Miner J L
Department of Animal Science, University of Nebraska, Lincoln 68583-0908, USA.
J Anim Sci. 2004 Mar;82(3):935-41. doi: 10.2527/2004.823935x.
Communication between adipose and other tissues has been hypothesized since at least the 1940s to be bidirectional. Despite this expectation, early progress was largely limited to adipose tissue's role in metabolism and storage of fatty acids, its development, and its response to endocrine and neural cues. However, efforts of the last decade have identified several molecules that are secreted from adipocytes, apparently for the purpose of signaling to other tissues. Cloning of the mouse obesity gene in 1994 is perhaps the most famous impetus for recognition that adipocytes are active in the regulation of multiple body functions. The product of this gene, leptin, has since been found to inhibit feeding, enhance energy expenditure, and stimulate gonadotropes. Evidence for the roles of other adipocyte-derived signals is being generated. Resistin is a protein that can cause whole-body insulin resistance. Its expression is correlated with body fatness and is inhibited by thiazolidinediones, perhaps mediating the association of type 2 diabetes with obesity, and the effectiveness of these drugs. Resistin and a related molecule, RELM alpha, can also inhibit differentiation of preadipocytes. Adiponectin/Acrp30 secretion from adipocytes is diminished in obese states. This protein can enhance use of fatty acids in lean tissues, inhibit glucose production by liver, and consequently decrease both blood glucose and BW. Adiponectin may also be responsible for the effectiveness of thiazolidinediones, given that these drugs promote adiponectin secretion. Secretion of complement proteins has been observed in adipocytes, and these interact to generate a signal called acylation-stimulating protein, which can promote triacylglycerol synthesis. These signals seem to be largely unique to adipocytes. Other signals are derived from adipose tissue, and it is unlikely that all the adipocyte's endocrine signals have been identified. Certainly, there is much to learn about how these signals function; however, it is clear that these biomedical research discoveries comprise a useful model for our study of growth and development in livestock.
至少从20世纪40年代起，人们就推测脂肪组织与其他组织之间的通讯是双向的。尽管有此预期，但早期进展在很大程度上仅限于脂肪组织在脂肪酸代谢和储存、其发育以及对内分泌和神经信号的反应方面的作用。然而，过去十年的研究已经鉴定出几种由脂肪细胞分泌的分子，其目的显然是向其他组织发出信号。1994年小鼠肥胖基因的克隆可能是促使人们认识到脂肪细胞在调节多种身体功能中发挥作用的最著名的推动力。此后发现该基因的产物瘦素可抑制进食、增加能量消耗并刺激促性腺激素细胞。其他源自脂肪细胞的信号的作用证据也在不断涌现。抵抗素是一种可导致全身胰岛素抵抗的蛋白质。其表达与体脂相关，并受到噻唑烷二酮类药物的抑制，这可能介导了2型糖尿病与肥胖的关联以及这些药物的有效性。抵抗素和一种相关分子RELMα也可抑制前脂肪细胞的分化。肥胖状态下脂肪细胞分泌的脂联素/Acrp30会减少。这种蛋白质可增强瘦组织中脂肪酸的利用，抑制肝脏产生葡萄糖，从而降低血糖和体重。鉴于这些药物可促进脂联素分泌，脂联素可能也是噻唑烷二酮类药物有效性的原因。在脂肪细胞中已观察到补体蛋白的分泌，这些补体蛋白相互作用产生一种称为酰化刺激蛋白的信号，该信号可促进三酰甘油的合成。这些信号似乎在很大程度上是脂肪细胞所特有的。其他信号源自脂肪组织，而且不太可能已经鉴定出脂肪细胞的所有内分泌信号。当然，关于这些信号如何发挥作用还有很多需要了解的；然而，很明显这些生物医学研究发现为我们研究家畜的生长发育提供了一个有用的模型。
