Distinct approaches to inhibit fructose-induced obesity

Abstract

Abstract Background Obesity is primarily a consequence of eating disorder. Drugs have been confirmed effective for weight loss more or less related to the functional connectivity in neural networks and metabolic pattern. Functional connectivity, amplitudes of neural signals, and the major ways of ATP productions were analyzed to discover the mechanisms of Metformin and Dapagliflozin. Methods Male ob/ob mice were divided into high-fat-diet fed (HFD), high-fat-diet fed with Metformin, and high-fat-diet fed with Dapagliflozin groups. Functional connectivity amplitude of low-frequency signal fluctuations and rCBV quantification were statistically analyzed in the linear mixed model, meanwhile, metabolic pattern of intestinal cells was also tested. Results Our results showed that Bold signaling responses, functional connectivity, and rCBV quantification tended to be attenuated in the Metformin-treated group compared to the HFD and Dapagliflozin groups. And only Dapagliflozin prevented fructose-induced hyper survival of intestinal cells and hypertrophy of intestinal villus by reducing glycolysis levels. Both Metformin and Dapagliflozin are effective for weight loss. Conclusions Our findings showed distinct mechanisms by which Dapagliflozin and Metformin inhibit obesity related eating disorders, combined use of both drugs Dapagliflozin and Metformin may be more beneficial for clinical improvement in fructose-induced obesity.