Ros M, Lobato M F, García-Ruíz J P, Moreno F J
Departamento de Biología Molecular, Universidad Autónoma de Madrid, Spain.
Mol Cell Biochem. 1990 Mar 27;93(2):185-94. doi: 10.1007/BF00226191.
Prolactin deficiency, induced by bromocryptine treatment, brought about reciprocal changes in the ability of adipocytes and acini isolated from lactating rats to synthesize lipids. The capacity to synthesize fatty acids and phospholipids decreased in the mammary gland and increased in adipocytes by bromocryptine treatment. In the mammary gland, the maximum potential activity of the pentose shunt as well as the specific activities of the pathway dehydrogenases were significantly reduced by bromocryptine treatment. Simultaneously, adipose tissue increased its lipogenic capacity but neither the maximum potential of the shunt nor the specific activities of the pentose phosphate shunt dehydrogenases were significantly changed with respect to the control lactating rats. Thus, a differential regulatory mechanism(s) of the pentose phosphate shunt activity appears to operate in these two tissues. Adipocytes from lactating rats showed a poor responsiveness to insulin in terms of lipid synthesis from glucose. In contrast, in adipocytes from bromocryptine treated rats insulin was able to increase lipid synthesis (105%). Sheep prolactin administration 'in vivo' partially reversed the effects of bromocryptine. These data suggest that prolactin mediates adipocytes resistance to insulin during lactation. Phospholipid synthesis, as occurred in fatty acid synthesis, is increased in adipose tissue and decreased in mammary gland by bromocryptine treatment. However, alpha 1-adrenergic stimulation increases phosphatidylinositol turnover to about the same percentages in both mammary gland acini and adipocytes from lactating rats independently of bromocryptine treatment.
溴隐亭治疗诱导的催乳素缺乏，导致从泌乳大鼠分离的脂肪细胞和腺泡合成脂质的能力发生相反变化。溴隐亭治疗使乳腺中脂肪酸和磷脂的合成能力降低，脂肪细胞中合成能力增加。在乳腺中，溴隐亭治疗显著降低了磷酸戊糖途径的最大潜在活性以及该途径脱氢酶的比活性。同时，脂肪组织增加了其生脂能力，但相对于对照泌乳大鼠，磷酸戊糖途径的最大潜在活性和磷酸戊糖途径脱氢酶的比活性均未发生显著变化。因此，磷酸戊糖途径活性的差异调节机制似乎在这两种组织中起作用。泌乳大鼠的脂肪细胞在从葡萄糖合成脂质方面对胰岛素反应较差。相反，在溴隐亭治疗大鼠的脂肪细胞中，胰岛素能够增加脂质合成（105%）。体内给予绵羊催乳素可部分逆转溴隐亭的作用。这些数据表明，催乳素介导泌乳期间脂肪细胞对胰岛素的抵抗。与脂肪酸合成一样，溴隐亭治疗使脂肪组织中的磷脂合成增加，乳腺中的磷脂合成减少。然而，α1-肾上腺素能刺激使泌乳大鼠乳腺腺泡和脂肪细胞中的磷脂酰肌醇周转率增加到大致相同的百分比，且与溴隐亭治疗无关。
