长期吃卡路里过高的食物会发胖。这一简单的道理背后实际上有很复杂的生物机理。众所周知，动物的脑在维持身体能量平衡方面起着很重要的调节作用。德国研究人员最近又发现，分布在脑和脊髓外的神经也参与影响动物胖瘦的过程。
动物脑部被称为下丘脑的部位已被发现是动物衡量自身所需能量和调节相应进食量的枢纽。能量很高的食物能使这种调节失衡，从而导致肥胖。德国马克斯·普朗克心肺研究所托布劳恩博士领导的一个研究小组发现，不仅脑部，动物脂肪组织中的神经也对造成肥胖产生影响。
据该研究所15日发表的新闻公报，研究人员培养出不具备Nscl－2基因的转基因鼠，Nscl－2基因只在神经细胞中发挥作用，这种实验鼠在成年之后要比正常鼠肥胖得多。进一步研究发现，转基因鼠的脂肪组织中神经、特别是细小的神经纤维要比正常情况少得多，因而转基因鼠脂肪组织中的信息传递明显减少。这应该是导致转基因鼠过胖的一个重要原因。
研究人员还意外发现，这些缺失Nscl－2基因的转基因鼠虽然肥胖，但并未因此罹患Ⅱ型糖尿病。他们认为，利用上述发现将来或许可以对人体脂肪细胞的成熟过程施加影响，从而改善人体的新陈代谢。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
