临床儿科杂志
臨床兒科雜誌
림상인과잡지
2015年
2期
170-173
,共4页
叶婷婷%黄艳红%方芳%刘冲霄%陈源文%董艳
葉婷婷%黃豔紅%方芳%劉遲霄%陳源文%董豔
협정정%황염홍%방방%류충소%진원문%동염
高脂饮食%子代%大鼠
高脂飲食%子代%大鼠
고지음식%자대%대서
high fat diet%offspring%rat
目的:探索母代高脂饮食对子鼠早期肝脏病理改变的影响及其可能机制。方法 SD雌性大鼠随机分成高脂饮食组(HF组)和对照组,至交配怀孕产仔,哺乳期母鼠继续原饮食并喂养子鼠至其3周龄,取子鼠肝脏组织,观察肝脏病理变化,并检测肝脏内过氧化物酶体增殖物激活受体α(PPARα)、长链脂酰辅酶A合成酶3(ACSL3)、肉毒碱棕榈酰基转移酶1α(CPT-1α)及3-羟基酰基辅酶A脱氢酶(Ehhadh)的基因表达变化。结果 HF组母鼠所育的子鼠3周龄时肝细胞胞浆内可见弥漫性空泡变性,小叶内可见点灶状坏死;HF组子鼠肝脏组织PPARα和Ehhadh基因表达水平明显高于对照组,而ACSL3基因表达则显著低于对照组,差异均有统计学意义(P<0.05);CPT-1α基因表达水平亦高于对照组子鼠,但两组间差异无统计学意义(P=0.19)。结论母鼠孕期持续至哺乳期的高脂饮食可引起子代早期肝内脂肪酸β氧化相关基因PPARα,CPT1α与Ehhadh表达代偿性增加,ACSL3表达降低,但尚不能逆转子代肝脏脂肪变性的发生。
目的:探索母代高脂飲食對子鼠早期肝髒病理改變的影響及其可能機製。方法 SD雌性大鼠隨機分成高脂飲食組(HF組)和對照組,至交配懷孕產仔,哺乳期母鼠繼續原飲食併餵養子鼠至其3週齡,取子鼠肝髒組織,觀察肝髒病理變化,併檢測肝髒內過氧化物酶體增殖物激活受體α(PPARα)、長鏈脂酰輔酶A閤成酶3(ACSL3)、肉毒堿棕櫚酰基轉移酶1α(CPT-1α)及3-羥基酰基輔酶A脫氫酶(Ehhadh)的基因錶達變化。結果 HF組母鼠所育的子鼠3週齡時肝細胞胞漿內可見瀰漫性空泡變性,小葉內可見點竈狀壞死;HF組子鼠肝髒組織PPARα和Ehhadh基因錶達水平明顯高于對照組,而ACSL3基因錶達則顯著低于對照組,差異均有統計學意義(P<0.05);CPT-1α基因錶達水平亦高于對照組子鼠,但兩組間差異無統計學意義(P=0.19)。結論母鼠孕期持續至哺乳期的高脂飲食可引起子代早期肝內脂肪痠β氧化相關基因PPARα,CPT1α與Ehhadh錶達代償性增加,ACSL3錶達降低,但尚不能逆轉子代肝髒脂肪變性的髮生。
목적:탐색모대고지음식대자서조기간장병리개변적영향급기가능궤제。방법 SD자성대서수궤분성고지음식조(HF조)화대조조,지교배부잉산자,포유기모서계속원음식병위양자서지기3주령,취자서간장조직,관찰간장병리변화,병검측간장내과양화물매체증식물격활수체α(PPARα)、장련지선보매A합성매3(ACSL3)、육독감종려선기전이매1α(CPT-1α)급3-간기선기보매A탈경매(Ehhadh)적기인표체변화。결과 HF조모서소육적자서3주령시간세포포장내가견미만성공포변성,소협내가견점조상배사;HF조자서간장조직PPARα화Ehhadh기인표체수평명현고우대조조,이ACSL3기인표체칙현저저우대조조,차이균유통계학의의(P<0.05);CPT-1α기인표체수평역고우대조조자서,단량조간차이무통계학의의(P=0.19)。결론모서잉기지속지포유기적고지음식가인기자대조기간내지방산β양화상관기인PPARα,CPT1α여Ehhadh표체대상성증가,ACSL3표체강저,단상불능역전자대간장지방변성적발생。
Objective To study the impact of maternal high-fat diet during pregnancy and lactation on hepatic steatosis in the early life of offspring rats and its possible mechanism. Methods Female Sprague-Dawley rats were fed either a high fat diet (HF) or control (C) diet for 8 weeks before mating and throughout gestation and ifrst 3 weeks of lactation. The expressions of hepatic fatty acid catabolism related genes, including peroxisome proliferator-activated receptor alpha (PPARα), acyl-CoA syn-thease long-chain family member3 (ACSL3), carnitine palmitoyltransferase-1α(CPT-1α) and 3-hydroxyacyl CoA dehydrogenase (Ehhadh) were determined in offspring liver tissue. The liver pathology was examined in offspring rats at 3 weeks of age. Results Pathohistological ifndings at 3 weeks of age showed that there were diffuse vacuolar degeneration in cytoplasm of hepatocytes and spot necrosis in hepatic lobular in the HF offspring liver. The mRNA expressions of PPARαand Ehhadh genes were markedly increased in the HF offspring as compared to the control group (P<0.05). The mRNA expression of CPT-1αgene was also higher in the HF offspring than that in control group (P=0.19). The level of ACSL3 gene expression, however, was markedly decreased (P<0.05). Conclusions Maternal high fat diet during pregnancy and lactation could result in an increased expression of genes related to hepatic fatty acidβ-oxidation, including PPARα, CPT1αand Ehhadh, but the liver steatosis cannot be reversed in the early life of offspring.