Laboratory of Nutritional Biochemistry, Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo, Hokkaido, Japan.
Metabolism. 2010 Jul;59(7):951-8. doi: 10.1016/j.metabol.2009.10.016. Epub 2009 Dec 16.
Dysregulation of visceral adipocytes increases the incidence of metabolic syndrome. Higher production of nonesterified fatty acid and changes in adipocytokine release may trigger insulin resistance. Many studies have suggested that calcium (Ca) deficiency is associated with insulin resistance; however, the mechanisms are poorly understood. We examined the effects of Ca deficiency on adrenaline-induced lipolysis and adipocytokine release in the early stages after weaning using freshly isolated adipocytes from mesenteric fat tissue of 3-week-old male Sprague-Dawley rats fed a normal-Ca (5 g/kg diet) or low-Ca (1 g/kg diet) diet for 4 weeks. The release rate of nonesterified fatty acid in the mesenteric adipocytes after stimulation with a low level of adrenaline (0.2 microg/mL) was much higher in the Ca-deficient group than in the control group. In contrast, adiponectin release in the mesenteric fat cells was lower in Ca-deficient rats. Leptin and tumor necrosis factor-alpha secretion showed a similar tendency without significant intergroup differences, and monocyte chemoattractant protein-1 release was not affected by Ca deficiency. We found that Ca deficiency reduced the average size of fat cells through a large increase in the number of cells slightly smaller than the average size, which may be associated with the changes in the properties of the mesenteric adipose tissue. Our present results suggest that a low intake of Ca in the early stages after weaning is associated with changes in the properties of mesenteric adipocytes, which may be linked to insulin resistance in the future.
内脏脂肪细胞的功能紊乱会增加代谢综合征的发病率。非酯化脂肪酸产量增加和细胞因子释放的变化可能会引发胰岛素抵抗。许多研究表明，钙（Ca）缺乏与胰岛素抵抗有关；然而，其机制尚不清楚。我们使用刚从 3 周龄雄性 Sprague-Dawley 大鼠的肠系膜脂肪组织中分离出来的脂肪细胞，研究了 Ca 缺乏对断奶后早期肾上腺素诱导的脂肪分解和细胞因子释放的影响，这些大鼠分别喂食正常 Ca（5 g/kg 饮食）或低 Ca（1 g/kg 饮食）饮食 4 周。低水平肾上腺素（0.2 μg/mL）刺激后，肠系膜脂肪细胞中非酯化脂肪酸的释放率在 Ca 缺乏组明显高于对照组。相比之下，Ca 缺乏大鼠的肠系膜脂肪细胞中脂联素的释放较低。瘦素和肿瘤坏死因子-α的分泌也表现出相似的趋势，但组间差异无统计学意义，单核细胞趋化蛋白-1 的释放不受 Ca 缺乏的影响。我们发现，Ca 缺乏通过大量数量稍小于平均大小的细胞来减少脂肪细胞的平均大小，这可能与肠系膜脂肪组织性质的变化有关。我们目前的结果表明，断奶后早期的低钙摄入与肠系膜脂肪细胞性质的变化有关，这可能与未来的胰岛素抵抗有关。
