ABSTRACT
DO-YOUNG PARK, YOUNG-TAE AHN, SE-HOON PARK, CHUL-SUNG HUH, SAE-ROM YOO, RINA YU, MI-KYUNG SUNG, ROBIN A. MCGREGOR, AND MYUNG-SOOK CHOI
6.1 INTRODUCTION
The gastrointestinal tract in an adult human contains approximately 1012 microorganisms per milliliter of luminal content and harbors approximately 500 to 1000 distinct bacteria species [1] collectively termed the microbiota. The gut microbiota plays an important role in the innate immune system and host metabolism[1]–[3]. There exists conflicting evidence whether the gut microbiota plays a role in obesity. Bäckhed et al. [4] observed that Germ-free (GF) B6 mice fed a chow diet appeared to be protected from excessive fat accumulation compared to conventional-
ized mice fed the same diet in both males and females. When GF animals were fed a Western-style, high-fat and sugar-rich diet, they appeared to be protected from diet-induced obesity [5]. However, another study reported that the absence of gut microbiota did not provide general protection from diet-induced obesity [6]. Mestdagh et al. [7] also reported that the total body fat content of GF C3H/Orl female mice fed a standard chow diet was not significantly different from that of conventional female mice fed the same diet. Therefore, the protection of GF mice from obesity appears to be dependent on diet and animal strain. Nevertheless, diet-induced obesity is reported to be associated with marked but reversible alterations in the mouse gut microbiota [8]. Hence the gut microbiota represents a therapeutic target with the potential to reverse existing obesity.
