食品科学

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过度营养与人体代谢和疾病关系的研究进展

庞广昌,陈庆森,胡志和,解军波   

  1. 天津市食品生物技术重点实验室,天津商业大学生物技术与食品科学学院,天津 300134
  • 出版日期:2013-08-15 发布日期:2013-09-03
  • 通讯作者: 庞广昌
  • 基金资助:

    “十二五”国家科技支撑计划项目(2012BAD29B07);国家自然科学基金项目(30871951)

Progress and Prospect of Overnutrition on Metabolism and Human Wellness

PANG Guang-chang,CHEN Qing-sen,HU Zhi-he,XIE Jun-bo   

  1. Tianjin Key Laboratory of Food Biotechnology, College of Biotechnology and Food Science, Tianjin University of Commerce,
    Tianjin 300134, China
  • Online:2013-08-15 Published:2013-09-03
  • Contact: PANG Guang-chang

摘要:

为了能够获得足够的营养,机体专门进化出一个营养传感系统,也就是以G蛋白偶联受体(GPCRs)为主体的营养传感系统。GPCRs通过钙离子通道、钠钾泵和植物神经系统对饮食中的营养进行计数,并将这些定量化的信号传递给大脑和相应器官,从而控制食欲。在营养和食欲控制失调时就会产生过度营养。生物除营养传感、计数和食欲控制系统之外还有一个营养的储存和消费控制系统,这个系统的主体就是mTOR。作为体内的营养传感系统,mTOR对糖、氨基酸和脂肪酸进行传感,从而控制糖、氨基酸和脂肪的合成与分解代谢,糖和脂肪的储存与消费同时控制细胞的周期、生长和增殖。机体从饮食中吸收的营养中的糖类以肝糖原和肌糖原的形式储存;以储脂,特别是皮下脂肪的形式储存脂肪,通过磷酸解和脂肪酸的β-氧化的形式及时满足机体的分解与合成代谢,以及各种生命活动对能量、还原力和中间代谢物的需求。当营养储存超过一定的极限时,mTOR将会激活机体的代谢和细胞增殖,以刺激对储存脂肪和糖元的消费。长期刺激基础代谢会造成多种代谢性疾病,特别是糖尿病、肥胖性炎症和癌症。一个普遍存在的自然现象是:生物的寿命与其代谢活性密切相关,代谢越旺盛的生物寿命越短,相反代谢越缓慢的生物寿命越长。近年来,已经有越来越多的研究结果证明:营养限制会延长寿命,不难推断,过度营养不仅会造成多种疾病,同时也会缩短人的寿命。本文将对这些问题进行综述,希望能引起大众的关注和学术界的进一步研究。

关键词: G蛋白偶联受体, 哺乳动物雷帕霉素靶蛋白, 营养, 信号通路, 代谢综合征

Abstract:

G protein coupled receptors (GPCRs) are developed for organisms to uptake enough foods during evolution. As
a primary nutrition sensor system, GPCRs are expressed in endocrine cells within the gut mucosa, and absorb nutrients and
quantitate them with voltage-gated calcium channels, sodium potassium pump and vegetative nervous system. These signals
are transmitted to brain for appetite control. GPCRs also coordinate with other chemosensory signaling elements. The release
of hormones can regulate energy and glucose homeostasis. The malfunction of GCPRs may be responsible for a variety of
metabolic dysfunctions associated with overfeeding or obesity. In addition, another nutrient sensor system, mammalian target
of rapamycin (mTOR) has been implicated as a sensor of nutrient sufficiency for dividing cells and is activated by essential
amino acids, glucose and lipids. mTOR is also involved in the mechanisms for efficient transition between anabolic states
and catabolic states. When nutrients are absorbed, the glucose will be transformed into liver glycogen or muscle glycogen
for future utilization, and the lipids will be stored in adipose tissue. The glycogen will be used in pyrophosphorolysis and the
lipids will be consumed by β-oxidation when energy is needed. When the nutrition storage exceeds some limits, mTOR will
activate many processes that generate or use a large amount of energy and glycogen. It is increasingly apparent that mTORactivated
metabolism impacts most major cellular functions, thus playing an oversized role in regulating basic cell behaviors
such as growth and proliferation, and many disease including cancer, obesity, and type 2 diabetes. Furthermore, there is
a ubiquitous natural phenomenon that the lifespan of an organism is closely related to its metabolic activity. The higher
the metabolism speed, the shorter the lifespan, and vice versa. In recent years, multiple studies have shown that calorie
restriction can prolong lifespan, so overnutrition may not only induce multiple diseases but also shorten lifespan. This review
describes recent findings regarding overnutrition-related diseases. The main purpose is to attract extensive attention and
broaden academic interest.

Key words: G proteincoupled receptors, mTOR, nutrition, signaling pathway, metabolic syndrome

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