中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2011年
7期
607-609
,共3页
黎慧清%陈璐璐%邓秀玲%张皎月%廖云飞%刘振华%宋惠杰
黎慧清%陳璐璐%鄧秀玲%張皎月%廖雲飛%劉振華%宋惠傑
려혜청%진로로%산수령%장교월%료운비%류진화%송혜걸
追赶生长%胃泌素%脂肪细胞%CCK2R
追趕生長%胃泌素%脂肪細胞%CCK2R
추간생장%위비소%지방세포%CCK2R
Catch-up growth%Gastrin%Adipocyte%CCK2R
24只Wistar大鼠分为正常对照组、限食组、追赶生长组,检测所有大鼠血糖、血脂、血清胃泌素,内脏脂肪体脂比、脂肪细胞CCK2R mRNA和蛋白水平.结果 显示限食组和正常组相比,血清胃泌素水平降低54%(P<0.05),内脏脂肪体脂比减少55%(P<0.05),脂肪细胞CCK2R mRNA和蛋白表达下降(2.19±0.18对3.2±0.24,0.11±0.03对0.15±0.04,P<0.05).追赶生长组血清胃泌素水平分别高于限食组72%和正常组31%(P<0.05),内脏脂肪体脂比高于限食组114%(P<0.05),达到正常对照组水平;同时脂肪细胞CCK2R mRNA和蛋白表达高于正常对照组(4.09±0.59对3.2±0.24,0.25±0.05对0.15±0.04,P<0.05).追赶生长大鼠内脏脂肪优先沉积的机制可能和胃泌素分泌增加及脂肪细胞CCK2R表达增加相关.
24隻Wistar大鼠分為正常對照組、限食組、追趕生長組,檢測所有大鼠血糖、血脂、血清胃泌素,內髒脂肪體脂比、脂肪細胞CCK2R mRNA和蛋白水平.結果 顯示限食組和正常組相比,血清胃泌素水平降低54%(P<0.05),內髒脂肪體脂比減少55%(P<0.05),脂肪細胞CCK2R mRNA和蛋白錶達下降(2.19±0.18對3.2±0.24,0.11±0.03對0.15±0.04,P<0.05).追趕生長組血清胃泌素水平分彆高于限食組72%和正常組31%(P<0.05),內髒脂肪體脂比高于限食組114%(P<0.05),達到正常對照組水平;同時脂肪細胞CCK2R mRNA和蛋白錶達高于正常對照組(4.09±0.59對3.2±0.24,0.25±0.05對0.15±0.04,P<0.05).追趕生長大鼠內髒脂肪優先沉積的機製可能和胃泌素分泌增加及脂肪細胞CCK2R錶達增加相關.
24지Wistar대서분위정상대조조、한식조、추간생장조,검측소유대서혈당、혈지、혈청위비소,내장지방체지비、지방세포CCK2R mRNA화단백수평.결과 현시한식조화정상조상비,혈청위비소수평강저54%(P<0.05),내장지방체지비감소55%(P<0.05),지방세포CCK2R mRNA화단백표체하강(2.19±0.18대3.2±0.24,0.11±0.03대0.15±0.04,P<0.05).추간생장조혈청위비소수평분별고우한식조72%화정상조31%(P<0.05),내장지방체지비고우한식조114%(P<0.05),체도정상대조조수평;동시지방세포CCK2R mRNA화단백표체고우정상대조조(4.09±0.59대3.2±0.24,0.25±0.05대0.15±0.04,P<0.05).추간생장대서내장지방우선침적적궤제가능화위비소분비증가급지방세포CCK2R표체증가상관.
Wistar rats(n=24) were divided into normal control group(NC), food restriction group(FR), and catch-up group(RN). Serum glucose,lipids, gastrin, the ratio of visceral fat to body fat, adipocyte CCK2R mRNA and protein levels were determined. Compared with NC group, FR rats had lower serum gastrin and visceral fat formation. The adipocyte CCK2R mRNA and protein levels of FR rats were lower than those of NC rats. Serum gastrin level of RN rats was higher than those of FR and NC rats(P<0.05). The ratio of visceral fat to body fat in RN rats increased compared with FR rats and was close to that of NC rats. The adipocyte CCK2R mRNA and protein levels of RN rats were higher than those of FR and NC rats. Gastrin and its receptor pathway possibly play a role in the mechanism of visceral fat accumulation in catch-up rats.