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饮食和表型对糖尿病SHR/N-cp大鼠肝脏及棕色脂肪组织脂肪细胞构成和5'-脱碘酶活性的影响

Effects of diet and phenotype on adipose cellularity and 5'-deiodinase activity of liver and brown adipose tissue of diabetic SHR/N-cp rats.

作者信息

Tulp O L, Hansen C T, McKee K, Michaelis O E

机构信息

Department of Nutrition and Food Sciences, Drexel University, Philadelphia, PA 19104.

出版信息

Comp Biochem Physiol A Comp Physiol. 1991;99(3):457-62. doi: 10.1016/0300-9629(91)90033-9.

DOI:10.1016/0300-9629(91)90033-9
PMID:1678339
Abstract
  1. Groups of lean and obese male SHR/N-cp rats were fed isoenergetic diets containing 54% carbohydrate as cornstarch (CS) or sucrose (SU) plus other nutrients from 5 weeks of age, and measures of adiposity, thyroxine 5' deiodinase (T4-5'DI) activity, and tissue and plasma triiodothyronine (T3) content determined at 9.5 months of age. 2. Body weights (BW) of obese greater than lean, and were greater when fed the SU than CS diet in both phenotypes. Phenotype effects (obese greater than lean) were present for fat pad weights and adipose cellularity in most primary adipose tissue depots, and diet effects (SU greater than CS) were present for epididymal and retroperitoneal depots in both phenotypes. 3. Interscapular brown adipose tissue (IBAT) and IBAT:BW ratios of obese greater than lean, and diet effects (SU greater than CS) were present for lean but not obese rats. Liver T4-5'DI activity and plasma and tissue T3 of lean greater than obese, while IBAT 5'DI activity of obese greater than lean in the CS diet. 4. These results indicate that obesity occurs in the SHR/N-cp rat as the result of hypertrophy and hyperplasia of adipose tissue, and that isoenergetic substitution of simple for complex carbohydrate exaggerates fat accretion in lean but not obese rats. Moreover, the obesity occurs in spite of greater mass, cellularity, and T4-5'DI activity of IBAT, consistent with a thermogenic defect in the obese phenotype of this strain.
摘要
  1. 从5周龄开始,给瘦型和肥胖型雄性SHR/N-cp大鼠喂以等能量饮食,其中碳水化合物含量为54%,分别为玉米淀粉(CS)或蔗糖(SU),并添加其他营养素。在9.5月龄时测定肥胖指标、甲状腺素5'脱碘酶(T4-5'DI)活性以及组织和血浆三碘甲状腺原氨酸(T3)含量。2. 肥胖大鼠的体重高于瘦型大鼠,且在两种表型中,喂食SU饮食时的体重均高于CS饮食。在大多数主要脂肪组织库中,脂肪垫重量和脂肪细胞构成存在表型效应(肥胖型大于瘦型),在两种表型的附睾和腹膜后脂肪库中存在饮食效应(SU大于CS)。3. 肥胖大鼠的肩胛间棕色脂肪组织(IBAT)及其与体重的比值高于瘦型大鼠,在瘦型大鼠中存在饮食效应(SU大于CS),而肥胖大鼠不存在。瘦型大鼠肝脏T4-5'DI活性以及血浆和组织T3水平高于肥胖大鼠,而在CS饮食中,肥胖大鼠的IBAT 5'DI活性高于瘦型大鼠。4. 这些结果表明,SHR/N-cp大鼠肥胖是脂肪组织肥大和增生的结果,简单碳水化合物等量替代复合碳水化合物会加剧瘦型而非肥胖型大鼠的脂肪堆积。此外,尽管IBAT质量、细胞构成和T4-5'DI活性更高,但仍出现肥胖,这与该品系肥胖表型中的产热缺陷一致。

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