Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women

Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women
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DOI:
10.1385/bter:112:2:109
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发表时间:
2006-08-01
影响因子:
3.9
通讯作者:
Franciscato Cozzolino, Silvia Maria
Franciscato Cozzolino, Silvia Maria
中科院分区:
生物学3区
文献类型:
--
作者:
Marreiro, Dilina do Nascimento;Geloneze, Bruno;Franciscato Cozzolino, Silvia Maria

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瘦素被认为是一种有助于调节体重的脂信号。锌可能在食欲调节中起重要作用,其给药可刺激瘦素的产生。然而,关于其对肥胖人群中瘦素水平的影响的文献报道很少。本研究旨在探讨补锌对胰岛素抵抗(IR)患者血清瘦素水平的影响。这是一项前瞻性的双盲、随机、临床、安慰剂对照研究。56名糖耐量正常的肥胖女性(年龄25-45岁,体重指数=36.2+/-2.3 kg/m(2))随机接受锌治疗,每天30 mg,共4wk。两组在年龄、BMI、卡路里摄入量、胰岛素浓度、胰岛素抵抗以及饮食、血浆、尿液和红细胞中锌浓度的基线值相似。用放射免疫法测定胰岛素和瘦素,用稳态模型评估(HOMA)评估胰岛素抵抗。用原子吸收光谱法测定血浆、红细胞和24小时尿中锌含量。4wk后,补锌组尿锌浓度由385.9+/-259.3升至470.2+/-241.2+/-mUg/24 h,但体重指数、空腹血糖、血浆和红细胞锌浓度均无明显变化。安慰剂组的胰岛素没有变化,而补充组的胰岛素显著下降。补锌组的HOMA也从5.8+/-2.6降至4.3+/-1.7(p<0.05),但安慰剂组没有变化。在安慰剂组中,瘦素没有变化。补锌组瘦素水平为23.6+/-12.3mU/L,无明显变化。来自有记录的胰岛素抵抗的独特肥胖个体的更多人类数据将有助于指导未来关于补锌(剂量更高或间隔更长)或不同措施的研究。
Leptin is thought to be a lipostatic signal that contributes to body weight regulation. Zinc might play an important role in appetite regulation and its administration stimulates leptin production. However, there are few reports in the literature on its role on leptin levels in the obese population. The present work assesses the effect of zinc supplementation on serum leptin levels in insulin resistance (IR). A prospective double-blind, randomized, clinical, placebo-controlled study was conducted. Fifty-six normal glucose-tolerant obese women (age: 25-45 yr, body mass index [BMI] = 36.2 +/- 2.3 kg/m(2)) were randomized for treatment with 30 mg zinc daily for 4 wk. Baseline values of both groups were similar for age, BMI, caloric intake, insulin concentration, insulin resistance, and zinc concentration in diet, plasma, urine, and erythrocytes. Insulin and leptin were measured by radioimmunoassay and IR was estimated by the homeostasis model assessment (HOMA). The determinations of zinc in plasma, erythrocytes, and 24-h urine were performed by using atomic absorption spectrophotometry. After 4 wk, BMI, fasting glucose, and zinc concentration in plasma and erythrocyte did not change in either group, although zinc concentration in the urine increased from 385.9 +/- 259.3 to 470.2 +/- 241.2 +/- mu g/ 24 h in the group with zinc supplementation (p < 0.05). Insulin did not change in the placebo group, whereas there was a significant decrease of this hormone in the supplemented group. HOMA also decreased from 5.8 +/- 2.6 to 4.3 +/- 1.7 (p < 0.05) in the zinc-supplemented group but did not change in the placebo group. Leptin did not change in the placebo group. In the zinc group, leptin was 23.6 +/- 12.3 mu g/ L and did not change. More human data from a unique population of obese individuals with documented insulin resistance would be useful in guiding future studies on zinc supplementation (with higher doses or longer intervals) or different measures.