Gayles E C, Pagliassotti M J, Prach P A, Koppenhafer T A, Hill J O
Section of Pediatric Nutrition, University of Colorado Health Sciences Center, Denver 80262, USA.
Am J Physiol. 1997 Jan;272(1 Pt 2):R188-94. doi: 10.1152/ajpregu.1997.272.1.R188.
The purpose of the current study was to examine the enzymatic profile [phosphofructokinase (PFK), beta-hydroxyacyl-CoA dehydrogenase (HADH), and citrate synthase (CS)] in gastrocnemius muscle, heart, and liver in rats allowed ad libitum access to a high-fat diet (HFD, 45% of kcal from corn oil). Male Wistar rats were fed a low-fat diet (LFD, 12% of kcal from corn oil) for a 2-wk baseline period after which some continued on the LFD and others were placed on the HFD. After 1 wk on the HFD, rats were categorized as obesity-resistant (OR), -intermediate (OI), or -prone (OP) on the basis of body weight gain (OR, lower tertile; OI, middle tertile; OP, upper tertile). At 1, 2, and 5 wk, rats from each group were killed (n = 9-14 from each group/time point) after a 24-h fast. At the end of the 5-wk dietary period, weight gain was 114.8 +/- 4.3 in LFD, 125.2 +/- 3.7 in OR, 147.1 +/- 4.1 in OI, and 173.7 +/- 3.5 g in OP rats (OP > OI > OR, LFD; P < 0.001). Energy intake was highly correlated with weight gain on the HFD at each time point (r > or = 0.72, P < 0.001). After 1 wk on the HFD, significant correlations between the ratio of PFK/HADH (an indication of the relative capacity for glycolysis vs. beta-oxidation, r = 0.4, P = 0.03) and HADH/CS (an indication of the capacity for beta-oxidation relative to total oxidative capacity, r = -0.56, P = 0.001) in the gastrocnemius muscle and weight gain were observed. At week 2, significant correlations between these ratios and weight gain were observed in the gastrocnemius, liver, and heart. In contrast, these ratios were not significantly correlated with weight gain at 5 wk. These results suggest that rats most susceptible to weight gain or a HFD are characterized by a continuous increase in energy intake (explaining approximately 50% of the variance in weight gain) and an early tissue enzymatic profile that favors carbohydrate over fat use.
本研究的目的是检测随意摄入高脂饮食（HFD，45%的千卡热量来自玉米油）的大鼠腓肠肌、心脏和肝脏中的酶谱[磷酸果糖激酶（PFK）、β-羟酰基辅酶A脱氢酶（HADH）和柠檬酸合酶（CS）]。雄性Wistar大鼠在为期2周的基线期喂食低脂饮食（LFD，12%的千卡热量来自玉米油），之后一些大鼠继续喂食LFD，另一些则改为HFD。在HFD喂养1周后，根据体重增加情况将大鼠分为抗肥胖（OR）、中度肥胖（OI）或易肥胖（OP）组（OR，体重增加处于较低三分位数；OI，体重增加处于中间三分位数；OP，体重增加处于较高三分位数）。在第1、2和5周，每组大鼠在禁食24小时后处死（每组/每个时间点n = 9 - 14）。在为期5周的饮食期结束时，LFD组大鼠体重增加114.8±4.3克，OR组为125.2±3.7克，OI组为147.1±4.1克，OP组为173.7±3.5克（OP > OI > OR，LFD组；P < 0.001）。在每个时间点，能量摄入与HFD组的体重增加高度相关（r≥0.72，P < 0.001）。在HFD喂养1周后，观察到腓肠肌中PFK/HADH比值（糖酵解与β-氧化相对能力的指标，r = 0.4，P = 0.03）和HADH/CS比值（β-氧化相对于总氧化能力的指标，r = -0.56，P = 0.001）与体重增加之间存在显著相关性。在第2周，在腓肠肌、肝脏和心脏中观察到这些比值与体重增加之间存在显著相关性。相比之下，在第5周这些比值与体重增加无显著相关性。这些结果表明，最易体重增加或易受HFD影响的大鼠的特征是能量摄入持续增加（解释了体重增加中约50%的变异）以及早期组织酶谱倾向于利用碳水化合物而非脂肪。
