Commerford S R, Pagliassotti M J, Melby C L, Wei Y, Hill J O
Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
Am J Physiol Regul Integr Comp Physiol. 2001 Jun;280(6):R1680-7. doi: 10.1152/ajpregu.2001.280.6.R1680.
Obesity results from positive energy balance and, perhaps, abnormalities in lipid and glycogen metabolism. The purpose of this study was to determine whether differences in lipogenesis, retention of dietary fat, and/or glycogenesis influenced susceptibility to dietary obesity. After 1 wk of free access to a high-fat diet (HFD; 45% fat by energy) rats were separated on the basis of 1 wk body weight gain into obesity-prone (OP; > or =48 g) or obesity-resistant groups (OR; < or =40 g). Rats were either studied at this time (OR1, OP1) or continued on the HFD for an additional 4 wk (OR5, OP5). Weight gain and energy intake were greater (P < or = 0.05) in OP vs. OR at both 1 (53 +/- 2 vs. 34 +/- 1 g; 892 +/- 27 vs. 755 +/- 14 kcal) and 5 (208 +/- 7 vs. 170 +/- 7 g; 4,484 +/- 82 vs. 4,008 +/- 72 kcal) wk, respectively. Rats were injected with (3)H(2)O and were either provided free access to an HFD meal containing labeled fatty acids (fed; n = 10 or 11/group) or were fasted (n = 10/group) overnight. The amount of food or (14)C tracer eaten overnight was equivalent between OP and OR rats. In liver, the fraction of (3)H retained in glycogen or lipid was not significantly different between OR and OP groups. Retention of dietary fat in the liver was not increased in OP rats. In adipose tissue, retention of (3)H was approximately 49% greater (P < or = 0.05) in OP1 vs. OR1 and approximately 30% greater in OP5 vs. OR5, but retention of dietary fat was not elevated in OP vs. OR. At the same time, fat pad weight (sum of epididymal, retroperitoneal, mesenteric) was 49% greater in OP1 rats vs. OR1 rats and 65% greater in OP5 vs. OR5 rats (P < or = 0.05). Thus a greater capacity for lipogenesis or retention of dietary fat does not appear to be included in the OP phenotype. The characteristic increase in energy intake associated with OP rats appears to be necessary and critical to accelerated weight and fat gain.
肥胖是由能量正平衡以及可能的脂质和糖原代谢异常导致的。本研究的目的是确定脂肪生成、膳食脂肪潴留和/或糖原生成的差异是否会影响对膳食性肥胖的易感性。在自由摄取高脂饮食（HFD；能量的45%为脂肪）1周后，根据1周的体重增加情况将大鼠分为肥胖倾向组（OP；体重增加≥48克）或肥胖抵抗组（OR；体重增加≤40克）。大鼠在此时（OR1、OP1）进行研究，或者继续给予HFD额外4周（OR5、OP5）。在第1周（53±2克对34±1克；892±27千卡对755±14千卡）和第5周（208±7克对170±7克；4484±82千卡对4008±72千卡）时，OP组的体重增加和能量摄入均显著高于OR组（P≤0.05）。给大鼠注射(3)H₂O，然后要么让它们自由摄取含有标记脂肪酸的HFD餐（喂食组；每组n = 10或11），要么禁食过夜（每组n = 10）。OP组和OR组大鼠过夜摄入的食物量或(14)C示踪剂量相当。在肝脏中，OR组和OP组之间糖原或脂质中保留的(3)H比例没有显著差异。OP组大鼠肝脏中膳食脂肪的潴留没有增加。在脂肪组织中，OP1组的(3)H潴留量比OR1组大约高49%（P≤0.05），OP5组比OR5组大约高30%，但OP组与OR组相比，膳食脂肪的潴留并没有升高。同时，OP1组大鼠的脂肪垫重量（附睾、腹膜后、肠系膜脂肪垫重量之和）比OR1组高49%，OP5组比OR5组高65%（P≤0.05）。因此，脂肪生成能力增强或膳食脂肪潴留似乎并不包含在OP表型中。与OP组大鼠相关的能量摄入特征性增加似乎是体重和脂肪加速增加所必需的且至关重要。
