Bessesen D H, Rupp C L, Eckel R H
Department of Medicine, University of Colorado Health Sciences Center, CO, USA.
Obes Res. 1995 Mar;3(2):179-89. doi: 10.1002/j.1550-8528.1995.tb00134.x.
Previous measurements of lipoprotein lipase (LPL) activity in adipose tissue (ATLPL) of lean and obese Zucker rats have consistently documented increased activity in obese rats relative to lean. Since LPL is considered to be rate limiting for the delivery of triglyceride fatty acids (TGFA) to muscle and adipose tissue, these data have been used to suggest that the metabolic partitioning of TGFA favors storage over oxidation in obese rats. To document the partitioning of TGFA directly, the fate of 14C labeled oleic acid (42nmols) was fed to lean, obese, and obese Zucker rats fed a hypocaloric diet designed to chronically reduce weight 25% below that of obese controls (reduced-obese). The amount of 14C recovered in CO2 over 6 hours following ingestion was significantly less in obese rats compared to lean (0.45 +/- 0.06 vs. 0.88 +/- 0.09nmols, p = .0004) and less still in the reduced obese group (0.34 +/- 0.06nmols p = .00003). Six hours after ingestion, the quantity of label found in adipose tissue was significantly greater in the obese rats compared to lean (14.51 +/- 1.92 vs. 1.38 +/- 0.29nmols p < .00001), but was intermediate in the reduced-obese group (9.23 +/- 0.98nmols p = .0003). At 2.2 hours there was significantly more label in skeletal muscle of lean rats compared to either obese or reduced-obese (2.33 +/- 0.24; 1.35 +/- 0.04nmols p = .01; 1.41 +/- 0.27nm p = .02). However, at 6 hours these differences between groups were no longer present. These finding Indicate that dietary fat is shunted away from oxidation toward storage in obese Zucker rats. Additionally it appears that there may be a relative block in the oxidation of TGFA that is taken up by skeletal muscle in obese rats. Finally the relative normalization of this partitioning defect in reduced-obese rats is at variance with what was suggested by previous measurements of tissue specific levels of LPL, and suggests an enhanced recirculation of fatty acids from adipose tissue to muscle in reduced-obese rats. This could occur through increased delivery of non-esterified fatty acids (NEFA) to muscle as a result of an increase in net lipolysis.
先前对瘦型和肥胖型 Zucker 大鼠脂肪组织脂蛋白脂肪酶（LPL）活性（ATLPL）的测量结果一致表明，肥胖大鼠的该活性相对于瘦型大鼠有所增加。由于 LPL 被认为是甘油三酯脂肪酸（TGFA）向肌肉和脂肪组织输送的限速因素，这些数据被用来表明，在肥胖大鼠中，TGFA 的代谢分配有利于储存而非氧化。为了直接记录 TGFA 的分配情况，将 14C 标记的油酸（42 纳摩尔）喂给瘦型、肥胖型以及食用低热量饮食的肥胖 Zucker 大鼠，该低热量饮食旨在使体重长期比肥胖对照组降低 25%（减重肥胖型）。摄入后 6 小时内，肥胖大鼠呼出的 CO2 中回收的 14C 量显著低于瘦型大鼠（0.45±0.06 对 0.88±0.09 纳摩尔，p = 0.0004），减重肥胖组更低（0.34±0.06 纳摩尔，p = 0.00003）。摄入 6 小时后，肥胖大鼠脂肪组织中发现的标记物数量显著多于瘦型大鼠（14.51±1.92 对 1.38±0.29 纳摩尔，p < 0.00001），但在减重肥胖组中处于中间水平（9.23±0.98 纳摩尔，p = 0.0003）。在 2.2 小时时，瘦型大鼠骨骼肌中的标记物显著多于肥胖型或减重肥胖型大鼠（2.33±0.24；1.35±0.04 纳摩尔，p = 0.01；1.41±0.27 纳摩尔，p = 0.02）。然而，在 6 小时时，各组之间的这些差异不再存在。这些发现表明，在肥胖 Zucker 大鼠中，膳食脂肪从氧化转向储存。此外，肥胖大鼠骨骼肌摄取的 TGFA 的氧化似乎可能存在相对障碍。最后，减重肥胖型大鼠这种分配缺陷的相对正常化与先前对 LPL 组织特异性水平的测量结果所暗示的情况不同，这表明在减重肥胖型大鼠中，脂肪酸从脂肪组织到肌肉的再循环增强。这可能是由于净脂解增加导致非酯化脂肪酸（NEFA）向肌肉的输送增加而发生的。
