長期吃卡路里過高的食物會發(fā)胖,。這一簡單的道理背后實際上有很復雜的生物機理。眾所周知,，動物的腦在維持身體能量平衡方面起著很重要的調(diào)節(jié)作用,。德國研究人員最近又發(fā)現(xiàn)，分布在腦和脊髓外的神經(jīng)也參與影響動物胖瘦的過程,。

動物腦部被稱為下丘腦的部位已被發(fā)現(xiàn)是動物衡量自身所需能量和調(diào)節(jié)相應進食量的樞紐,。能量很高的食物能使這種調(diào)節(jié)失衡，從而導致肥胖,。德國馬克斯·普朗克心肺研究所托布勞恩博士領(lǐng)導的一個研究小組發(fā)現(xiàn),，不僅腦部，動物脂肪組織中的神經(jīng)也對造成肥胖產(chǎn)生影響,。

據(jù)該研究所15日發(fā)表的新聞公報,，研究人員培養(yǎng)出不具備Nscl－2基因的轉(zhuǎn)基因鼠，Nscl－2基因只在神經(jīng)細胞中發(fā)揮作用,，這種實驗鼠在成年之后要比正常鼠肥胖得多,。進一步研究發(fā)現(xiàn)，轉(zhuǎn)基因鼠的脂肪組織中神經(jīng),、特別是細小的神經(jīng)纖維要比正常情況少得多,，因而轉(zhuǎn)基因鼠脂肪組織中的信息傳遞明顯減少。這應該是導致轉(zhuǎn)基因鼠過胖的一個重要原因,。

研究人員還意外發(fā)現(xiàn),，這些缺失Nscl－2基因的轉(zhuǎn)基因鼠雖然肥胖，但并未因此罹患Ⅱ型糖尿病,。他們認為,，利用上述發(fā)現(xiàn)將來或許可以對人體脂肪細胞的成熟過程施加影響,，從而改善人體的新陳代謝。（生物谷Bioon.com）

生物谷推薦原始出處：

PLoS ONE 4(5): e5516. doi:10.1371/journal.pone.0005516

Defective Peripheral Nerve Development Is Linked to Abnormal Architecture and Metabolic Activity of Adipose Tissue in Nscl-2 Mutant Mice

Karen Ruschke1,2,4, Henning Ebelt1, Nora Kl?ting2, Thomas Boettger4, Kay Raum3, Matthias Blüher2, Thomas Braun1,4*

1 Institute of Physiological Chemistry, University of Halle-Wittenberg, Halle, Germany, 2 Department of Medicine, University of Leipzig, Leipzig, Germany, 3 Julius Wolff Institute and Center for Musculoskeletal Surgery, Charité-Universit?tsmedizin Berlin, Berlin, Germany, 4 Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany

Background

In mammals the interplay between the peripheral nervous system (PNS) and adipose tissue is widely unexplored. We have employed mice, which develop an adult onset of obesity due to the lack the neuronal specific transcription factor Nscl-2 to investigate the interplay between the nervous system and white adipose tissue (WAT).

Methodology

Changes in the architecture and innervation of WAT were compared between wildtype, Nscl2?/?, ob/ob and Nscl2?/?//ob/ob mice using morphological methods, immunohistochemistry and flow cytometry. Metabolic alterations in mutant mice and in isolated cells were investigated under basal and stimulated conditions.

Principal Findings

We found that Nscl-2 mutant mice show a massive reduction of innervation of white epididymal and paired subcutaneous inguinal fat tissue including sensory and autonomic nerves as demonstrated by peripherin and neurofilament staining. Reduction of innervation went along with defects in the formation of the microvasculature, accumulation of cells of the macrophage/preadipocyte lineage, a bimodal distribution of the size of fat cells, and metabolic defects of isolated adipocytes. Despite a relative insulin resistance of white adipose tissue and isolated Nscl-2 mutant adipocytes the serum level of insulin in Nscl-2 mutant mice was only slightly increased.

Conclusions

We conclude that the reduction of the innervation and vascularization of WAT in Nscl-2 mutant mice leads to the increase of preadipocyte/macrophage-like cells, a bimodal distribution of the size of adipocytes in WAT and an altered metabolic activity of adipocytes.