| Summary: | 碩士 === 國立臺灣大學 === 動物科學技術學研究所 === 104 === Obesity, which has reached epidemic proportions globally, may induce metabolic syndromes in relation to cause of death. Leptin can suppress food intake and thereby lead to weight loss through binding leptin receptor on the hypothalamus. Suppressor of cytokine signaling (SOCS) proteins is one of the mediator reducing leptin sensitivity by inhibition of the phosphorylation of signal transducer and activator of transcription-3 (STAT3), an intracellular leptin-signaling mediator. Lactobacillus rhamnosus GG (LGG) was proved to be highly correlated with SOCS3. The purpose of this study is to expand the comprehension of the relation between L. rhamnosus GG and host energy metabolism. 8-week-old of C57BL/6J male mice were devided into treatment groups, ND (normal diet / PBS treatment) , HFD (high-fat diet / PBS treatment), LL (high-fat diet / 108 CFU L. rhamnosus GG) and LH (high-fat diet / 1010 CFU/mL L. rhamnosus GG). The grow performance, leptin sensitivity, and gut microbiota composition of the mice were assayed. The results show that, L. rhamnosus GG may decrease lipid deposition, high-dosed L. rhamnosus GG effectively maintained leptin sensitivity. In LH group, their body weight dropped off more clearly after leptin i.p. injection than saline i.p. injection. Also, the levels of serum leptin were significantly higher in L. rhamnosus GG -treated mice than those in the PBS-treated mice (p<0.05). In addition, leptin-injected mice presented significantly higher expression of SOCS-3 in hypothalamus than saline-injected mice (p<0.001) in LH group. Finally, L. rhamnosus GG could establish a healthy intestinal environment to prevent the damage cause by pathogens. Ileum sections showed that L. rhamnosus GG -treated mice had significant longer villi length and villi length-crypt depth ratio than HFD group. In conclusion, L. rhamnosus GG plays an important role in modulating serum leptin levels and giving rise to the enhancement of leptin sensitivity and intestinal health in diet-induced obesity.
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