation in adipose tissues, as confirmed by immunochemical, flow cytometric, and gene expression analyses. Tumor necrosis factor-␣ and interleukin-6 mRNA levels in white adipose tissue and plasma nonesterified fatty acid levels were increased in transgenic mice. aP2-MCP-1 mice showed insulin resistance, suggesting that inflammatory changes in adipose tissues may be involved in the development of insulin resistance. Insulin resistance in aP2-MCP-1 mice was confirmed by hyperinsulinemic euglycemic clamp studies showing that transgenic mice had lower rates of glucose disappearance and higher endogenous glucose production than wild-type mice. Consistent with this, insulin-induced phosphorylations of Akt were significantly decreased in both skeletal muscles and livers of aP2-MCP-1 mice. MCP-1 pretreatment of isolated skeletal muscle blunted insulin-stimulated glucose uptake, which was partially restored by treatment with the MEK inhibitor U0126, suggesting that circulating MCP-1 may contribute to insulin resistance in aP2-MCP-1 mice. We concluded that both paracrine and endocrine effects of MCP-1 may contribute to the development of insulin resistance in aP2-MCP-1 mice.
Heat stress affects endocrine systems in cows. This study investigated changes in insulin and glucagon secretion between thermoneutral (TN; 18 degrees C, relative humidity [RH] 60%) and hot (28 degrees C, RH 60%) environments in lactating cows. Glucose, arginine, and butyrate were administered i.v. to four cows (mean, at 83 d postpartum) in each environment. Blood was collected via a jugular catheter at regular intervals. Heat exposure resulted in a marked increase in respiration rate and rectal temperature. A decrease in milk yield was also observed during heat exposure. Basal insulin concentrations were elevated, and basal glucose concentrations tended to be lower in the hot environment. Peak values of insulin and glucagon following the arginine injection were significantly higher in the hot than in the TN environment. The insulin peak value in response to the butyrate infusion was also higher during the heat exposure. However, insulin and glucagon responses to the glucose load were not affected by heat stress. The increase in plasma glucose concentration following arginine injection was inhibited by the heat exposure. In conclusion, heat stress resulted in a higher insulin secretion in lactating cows. Glucagon secretion in response to the arginine injection was enhanced, but the rise in plasma glucose was inhibited by heat exposure. These changes would be related to a reduction in milk yield during heat stress.
Abstract:The relationship among ultrasonic vocalization (USV), prolactin and maternal behavior was investigated in lactating rat mothers and their pups. The lactating mother had a cannula inserted into the external jugular vein, and was exposed to USVs emitted from a pup immediately. Changes of prolactin and maternal behavior were determined. Prolactin increased dramatically during exposure to USVs, when maternal search, retrieving and nest building behavior appeared significantly. These results suggested that the relationship among USV, prolactin and maternal behavior was included in communication between lactating mother and pup. Key words: lactating rat, maternal behavior, prolactin, ultrasonic vocalization (USV) tion between lactation mother and pup in rodents might include relationships involving prolactin, maternal behavior and USVs. In the present age, the relationship between parent and child is becoming weak in human being, therefore the basic study of the communication using laboratory animals is significant.In this study, we tried to verify the relationship among USV, prolactin and maternal behaviors by the exposing lactation mother with a cannula inserted into the external jugular vein to USVs.
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