澳大利亚某研究团队发现肝脏可能是调节体重的关键。他们发现肝脏可通过与大脑的“沟通”来调节体重。这项研究将会发表在《Diabetes》上。

墨尔本大学以及奥斯汀健康的研究人员指出，人体内有一个天生的系统，可以限制因食用高脂肪食物而引起的体重过度增加。然而，这个系统仅对正常饮食的饱和脂肪酸起作用，而对食用脂肪及高糖饮食的人则不起作用。

该研究团队来自墨尔本大学的分子肥胖实验室，他们发现当食用高脂食物时，肝脏中的一种酶的量会升高，并且这种酶向大脑传递信号以抑制刺激食欲的基因。简单来说，就是当食用脂肪后，大脑“告诉”身体应该要减少食物的摄入量，从而控制体重的增加。

研究人员将体内有高水平FBPase酶的小鼠与含有正常水平FBPase酶的小鼠作了比较。含有更多FBPase酶的小鼠体内的脂肪组织只有正常水平的鼠的一半，并且进食量较少。当研究人员切断肝脏和大脑之间的沟通“渠道”后，高水平FBPase酶小鼠也会吃较多的食物。既往研究表明，FBPase酶的主要作用是在肝脏中产生葡萄糖，但研究人员发现，它对于体重的调节作用更重要。

墨尔本大学的研究人员Barbara Fam博士说：“实际上，我们认为FBPase酶过度表达的小鼠会显示出糖尿病的征象，因为FBPase酶可使肝脏产生更多的葡萄糖。然而，当我们对小鼠进行更深层次的研究时，我们惊奇地发现FBPase酶诱发了大量的激素，这种激素能影响小鼠食欲。”

“结果表明，高脂肪饮食引起肝脏内FBPase酶的增多，作为一种负反馈机制以限制体重进一步增加。更重要的是，FBPase酶在正常的生理情况下，对控制体重不起作用，只有当这个体系处于过度营养负荷的情况下才起作用。当人们长期食用脂肪和糖时，它能对身体产生众多不同的影响。”Barbara Fam补充说。她解释说，肝脏将来或能成为治疗肥胖和2型糖尿病的新靶点。

此项研究表明，肝FBPase酶不仅可作为糖代谢的“调解员”，也可作为一个重要的调节食欲和脂肪的“协调员”。目前，还需要进一步研究，以证实这种观点。

原文：

A team of Australian researchers have found that the liver could hold the key to treating obesity . They found that the liver plays a major role in regulating weight by communicating with the brain . The study will be published in the Journal of Diabetes

University of Melbourne researchers and those from Austin Health have noted that the body has an innate system in place to limit excessive weight gain caused by eating fatty foods. However, the system only works in response to saturated fat in a normal diet and would not stop obesity in people who ate fat and sugar-laden diets.

The team belonging to the university's Molecular Obesity Laboratory found that an enzyme in the liver increased when fatty foods were consumed and sent a signal to the brain to reduce appetite-stimulating genes. The overall affect was that after fat was consumed the brain told the body to reduce its food intake, thereby limiting weight gain.

The researchers compared higher levels of the enzyme, called FBPase, in mice with normal levels in another group. The animals with more FBPase had half the amount of fatty tissue and ate less food than those mice without the extra enzymes. When the researchers severed the communication links between the liver and the brain, the mice ate more food, even though they had higher levels of the enzymes. FBPase's main role is to produce glucose in the liver, but researchers found it is more important in regulating body weight.

Melbourne University researcher Dr Barbara Fam said people who eat a fatty diet would still become overweight, but the system probably limited the amount of weight gained. “We actually thought that the mouse with the over-expressed enzyme would show signs of becoming diabetic since the enzyme is important in producing more glucose from the liver. However when we studied our mice in more depth, we were very surprised to see that this enzyme triggered a number of hormones that influence the control of appetite,” said Dr Barbara Fam said.

“The results suggest that consumption of a diet high in fat, causes an increase in liver FBPase that was likely put in place as a negative feedback mechanism to limit further weight gain. Importantly, FBPase does not function to control body weight under normal physiological circumstances but acts only when the system is exposed to excess nutrients such as fat. When people eat diets loaded with fat and sugars particularly over the long term, it can have a number of different effects on the body but it appears that we actually have in place an innate system that protects us from any further weight gain that could happen while eating these type of diets,” she added. She explained the liver could in future be considered as a target for treating weight-related conditions including obesity  and type 2 diabetes .

More needs to be investigated to verify this in further trials, however this study has demonstrated that liver FBPase should be viewed not only as a mediator of glucosemetabolism but also as an important regulator of appetite and fat.

相关文献：

The role of liver fructose-1,6-bisphosphatase in regulating appetite and adiposity.

Diabetes 2012;615:1122-32

Visinoni S Khalid NF Joannides CN Shulkes A Yim M Whitehead J Tiganis T Lamont BJ Favaloro JM Proietto J Andrikopoulos S Fam BC

Department of Medicine, University of Melbourne, Heidelberg, Victoria, Australia.