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脂联素受体AdipoR1和AdipoR2在瘦大鼠和肥胖Zucker大鼠中的表达。

Expression of the adiponectin receptors AdipoR1 and AdipoR2 in lean rats and in obese Zucker rats.

作者信息

Beylot Michel, Pinteur Claudie, Peroni Odile

机构信息

INSERM U499, Metabolic and Renal Physiolopathology, Faculté RTH Laennec, 69008 Lyon, France.

出版信息

Metabolism. 2006 Mar;55(3):396-401. doi: 10.1016/j.metabol.2005.09.016.


DOI:10.1016/j.metabol.2005.09.016
PMID:16483885
Abstract

The adiponectin receptors, AdipoR1 and AdipoR2, are thought to transmit the insulin-sensitizing effects of adiponectin, an adipokine secreted by adipocytes. Modifications of their expression in insulin-sensitive tissues (skeletal muscle, liver, and adipose tissue) could therefore play a role in the control of insulin sensitivity and the development of insulin resistance. Recent data in mice supported this possibility. We examined whether the expression of adiponectin receptors (messenger RNA [mRNA] concentrations) is controlled in vivo in rats (Wistar) by nutritional factors (high-fat [HF] vs high-carbohydrate diet, fasting vs fed state) and whether this expression is decreased in an experimental model of insulin resistance, the obese Zucker rat. In Wistar rats, neither an HF diet nor fasting modified the mRNA concentrations of AdipoR1 in muscle, liver, or adipose tissue; the only modification observed was a decrease (P < .05) in AdipoR2 mRNA level in the liver of rats fed with an HF diet. In obese Zucker rats compared with their lean controls, neither AdipoR1 nor AdipoR2 expression was modified in muscle. AdipoR2 expression was slightly decreased in adipose tissue, whereas the expression of both AdipoR1 and AdipoR2 was increased (P < .05) in the liver of obese Zucker rats. In conclusion, contrary to what was reported in mice, the expression of adiponectin receptors in rats is poorly responsive to changes in nutritional conditions and is not decreased in a model of insulin resistance. These results do not support an important role for the expression of AdipoR1 and AdipoR2 in the modulation of sensitivity to insulin.

摘要

脂联素受体AdipoR1和AdipoR2被认为可传递脂联素的胰岛素增敏作用,脂联素是一种由脂肪细胞分泌的脂肪因子。因此,其在胰岛素敏感组织(骨骼肌、肝脏和脂肪组织)中的表达变化可能在胰岛素敏感性调控及胰岛素抵抗的发生发展中发挥作用。近期小鼠实验数据支持了这一可能性。我们研究了在大鼠(Wistar)体内,营养因素(高脂饮食与高碳水化合物饮食、禁食与进食状态)是否控制脂联素受体的表达(信使核糖核酸[mRNA]浓度),以及在胰岛素抵抗实验模型——肥胖Zucker大鼠中该表达是否降低。在Wistar大鼠中,高脂饮食和禁食均未改变肌肉、肝脏或脂肪组织中AdipoR1的mRNA浓度;唯一观察到的变化是高脂饮食喂养的大鼠肝脏中AdipoR2 mRNA水平降低(P<0.05)。与瘦的对照大鼠相比,肥胖Zucker大鼠肌肉中AdipoR1和AdipoR2的表达均未改变。脂肪组织中AdipoR2表达略有降低,而肥胖Zucker大鼠肝脏中AdipoR1和AdipoR2的表达均增加(P<0.05)。总之,与小鼠实验结果相反,大鼠脂联素受体的表达对营养状况变化反应较弱,且在胰岛素抵抗模型中未降低。这些结果不支持AdipoR1和AdipoR2表达在调节胰岛素敏感性方面起重要作用。

相似文献

[1]
Expression of the adiponectin receptors AdipoR1 and AdipoR2 in lean rats and in obese Zucker rats.

Metabolism. 2006-3

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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引用本文的文献

[1]
Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin.

Chem Senses. 2019-7-17

[2]
Long-Term Impact of Neonatal Intake of Oleanolic Acid on the Expression of AMP-Activated Protein Kinase, Adiponectin and Inflammatory Cytokines in Rats Fed with a High Fructose Diet.

Nutrients. 2019-1-22

[3]
From Placenta to Polycystic Ovarian Syndrome: The Role of Adipokines.

Mediators Inflamm. 2016

[4]
A novel role of globular adiponectin in treatment with HFD/STZ induced T2DM combined with NAFLD rats.

ScientificWorldJournal. 2014-2-6

[5]
Cardiac hypertrophy and fibrosis in the metabolic syndrome: a role for aldosterone and the mineralocorticoid receptor.

Int J Hypertens. 2011

[6]
Adiponectin receptor signalling in the brain.

Br J Pharmacol. 2012-1

[7]
High-fat diet and glucocorticoid treatment cause hyperglycemia associated with adiponectin receptor alterations.

Lipids Health Dis. 2011-1-18

[8]
Hepatic expression of adiponectin receptors increases with non-alcoholic fatty liver disease progression in morbid obesity in correlation with glutathione peroxidase 1.

Obes Surg. 2011-4

[9]
APPL1: role in adiponectin signaling and beyond.

Am J Physiol Endocrinol Metab. 2009-1

[10]
Adiponectin deficiency exacerbates lipopolysaccharide/D-galactosamine-induced liver injury in mice.

World J Gastroenterol. 2006-6-7

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