| Epidemiological survey showed that fatty acids intake increased year by year and theproportion of Europeans’fatty acids uptake has risen to28%-42%of the total energy. It iswell documented that high-fat Mediterranean diet rich in n-3polyunsaturated fatty acids incan reduce the morbidity of diabetes in today’s dietary environment. With increasing oftotal energy intake, n-6polyunsaturated fatty acids are generally excessive, but n-3polyunsaturated fatty acids are often seriously inadequate in diet. n-3play a moreimportant role on reducing blood fat and prevent cardiovascular diseases andanti-inflammatory function than n-6. As we known, a single certain types of fatty acidsintake can not balance a reasonable ratio of the two intake nutritionally we advocated.Inflammatory factors activated by Toll-like recognition receptor4(TLR4) can impair insulin signaling pathway. TLR4is a transmembrane receptor regulating the innateimmune response by inducing signaling cascade kinases and activation of transcriptionfactors pathogen immune to produce pro-inflammatory cytokines, chemokines,eicosanoids, reactive oxygen species to affect the innate immune system. When insulinresistance happens, a variety of pro-inflammatory pathways are activated. Inflammatoryfactors directly interfere with the normal function of insulin signal transduction pathway.Ultimately, the development of chronic inflammation may impair insulin sensitivity, whichcan lead to dysfunction of vital organs of the body, closely related to mitochondrialdysfunction if these inflammatory cytokines can not be effectively regulated,In this study, we would explore the proper n-6to n-3dietary ratio of high-fat diet andwhether it can influence the level of TLR4expression levels to reduce inflammation levelto improve the morphology and function of rat skeletal muscle mitochondria, which mayprovide a scientific basis for clinical dietary in the treatment of type II diabetes.Methods:40male SD rats, born in21days, were randomly divided into four groups afteradaptively fed for1week, given the different proportions and types of high-fat diet. Theywere divided into4groups: normal control group, high saturated fatty acids group, highpolyunsaturated fatty acids n-3/n-61:1group, highly polyunsaturated fatty acids n-3/n-61:4. The experimental period was16weeks, rats were fed in single cage with free accessto water and food. Recorded daily food intake and the remaining amount weighed onceevery7days (9:00-10:00), measured the levels of OGTT and ITT by tail-cut every twoweeks from the beginning of the fourth week of experiment. At16week, TG, TC, seruminsulin levels ands inflammatory factors level were detected from eyes blood, and sacrificeanimals (12hours of fasting).Adipose of epididymis and perinephritis were removed andweighed, part of the fresh soleus muscle tissue were collected for the extraction ofmitochondria and the detection of SOD and MDA; another were cut with a sharp blade tinto small pieces (about1mm2of the longitudinal section of the long strip) intopre-cooled2.5%glutaraldehyde (1month of storage life) for electron microscopy;the remaining rat soleus muscle tissue were quickly placed at-80℃for determination ofTLR4protein.Results:1. Compared with NC group, SFA, PUFA1:1and PUFA1:4groups’ weight and body fatratio increased visibly (P <0.05).PUFA1:1compared with PUFA1:4group may play amore obvious improvement on blood lipid metabolism and hyperinsulinemia (P <0.05).2. Glucose tolerance test results show that SFA group, blood glucose regulating abilityof PUFA1:1group and PUFA1:4group rats are not significantly impaired, comparedwith NC group.Insulin tolerance test results show that blood glucose regulatingability of SFA group are severely damaged, however,1:4group has a significantdifference with SFA group (P <0.05).3. ISI level of SFA group and PUFA1:4group decreased visibly (P <0.05), while FPG,FINS and ISI of PUFA1:1group kept a normal level as NC group.4. TLR4, IL-6, TNF-alpha and CRP levels of SFA group and PUFA1:4group elevatedsignificantly higher than the normal group and PUFA1:1group (P <0.05).There is nosignificant difference between NC group and PUFA1:1group,but the data indicatedthat serum inflammatory level of PUFA1:4group seemed increase obviouslycompared with PUFA1:1group(P <0.05).5. TEM results show that SFA rats skeletal muscle mitochondria seems swelling fusionpathological phenomena, PUFA1:4also showed a decrease in the number ofmitochondria and visible lipid droplets.PUFA1:1group and NC group seems in aphysiological condition.6. Compared with NC group,SOD level of the SFA group and PUFA1:4groupdecreased significantly (P <0.01),SOD level of PUFA1:1group has no significantdifference with NC group, but a significant one with PUFA1:4(P <0.05). Comparedwith NC group, MDA levels of SFA and PUFA1:4increased significantly (P <0.05),PUFA1:1group compared with NC group is no significant difference, but a significant one with PUFA1:4group.Conclusion:1. We confirmed that PUFA1:1group can improve blood lipid metabolism and ISI inobesity and insulin resistance rat models, but not PUFA1:4group.2. PUFA1:1group probably can reduce pro-inflammatory Il-6, TNF-α and CRP level ofskeletal muscle in rats by inhibiting TLR4expression.3. PUFA1:1group may make a protective effect on normal morphological andphysiological function of rat skeletal muscle mitochondria, which may be related ton-3decreasing the level of inflammation via TLR4. |
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