Leite Nayara de Carvalho, Montes Elisangela Gueiber, Fisher Stefani Valéria, Cancian Cláudia Regina Capriglioni, de Oliveira Júlio Cezar, Martins-Pinge Marli Cardoso, Kanunfre Carla Cristine, Souza Kleber Luiz Araujo, Grassiolli Sabrina
Department of Structural and Functional Biology, Institute of Biology, UNICAMP, Campinas, São Paulo, Brazil.
Department of General Biology, State University of Ponta Grossa, Ponta Grossa, Parana, Brazil.
Metabolism. 2015 Sep;64(9):1122-33. doi: 10.1016/j.metabol.2015.05.003. Epub 2015 May 7.
Obesity-induced abnormalities, such as insulin resistance, dyslipidemia and hypertension, are frequently correlated with low-grade inflammation, a process that may depend on normal spleen function. This study investigated the role of the spleen in the obesity induced by monosodium glutamate (MSG) treatment.
MATERIALS/METHODS: MSG-obese and lean control (CON) rats were subjected to splenectomy (SPL) or non-operated (NO).
MSG-NO rats presented a high adipose tissue content, insulin resistance, dyslipidemia and islet hypersecretion, accompanied by hypertrophy of both pancreatic islets and adipocytes when compared with CON-NO rats. In addition, changes in nitric oxide response were found in islets from the MSG-NO group without associated alterations in inducible nitric oxide synthase (iNOS) or IL1β expression. MSG-NO also presented increased leukocyte counts and augmented LPS-induced nitric oxide production in macrophages. Splenectomy of MSG-obese animals decreased insulin hypersecretion, normalized the nitric oxide response in the pancreatic islets, improved insulin sensitivity and reduced hypertrophy of both adipocytes and islets, when compared with MSG-NO rats.
Results show that splenectomy attenuates the progression of the obesity modulating pancreas functions in MSG-obese rats.
肥胖引起的异常情况，如胰岛素抵抗、血脂异常和高血压，常与低度炎症相关，这一过程可能依赖于正常的脾脏功能。本研究调查了脾脏在谷氨酸钠（MSG）诱导的肥胖中的作用。
材料/方法：将MSG诱导肥胖的大鼠和瘦素对照（CON）大鼠进行脾切除术（SPL）或假手术（NO）。
与CON-NO大鼠相比，MSG-NO大鼠脂肪组织含量高，存在胰岛素抵抗、血脂异常和胰岛分泌亢进，同时伴有胰岛和脂肪细胞肥大。此外，在MSG-NO组的胰岛中发现一氧化氮反应发生变化，但诱导型一氧化氮合酶（iNOS）或IL1β表达无相关改变。MSG-NO组的白细胞计数也增加，巨噬细胞中脂多糖诱导的一氧化氮生成增强。与MSG-NO大鼠相比，对MSG诱导肥胖的动物进行脾切除可减少胰岛素分泌亢进，使胰岛中的一氧化氮反应正常化，提高胰岛素敏感性，并减少脂肪细胞和胰岛的肥大。
结果表明，脾切除术可减弱MSG诱导肥胖大鼠的肥胖进展，调节胰腺功能。
