RESUMEN
Objective@#To study the effects of resistant dextrin (RD) on liver fat deposition in high-fat diet-fed (HFD) mice, and to further explore whether it can regulate the AMPK signaling pathway.@*Methods@#Thirty-six 4-week-old male C57BL/6 mice were randomly divided into three groups: normal control group (chow), high-fat diet group (HFD), and high-fat diet+ resistant dextrin group (HFD+ RD, 10 g·kg-1·d-1). After 12 weeks of intervention, the liver tissues and serum samples were collected. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine transaminase (ALT) levels and liver TG were measured. Liver tissue HE and oil red O staining were performed to observe hepatocyte steatosis and liver fat deposition. Quantitative real-time PCR was performed to detect the relative expression of fatty acid synthesis related genes SREBP1, ACC, SCD1 in the liver tissue, and Western blot was performed to detect relative protein levels of pAMPK, SREBP1, Fasn, and ACC in the liver.@*Results@#Compared with chow group, the body weight gain, fasting blood glucose (FBG), serum TC, LDL-C, HDL-C, and ALT levels were increased in HFD group (P<0.01), and serum AST level was also increased (P<0.05). Moreover, liver oil red O staining revealed that liver fat deposition was much more obvious in HFD group than that in chow group, and liver TG was also increased in HFD group (P<0.01). The mRNA levels of SREBP1 and ACC were increased in HFD group compared with that in chow group, and the protein level of pAMPK was reduced in HFD group (P<0.05). As compared with HFD group, the body weight gain, serum TG, TC, LDL-C, HDL-C and ALT levels were significantly reduced in RD group (P<0.01), and FBG level was also reduced (P<0.05). Moreover, RD treatment alleviated liver fat deposition and TG accumulation (P<0.01). The mRNA levels of SREBP1, ACC, and SCD1 were all reduced in RD group compared with HFD group. The protein level of pAMPK was increased, and the expression of Fasn was reduced with RD treatment (P<0.01).@*Conclusion@#Resistant dextrin improves liver fat deposition and activates the AMPK signaling pathway in HFD-fed mice.
RESUMEN
Objective: To investigate the effect of resistant dextrin on insulin resistance in db/db mice and preliminarily explore potential molecular mechanisms. Methods: Ten 8-week-old db/db mice were randomly assigned into two groups, i.e., control group and resistant dextrin group, which were administered with distilled water and resistant dextrin by gavage for 9 weeks, respectively. Fasting blood glucose (FBG) and body weight were measured every week. Intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) were performed separately at the 8th and 9th week. Fasting serum insulin (FINS) was measured, homeostasis model assessment insulin resistance (HOMA-IR) index was calculated, and triacylglycerol (TAG), total cholesterol (TC), low density lipoprotein-cholesterol (LDL-Ch), high density lipoprotein-cholesterol (HDL-Ch) were detected after the mice were sacrificed. The relative expression of Ir, Irs-1, Pi3k, Akt, and Glut-2 in insulin signaling pathways in the liver was determined by real-time quantitative PCR. The expression of IRS-1, p-AKT, GLUT-2 in the liver were determined by Western blotting. Results: After 9 weeks of treatment with resistant dextrin, the body weight of the resistant dextrin group decreased, but the difference was not statistically significant (P=0.384); FINS decreased, and HOMA-IR index significantly decreased (P=0.032); insulin resistance was significantly improved (all P<0.05); the blood biochemical parameters, including TAG, TC, LDL-Ch, and HDL-Ch were lower, but only LDL-Ch was statistically different (P=0.034); the expression of Ir, Irs-1, Akt, and Glut-2 mRNA in the liver significantly increased (all P<0.05); the expression of IRS-1 and GLUT-2 proteins also significantly increased (P=0.026, P=0.039). Conclusion: Resistant dextrin may improve insulin resistance in db/db mice by enhancing insulin signaling pathway.