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Levels. BBR reversed the elevated plasma lipid PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26499173 profiles of the NAFLD

Levels. BBR reversed the elevated plasma lipid profiles of the NAFLD + BBR group (TG: 0.70 ?0.16; TC: 1.55 ?0.21; LDL: 0.25 ?0.07) to levels similar to the NCD group (TG: 0.72 ?0.05; TC: 1.66 ?0.06; LDL: 0.24 ?0.03), particularly the TG and LDL levels (Fig. 4a and b). During the entire trial, differences were not observed in the FFA levels between the three groups (P > 0.05, data not shown).Berberine inhibited hepatic lipogenesis and promoted fatty acid oxidation in skeletal muscleThe new synthesis of triglycerides in the liver displayed an increasing trend in the NAFLD group (3.47 ?0.53 vs NCD: 3.05 ?0.56, P > 0.05). Compared with the NAFLD group, BBR significantly reduced hepatic lipogenesis (NAFLD + BBR: 2.25 ?0.44, P < 0.05) (Fig. 5e). The rates of fatty acid oxidation in skeletal muscle decreased dramatically in the NAFLD group (3.07 ?1.70 , P < 0.05), but no difference was observed between the NCD (6.01 ?1.93 ) and NAFLD + BBR (5.04 ?0.98 ) groups (Fig. 5f ).Changes in liver morphologyBerberine decreased Raglu, Ragly, GNG from glycerol and the percent of glycerol converted to glucose ( )Although significant differences in Ragly were not observed between the three groups, Ragly was still the highest in the NAFLD group (69.74 ?27.95) and was similar in the NCD (47.64 ?6.36) and NAFLD + BBR (49.36 ?18.60) groups (Fig. 5a). Raglu was significantly increased in the NAFLD group (111.32 ?51.88, P < 0.05, vs NCD or NAFLD + BBR), whereas the NCD (67.24 ?12.68) and NAFLD + BBR (57.97 ?10.44) groups had similar Raglu values (Fig. 5b). The GNG from glycerol primarily increased in the NAFLD group (16.64 ?7.93, P < 0.05, vs NCD or NAFLD + BBR), whereas it was comparable in the NCD (3.63 ?1.44) and NAFLD + BBR (5.09 ?2.82) groups (Fig. 5c). Similarly, the percent of glycerol converted to glucose displayed the same trend (P < 0.05, NAFLD: 25.82 ?13.03 ; NCD: 7.81 ?3.49 ; NAFLD + BBR: 10.32 ?5.57 ) (Fig. 5d).Under the light microscope, normal liver tissue structures and well-arranged hepatic lobules without liquid droplets were observed in the NCD group (Fig. 6a), whereas a disordered arrangement of the hepatic lobules and fatty degeneration of the hepatocytes was observed in the NAFLD group (Fig. 6b). However, the injury to the hepatic lobules and hepatocyte steatosis observed in the rats in the NAFLD + BBR group were all noticeably improved (Fig. 6c).Discussion NAFLD is already considered a critical hepatic manifestation of metabolic syndrome [4]. In addition, dietary habits and genetic background are thought to be responsible for the pathogenesis and development of hyperlipidemia with NAFLD; therefore, many mouse and rat models of NAFLD have been induced by feeding the animals a high-fat-diet in previous studies [4, 20, 21]. In our study, the rat model of NAFLD was also successfully established by PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28396122 providing nourishment with a high-fat diet for 16 weeks, at which time, the body weight was greatly increased. Meanwhile, increased fasting insulin concentrations, HOMA-IR and decreased ISI were observed in the rats with NAFLD. This result verifiedFig. 4 Changes in the TG and LDL concentrations in the three groups at the 0th, 16th, and 32nd weeks. The TG (a) and LDL (b) levels were higher in the two HFD groups at Leupeptin hemisulfate the 16th week, but the differences between the groups were not significant. Over the next 16 weeks, BBR reversed the elevated TG and LDL levels to levels similar to the NCD group. The data are expressed as the means ?SEM. P < 0.05, NCD vs.

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