The Role of Momordica charantia in Resisting Obesity

Abstract

Momordica charantia (M. charantia), commonly known as bitter gourd, bitter melon, kugua, balsam pear, or karela, is a tropical and sub-tropical vine belonging to the Cucurbitaceae family. It has been used to treat a variety of diseases in the traditional medicine of China, India, and Sri Lanka. Here, we review the anti-obesity effects of various bioactive components of M. charantia established at the cellular and organismal level. We aim to provide links between various bioactive components of M. charantia and their anti-obesity mechanism. An advanced search was conducted on the worldwide accepted scientific databases via electronic search (Google Scholar, Web of Science, ScienceDirect, ACS Publications, PubMed, Wiley Online Library, SciFinder, CNKI) database with the query TS = "Momordica charantia" and "obesity". Information was also obtained from International Plant Names Index, Chinese Pharmacopoeia, Chinese herbal classic books, online databases, PhD and MSc dissertations, etc. First, studies showing the anti-obesity effects of M. charantia on the cells and on animals were classified. The major bioactive components that showed anti-obesity activities included proteins, triterpenoids, saponins, phenolics, and conjugated linolenic acids. Their mechanisms included inhibition of fat synthesis, promotion of glucose utilization, and stimulation of auxiliary lipid-lowering activity. Finally, we summarized the risks of excessive consumption of M. charantia and the application. Although further research is necessary to explore various issues, this review establishes the therapeutic potential of M. charantia and it is highly promising candidate for the development of anti-obesity health products and medicines.

Keywords: Momordica charantia; anti-obesity; bioactive components; mechanisms.

Figure 1

Chemical structure of saponins and triterpenes isolated from M. charantia.

Figure 2

Chemical structure of phenolics and flavonoids isolated from M. charantia.

Figure 3

Chemical structure of fatty acids isolated from M. charantia.

Figure 4

Possible mechanisms contributing to the inhibition of fat synthesis and glucose utilization of M. charantia. M. charantia stimulates glucose transporter 4 (GluT-4) to migrate to the cell membrane and mediate glucose uptake by increasing adiponectin, and the adenosine monophosphate-activated protein kinase (AMPK) activity. In addition, M. charantia blocks the expression of PPARγ, and PPARγ downstream pathway including C/EBPα and PI3K to reduce the accumulation of fat.

Figure 5

Possible mechanisms contributing to the auxiliary lipid-lowering activity of M. charantia. M. charantia reduce the elevated levels of serum cholesterol, phospholipids, triglyceride (TG), and low-density lipoprotein (LDL). On the contrary, M. charantia increases the high-density lipoprotein (HDL) level by elevating lipid flow in the tissues.