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首页> 外文期刊>Life sciences >Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity.
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Adrenal medullary function and expression of catecholamine-synthesizing enzymes in mice with hypothalamic obesity.

机译：下丘脑肥胖小鼠的肾上腺髓质功能和儿茶酚胺合成酶的表达。

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The mechanisms underlying the onset of obesity are complex and not completely understood. An imbalance of autonomic nervous system has been proposed to be a major cause of great fat deposits accumulation in hypothalamic obesity models. In this work we therefore investigated the adrenal chromaffin cells in monosodium glutamate (MSG)-treated obese female mice. Newborn mice were injected daily with MSG (4 mg/g body weight) or saline (controls) during the first five days of life and studied at 90 days of age. The adrenal catecholamine content was 56.0% lower in the obese group when compared to lean controls (P < 0.0001). Using isolated adrenal medulla we observed no difference in basal catecholamine secretion percentile between obese and lean animals. However, the percentile of catecholamine secretion stimulated by high K+ concentration was lower in the obese group. There was a decrease in the tyrosine hydroxylase enzyme expression (57.3%, P < 0.004) in adrenal glands of obese mice. Interestingly, the expression of dopamine beta-hydroxylase was also reduced (47.0%, P < 0.005). Phenylethanolamine N-methyltransferase expression was not affected. Our results show that in the MSG model, obesity status is associated with a defective adrenal chromaffin cell function. We conclude that in MSG obesity the low total catecholamine content is directly related to a decrease of key catecholamine-synthesizing enzymes, which by its turn may lead to a defective catecholamine secretion.
机译：肥胖发作的潜在机制很复杂，尚未完全了解。有人提出自主神经系统失衡是下丘脑肥胖模型中大量脂肪堆积的主要原因。因此，在这项工作中，我们研究了味精（MSG）处理的肥胖雌性小鼠的肾上腺嗜铬细胞。在生命的前五天内，每天给新生小鼠注射味精（4 mg / g体重）或生理盐水（对照组），并在90天时进行研究。与瘦对照组相比，肥胖组的肾上腺儿茶酚胺含量降低了56.0％（P <0.0001）。使用分离的肾上腺髓质，我们观察到肥胖动物和瘦动物的基础儿茶酚胺分泌百分率没有差异。然而，在肥胖组中，高K +浓度刺激的儿茶酚胺分泌百分率较低。肥胖小鼠肾上腺的酪氨酸羟化酶表达降低（57.3％，P <0.004）。有趣的是，多巴胺β-羟化酶的表达也降低了（47.0％，P <0.005）。苯乙醇胺N-甲基转移酶的表达不受影响。我们的结果表明，在MSG模型中，肥胖状态与肾上腺嗜铬细胞功能缺陷有关。我们得出的结论是，在MSG肥胖症中，低的儿茶酚胺总含量与关键的儿茶酚胺合成酶的减少直接相关，这反过来可能导致儿茶酚胺分泌不良。

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