Mizuma H, Abadie J, Prasad C
Department of Medicine, LSU Medical Center, New Orleans 70112.
Peptides. 1994;15(3):447-52. doi: 10.1016/0196-9781(94)90203-8.
Enterostatin or Val-Pro-Asp-Pro-Arg (VPDPR) is the amino-terminal pentapeptide of procolipase; VPDPR is generated during tryptic activation of procolipase to lipase. In rodents, exogenous VPDPR has been shown to cause a selective decrement in fat appetite. To understand the mechanism(s) underlying the action of this peptide, we have studied the effects of corticosterone, an adrenal hormone known to modulate caloric intake, on VPDPR-mediated inhibition of appetite. The results of this study show a significant increase in the inhibition of total caloric intake by 250 micrograms/kg VPDPR following corticosterone treatment (control, 2.3%; corticosterone treated, 22.7%). Furthermore, the decrement in the caloric intake in corticosterone-treated rats was exclusively due to the loss of fat intake.
肠抑胃素或缬氨酸-脯氨酸-天冬氨酸-脯氨酸-精氨酸(VPDPR)是前脂酶的氨基末端五肽;VPDPR是在前脂酶被胰蛋白酶激活成为脂肪酶的过程中产生的。在啮齿动物中,外源性VPDPR已被证明会导致脂肪食欲选择性下降。为了解这种肽作用的潜在机制,我们研究了皮质酮(一种已知可调节热量摄入的肾上腺激素)对VPDPR介导的食欲抑制的影响。这项研究结果表明,皮质酮处理后,250微克/千克VPDPR对总热量摄入的抑制作用显著增加(对照组为2.3%;皮质酮处理组为22.7%)。此外,皮质酮处理的大鼠热量摄入的减少完全是由于脂肪摄入量的减少。