Diet control of host-gut microbiota interactions in wild type and congenital leptin deficient mice interrelated to development of obesity and its complications

Changes in environmental and genetic factors are vital to development of obesity and its complications. Induction of obesity and type 2 diabetes by both leptin deficient (ob/ob) and high fat diet (HFD) has been verified in an animal model. In the present experiment, three types of diets (normal diet; ND, HFD and high sucrose diet; HSD) and two types of genetic mice (Wide type: WT & ob/ob) were used to explore the relationship among diet supplements, gut microbiota, host genetics and metabolic status. High fat diet increased the body, fat and liver weight in both ob/ob and WT mice, but HSD did not. High fat diet also resulted in dyslipidemia, as well as increased serum transaminases and fasting glucose in ob/ob mice but not in WT mice, while HSD did not. Moreover, HFD led to brain BDNF elevation in WT mice and reduction in ob/ob mice, whereas HSD did not. Both HFD and HSD dominated over host genotypes in altering gut microbiota. Taken together, diets more intensively disturbed the structure of gut microbiota in excess of genetic change, particularly under leptin deficient conditions. Different responses of host genotypes may contribute to the development of metabolic disorder phenotypes linked with gut microbiota alterations.