Lee Soo-Lim, Kwak Eun-Hee, Kim Yang-Ha, Choi Je-Yong, Kwon Soon-Tae, Beattie John H, Kwun In-Sook
Department of Food Science and Nutrition, Andong National University, Andong, South Korea.
J Med Food. 2003 Winter;6(4):281-9. doi: 10.1089/109662003772519822.
Zinc deficiency in animals causes impaired growth and anorexia, and the mechanisms for these symptoms of zinc deficiency are not yet clear. We investigated whether circulating leptin levels and gene expression would be dysregulated under zinc deficiency and what would be the implications for appetite in rats. In study 1, 24 Sprague-Dawley rats were provided consecutively with three different dietary zinc intake levels: Zn-adequate (30 mg/kg of diet), Zn-depleted (1 mg/kg of diet), and Zn-replete (50 mg/kg of diet), for 1, 2, and 2 weeks, respectively. At the end of each dietary period, one-third of the rats were killed. In study 2, rats were assigned to one of the four Zn diet groups: Zn-adequate (30 mg/kg of diet), pair-fed (30 mg/kg of diet), Zn-deficient (1 mg/kg of diet), or Zn-sufficient (50 mg/kg of diet), and were fed for 4 weeks. Tissue Zn and serum leptin were measured, and leptin gene expression in adipose tissues (inguinal and abdominal) was determined by reverse transcription-polymerase chain reaction and northern blotting. Blood subfractions as plasma, red blood cells, and mononuclear cells and liver Zn level were decreased during the Zn-depletion period (P <.05). Serum leptin showed a tendency to increase during the Zn-depletion period and decreased back to the level of the Zn-repletion period. Leptin mRNA levels in inguinal adipocytes also increased during the Zn-depletion (P <.05) and Zn-deficient periods, which is consistent with the change in serum leptin. However, the decrease in leptin mRNA in abdominal adipocytes was not consistent with the increase in inguinal leptin levels and the change in serum leptin. Increased leptin levels in linguinal adipocytes is consistent with the expected physiological change of a decrease in appetite under Zn deficiency. However, before coming to any firm conclusion, further studies on adipose tissue-specific leptin expression, including the appetite-related neuropeptides, are necessary for clarifying the cause of lower appetite in zinc deficiency.
动物缺锌会导致生长发育受阻和食欲不振，而缺锌出现这些症状的机制尚不清楚。我们研究了在缺锌情况下循环瘦素水平和基因表达是否会失调，以及这对大鼠食欲有何影响。在研究1中，给24只斯普拉格-道利大鼠连续提供三种不同的膳食锌摄入量水平：锌充足（30毫克/千克饲料）、锌缺乏（1毫克/千克饲料）和锌补充（50毫克/千克饲料），分别持续1周、2周和2周。在每个饮食阶段结束时，处死三分之一的大鼠。在研究2中，将大鼠分为四个锌饮食组之一：锌充足（30毫克/千克饲料）、配对喂养（30毫克/千克饲料）、缺锌（1毫克/千克饲料）或锌充足（50毫克/千克饲料），并喂养4周。测量组织锌和血清瘦素，并通过逆转录-聚合酶链反应和Northern印迹法测定脂肪组织（腹股沟和腹部）中的瘦素基因表达。在锌缺乏期，血浆、红细胞和单核细胞等血液亚组分以及肝脏锌水平降低（P<.05）。血清瘦素在锌缺乏期有升高趋势，然后又降至锌补充期的水平。腹股沟脂肪细胞中的瘦素mRNA水平在锌缺乏期和缺锌期也升高（P<.05），这与血清瘦素的变化一致。然而，腹部脂肪细胞中瘦素mRNA的降低与腹股沟瘦素水平的升高以及血清瘦素的变化不一致。腹股沟脂肪细胞中瘦素水平的升高与缺锌时食欲下降的预期生理变化一致。然而，在得出任何确凿结论之前，有必要对脂肪组织特异性瘦素表达进行进一步研究，包括与食欲相关的神经肽，以阐明缺锌时食欲降低的原因。
