Ovarian modulation of lipoprotein lipase activity in white adipose tissue of ground squirrels

Golden-mantled ground squirrels were ovariectomized (OVX) or Sham-OVX during the weight gain phase of the circannual body weight cycle. Other squirrels, OVX or Sham-OVX during the weight loss phase, were subcutaneously implanted with estradiol-filled or empty Silastic capsules. The mass of several fat pads as well as adipose tissue lipoprotein lipase (LPL) activity were determined at autopsy. Ovariectomy at either phase of the annual cycle was without effect on body weight. However, LPL activity of the parametrial fat pad was increased in OVX as compared to Sham-OVX squirrels. Fourteen days of estradiol treatment during the weight loss phase decreased the mass and LPL activity of the retroperitoneal fat depot but did not affect these parameters in perirenal adipose tissue. Although estradiol exerts different or opposite effects on body mass and food intake of rats and ground squirrels, ovariectomy and estrogen treatment affect LPL activity in a similar fashion in both species.     

Adipose tissue lipoprotein lipase activity in rats with obesity-inducing hypothalamic knife cuts

Three experiments examined the effects of obesity-inducing parasagittal hypothalamic knife cuts on adipose tissue lipoprotein lipase (LPL) activity in female rats. Knife cuts induced a 4-fold increase in adipose tissue LPL activity. Knife-cut rats with controlled insulin levels were hyperphagic but showed no increase in adipose tissue LPL activity or body weight gain. Prevention of the hyperphagia by food restriction also blocked the changes in LPL activity and weight gain. Finally, exogenous insulin treatment increased adipose tissue LPL activity in the absence of hyperphagia in neurologically-intact rats. We conclude that increased adipose tissue LPL activity may play a permissive role in the development of hypothalamic obesity, with the increase in enzyme activity being secondary to knife-cut-induced hyperinsulinemia.     

Adipose tissue lipoprotein lipase activity in rats maintained at a reduced body weight

Male rats fed a cellulose-diluted diet maintained a reduced body weight. Adipose tissue lipoprotein lipase (LPL) activity decreased after two days of cellulose feeding, but was not different from chow-fed control levels with weight stabilized at 90% or 70% of the control group. Plasma triglyceride concentration decreased with weight loss and remained depressed with stabilized reduced weight. Regaining lost weight had no effect on LPL activity when compared with chow-fed controls or with levels obtained for the weight-reduced group. However, plasma triglyceride concentration returned to chow-fed control levels with weight gain. The disparity between these results and those obtained in obese human beings lends support to the hypothesis that the increase in adipose tissue LPL activity in weight-reduced obese human beings is indicative of a defect in regulation of adipose tissue metabolism.     

Responses of adipose and muscle lipoprotein lipase to chronic infection and subsequent acute lipopolysaccharide challenge

Infection of male Swiss Webster mice with Toxoplasma gondii or Neospora caninum leads to long-term alterations in energy balance. Following an initial 20 to 30% weight loss in all T. gondii-infected mice, half of the animals regain most of the lost weight (gainers), whereas the others maintain their low body weight (nongainers). Infection with N. caninum does not elicit weight loss. Lipoprotein lipase (LPL), the enzyme responsible for plasma triglyceride (TG) clearance and partitioning among tissues, is under tissue-specific modulation associated with energy balance. It is also a major determinant of infection-induced hypertriglyceridemia. This study aimed to assess the long-term modulation of adipose and muscle LPL activity in mice infected with T. gondii or N. caninum, to evaluate the effects of subsequent acute lipopolysaccharide (LPS) administration, and to relate LPL modulation in these conditions with infection-related changes in body weight gain. Twenty-eight days after infection, LPL activity in muscle of both gainer and nongainer T. gondii-infected mice was reduced by 40 to 50% compared with the levels in controls and N. caninum-infected mice, whereas LPL activity in adipose depots remained unchanged in all infected groups compared to the level in controls. LPS (from Escherichia coli, 100 ng/kg) injection induced a global reduction in adipose LPL in all groups, as assessed 90 min later. In both T. gondii-infected subgroups, muscle LPL was not further reduced by LPS treatment, whereas it was decreased by 40 to 50% in muscles of control and N. caninum-infected mice. Pre-LPS TG levels in plasma were similar in all groups. LPS greatly increased TG levels in plasma in both control and N. caninum-infected animals, whereas it did not alter those of T. gondii-infected gainer or nongainer animals. These results show that (i) independently of the extent of postinfection weight gain, long-term infection with T. gondii chronically reduces muscle LPL, which becomes unresponsive to acute endotoxemia; (ii) modulation of tissue LPL activity during chronic T. gondii infection favors TG partitioning towards adipose tissue; and (iii) skeletal muscle LPL is a key determinant of the acute response of triglyceridemia to LPS.     

Growth and development of gastrocnemius muscle in S 5B/PL and Osborne-Mendel rats overfed during nursing

Three techniques for overfeeding rat pups were used from birth to 24 days of age to assess their effect on growth and development in an obesity susceptible (OM) and an obesity resistant (S 5B/P1) strain of rat. These included: (1) Feeding a semi-purified high fat rather than low fat diet to the dams (alters the energy content of milk); (2) Raising pups in litters of 3 rather than 6; and (3) Force feeding of milk in lieu of any force feeding. In OM rats there was no difference in lean body mass (excludes heart, liver and kidney) (LBM) gastrocnemius muscle weights, cell number and protein content of muscle. Body weights and gastrocnemius muscle triglycerides were significantly higher in OM rats fed the high fat diet than in those fed the low fat diet. S 5B/P1 (S) rats treated in the same manner as OM, showed no significant differences in body weight, LBM, gastrocnemius muscle weight or content of DNA, protein or triglycerides. Protein and DNA for 100 g fresh gastrocnemius muscle were similar for the two strains even though the muscle was 1 1/2 times heavier in OM than in S rats. Muscle triglycerides were higher in OM than in S rats.     

Reduced accumbens dopamine in Sprague-Dawley rats prone to overeating a fat-rich diet

Obese humans and animals exhibit reduced functioning of the dopamine (DA) system in the nucleus accumbens (NAc). The question addressed here is whether this change in NAc DA can be detected in Sprague-Dawley rats that are prone to obesity on a fat-rich diet but still at normal body weight. Rats were subgrouped as “obesity-prone” (OP) or “obesity-resistant” (OR), based on their weight gain during 5 days of access to a high-fat diet, and were then shifted to a lower-fat chow diet before microdialysis testing was performed. The OP rats compared to OR rats exhibited markedly reduced basal levels of DA in the NAc. After a high-fat challenge meal, both OP and OR rats showed a significant increase in extracellular DA and its metabolites; however, the NAc DA of the OP rats still remained at reduced levels. Also, the increase in DA and metabolite levels observed in OR rats after systemic administration of a fat emulsion was not evident in the OP rats, which instead showed no change in DA and a decrease in its metabolites. These results demonstrate, first, that fat can stimulate accumbal DA release and, second, that outbred rats prone to overeating and becoming obese on a palatable, fat-rich diet exhibit reduced signaling in the mesolimbic DA system while still at normal weight, suggesting that it may be causally related to their excess consummatory behavior.     

Repeated hypothalamic stimulation with neuropeptide Y increases daily carbohydrate and fat intake and body weight gain in female rats

Neuropeptide Y (NPY), repeatedly injected in the hypothalamic paraventricular nucleus (PVN), produces dramatic obesity and overeating in female rats maintained on a single nutritionally complete diet. In the present study, we investigated whether these effects could also be obtained in animals with a choice of three pure macronutrients: protein, carbohydrate, and fat. Female rats with indwelling PVN cannulas were injected with NPY (235 pmol) or its saline vehicle every 8 hr for 6 days. A third group was left undisturbed. Consumption of each macronutrient and body weight were measured every 24 hr for 6 days preinjection, 6 days during injections, and 21 days after the injections were terminated. Relative to vehicle or preinjection rates of body weight gain (approximately 1.5 g/day), NPY dramatically enhanced weight gain to a rate of 9.3 g/day and more than doubled total daily food intake. This augmentation was accounted for by increases in carbohydrate intake (+26.4 kcal/day) and fat intake (+48.5 kcal/day), with no significant potentiation of protein consumption. When the NPY injections were terminated, body weight and macronutrient intake returned to control levels within 1 or 2 weeks. These findings are consistent with a role for NPY in hypothalamic mechanisms of macronutrient intake and body weight regulation and suggest that disturbances in brain NPY may contribute to the development of eating and weight disorders.     

Responses of Adipose and Muscle Lipoprotein Lipase to Chronic Infection and Subsequent Acute Lipopolysaccharide Challenge

Infection of male Swiss Webster mice with Toxoplasma gondii or Neospora caninum leads to long-term alterations in energy balance. Following an initial 20 to 30% weight loss in all T. gondii-infected mice, half of the animals regain most of the lost weight (gainers), whereas the others maintain their low body weight (nongainers). Infection with N. caninum does not elicit weight loss. Lipoprotein lipase (LPL), the enzyme responsible for plasma triglyceride (TG) clearance and partitioning among tissues, is under tissue-specific modulation associated with energy balance. It is also a major determinant of infection-induced hypertriglyceridemia. This study aimed to assess the long-term modulation of adipose and muscle LPL activity in mice infected with T. gondii or N. caninum, to evaluate the effects of subsequent acute lipopolysaccharide (LPS) administration, and to relate LPL modulation in these conditions with infection-related changes in body weight gain. Twenty-eight days after infection, LPL activity in muscle of both gainer and nongainer T. gondii-infected mice was reduced by 40 to 50% compared with the levels in controls and N. caninum-infected mice, whereas LPL activity in adipose depots remained unchanged in all infected groups compared to the level in controls. LPS (from Escherichia coli, 100 ng/kg) injection induced a global reduction in adipose LPL in all groups, as assessed 90 min later. In both T. gondii-infected subgroups, muscle LPL was not further reduced by LPS treatment, whereas it was decreased by 40 to 50% in muscles of control and N. caninum-infected mice. Pre-LPS TG levels in plasma were similar in all groups. LPS greatly increased TG levels in plasma in both control and N. caninum-infected animals, whereas it did not alter those of T. gondii-infected gainer or nongainer animals. These results show that (i) independently of the extent of postinfection weight gain, long-term infection with T. gondii chronically reduces muscle LPL, which becomes unresponsive to acute endotoxemia; (ii) modulation of tissue LPL activity during chronic T. gondii infection favors TG partitioning towards adipose tissue; and (iii) skeletal muscle LPL is a key determinant of the acute response of triglyceridemia to LPS.     

Lack of diet-induced thermogenesis in brown adipose tissue of obese medial hypothalamic-lesioned rats

Radiofrequency heat lesions were made in the medial hypothalamus of 12-week old male and female Holtzman rats. Two to three days later rats were offered a palatable cafeteria diet in addition to chow or were fed chow alone for the next 3-4 weeks. Male lesioned rats were only slightly hyperphagic on the chow diet and gained little extra weight. When fed the cafeteria diet, energy intake of male lesioned rats almost doubled in comparison with chow-fed lesioned rats and a very rapid extra weight gain occurred. Despite the marked hyperphagia, thermogenesis in brown adipose tissue was suppressed in the cafeteria-fed lesioned rats, as indicated by low mitochondrial guanosine diphosphate (GDP) binding. In female rats, lesions induced much greater hyperphagia and body weight gain than in male rats, particularly when they ate the cafeteria diet. Again, thermogenesis in brown adipose tissue was suppressed in the cafeteria-fed female lesioned rats. The proportion of energy derived from carbohydrate was not altered by the cafeteria diet in either male or female rats, whether lesioned or not, but there was an increase in the proportion of energy derived from fat at the expense of protein. No sex differences in food selection were observed. The accumulation of body fat was always greater in female lesioned rats than in male lesioned rats for similar food intakes. It is concluded that medial hypothalamic lesions prevent the normal occurrence of diet-induced thermogenesis in brown adipose tissue despite extreme overeating by the rats of a palatable cafeteria diet.     

High fat/sucrose feeding attenuates the hypertension of spontaneously hypertensive rats

To assess the caloric and cardiovascular effects of dietary obesity on an important animal model of hypertension research, 60-day-old male spontaneously hypertensive (SHR) rats were fed either Agway pelleted chow (Pellet), a diet enriched in fat and sucrose (HF/M), or alternated (Cycled) between 2-week periods of HF/M diet and Agway pelleted chow. After 14 weeks, HF/M feeding elevated the body weight of SHR rats by 15% over the body weight of pellet-fed control rats. This relative obesity was accompanied by heavier white (retroperitoneal) and brown (interscapular) fat pads, heavier heart weights, and tachycardia. Paradoxically, the systolic blood pressure levels of SHR rats fed the HF/M diet were reduced. Ruled out as an explanation for the blood pressure reduction was the relative polyunsaturated to saturated fat (P/S) rati of the diet. The hypertension of SHR rats may be due in part to the effects of an underlying metabolic problem that is counteracted by the effects of HF/M feeding; HF/M feeding not only elevated body weight but also reversed the hypoinsulinemia found in pellet-fed SHR rats. The Cycled group evidenced large up-and-down swings in caloric intake that coincided with HF/M and Pellet feeding; this produced modest staircase-like changes in body weight gain. Similar to the HF/M group, the systolic blood pressure level of the Cycled group was also reduced in comparison to the blood pressure level of the Pellet group. However, the Cycled group was found to be more responsive to the pressor effects of intravenous phenylephrine, an alpha-adrenergic agonist.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of the detraining status on high-fat diet induced fat accumulation in the adipose tissue and liver in female rats

The purpose of the present study was to investigate the effects of a high-fat diet (HFD) in previously trained rats that have been detrained for different periods. Two groups of female rats were, first, either treadmill trained for 8 weeks or remained sedentary (Sed). Trained animals, thereafter, remained inactive for 4 weeks (Inact-4 weeks), while fed a standard diet, before being submitted to a high-fat diet (42% kcal of fat) for an additional 2 or 6 weeks. The order was reversed in a 3rd group in which rats were first kept sedentary for 4 weeks before being submitted to the same 8-week training program that ended with the initiation of the HFD (Inact-0 week). Fat accumulation in the mesenteric depot (P<0.05) and in the sum of 3 intra-abdominal (urogenital, retroperitoneal, and mesenteric; P=0.065) tissues in response to the HF feeding was higher in trained rats kept inactive for 4 weeks than in Sed and Inact-0 week animals. Liver triacylglycerol accumulation also showed a tendency to be higher (P<0.07) in Inact-4 weeks than in Inact-0 week rats. These changes were not associated with significant changes in fat cell diameter and number in the mesenteric adipose tissue. When rats in all groups were subdivided into obesity prone (OP) and obesity resistant (OR) on the basis of the change in body weight gain in response to the HFD, liver lipid infiltration was higher (P<0.01) in OP Inact-4 weeks rats than in all other groups. The present results indicate that previously trained rats that have been inactive for a while maintain higher body adiposity in response to a HFD than in freshly inactive and sedentary rats.     

Effects of testosterone on body weight and adipose tissue: role of aromatization

Treatment of castrated male rats with low doses of testosterone propionate (TP; 0.2 mg/day) increases food intake and body weight gain, but long-term treatment with a higher dose of TP (1 mg/day) reduces body weight gain and carcass fat content. Concurrent treatment with androsta-1,4,6-triene-3, 17-dione (ATD), which blocks the aromatization of androgens to estrogens, prevents the weight-reducing effects of high doses of TP. Long-term treatment with 1 mg TP/day also depletes cytoplasmic estrogen receptors and reduces lipoprotein lipase activity in epididymal fat pads. Both of these effects are blocked by concurrent treatment with ATD. These findings suggest that in male rats given high doses of TP, estrogenic metabolites of the androgen may reduce body weight gain by direct effects on adipose tissue metabolism, including lipoprotein lipase activity. These mechanisms may underlie the reductions in body weight and carcass fat content seen in gondadally-intact, sexually-active male rats.     

Ascorbic acid oral treatment modifies lipolytic response and behavioural activity but not glucocorticoid metabolism in cafeteria diet‐fed rats

Aim: To analyse the effects of vitamin C (VC), a potent dietary antioxidant, oral supplementation on body weight gain, behavioural activity, lipolytic response and glucocorticoid metabolism in the early stages of diet‐induced overweight in rats. Methods: Food intake, locomotive activity and faecal corticosterone were assessed during the 14 day trial period. After 2 weeks, the animals were sacrificed and the body composition, biochemical markers and lipolytic response from isolated adipocytes from retroperitoneal white adipose tissue were examined. Results: The intake of a high‐fat diet by rats induced a significant increase in body weight, adiposity and insulin resistance markers as well as a decrease in faecal corticosterone levels compared with standard diet‐fed rats. Interestingly, the animals fed on the cafeteria diet showed a significant increase in the isoproterenol‐induced lipolytic response in isolated adipocytes. Furthermore, this cafeteria‐fed group showed a reduced locomotive behaviour than the control rats. On the other hand, oral VC supplementation in animals receiving the high‐fat diet restored the cafeteria diet effect in some of the analysed variables such as final body weight and plasma insulin to control group levels. Remarkably, increases in locomotive behaviour and a significant decrease in the lipolytic response induced by isoproterenol on isolated adipocytes from animals treated with VC were observed. Conclusion: This work demonstrates that an oral ascorbic acid supplementation has direct effects on behavioural activity and on adipocyte lipolysis in early obesity stages in rats, which could indicate a protective short‐term role of this vitamin against adiposity induced by chronic high‐fat diet consumption.     

Repeated fasting/refeeding elevates plasma leptin without increasing fat mass in rats

It is known that repeated fasting and refeeding increase capacity of fat storage in adipose tissue as an adaptive response to fasting. However, the amount of weight gain in fasted/refed animals falls behind the control level in most rodent studies. Leptin, an adipocyte-derived hormone that impacts on energy homeostasis, may be up-regulated by repeated cycles of fasting and refeeding. In this study, we investigated the adaptive response of leptin to repeated cycles of 1-day fasting and 1-day refeeding for 42 days in rats. The repeated fasting and refeeding (RFR) rats gained less body weight than the controls. Daily food intake of the RFR rats was decreased after Day 16 and remained suppressed. Circulating leptin levels of the RFR rats were significantly elevated at Day 35 compared with the controls and at Day 44 compared with the controls and pair-fed (PF) rats. Leptin mRNA levels of these rats were also significantly increased in retroperitoneal white adipose tissue (RT-WAT) compared with the controls and PF rats. Moreover, hypothalamic proopiomelanocortic (POMC) gene expression was augmented in the RFR rats compared with the controls and PF rats. However, there was no statistical difference in percent visceral fat mass among the experimental groups. Lipoprotein lipase (LPL) mRNA levels of RFR rats were significantly increased in RT-WAT compared with the controls and PF rats. These data indicated that leptin was up-regulated in response to chronic repeated fasting and refeeding cycles without a concomitant increase in adiposity, and the augmented leptin levels were associated with an increase in POMC gene expression, reduced food intake, and diminished body weight gain.     

Lack of diet-induced thermogenesis following lesions of paraventricular nucleus in rats

The effects of electrolytic lesions in the hypothalamus paraventricular nucleus were studied in adult male and female Sprague-Dawley rats, fed different diets, consisting of either palatable human food plus chow (cafeteria diet) or chow alone. The results showed that both cafeteria diet and lesions induced an increase in energy intake and weight gain in rats of both sexes. Oxygen consumption rate and colonic temperature were significantly decreased by lesions, while cafeteria diet increased the same parameters only in intact animals. The lesion decreased weight, protein and DNA, and temperature of brown adipose tissue, while cafeteria diet increased the values considered in brown adipose tissue of sham-injured rats, but not in lesioned animals. The response to norepinephrine administration was significantly greater in intact rats and those fed cafeteria diet. The results suggest that the larger body weight gain observed in lesioned rats, particularly evident in rats fed cafeteria diet, is partly due to the disappearance of diet-induced thermogenesis that depends on the reduced mass and functional activity of brown adipose tissue.     

重组腺相关病毒介导的VLDLR基因对2型糖尿病大鼠脂代谢紊乱的作用

目的： 探索增加极低密度脂蛋白受体 (VLDLR) 基因表达对2型糖尿病大鼠脂代谢紊乱和动脉粥样斑块的影响。方法: 构建携带人VLDLR基因的重组腺相关病毒载体（rAAV-VLDLR）。高脂高糖饮食8周后尾静脉注射小剂量链脲佐菌素(STZ)造2型糖尿病动物模型,VLDLR治疗组大鼠注射rAAV-VLDLR,糖尿病对照组注射rAAV-0。RT-PCR及Western blotting分别检测大鼠骨骼肌、心脏、主动脉、肝脏、脂肪VLDLR mRNA及蛋白表达水平。检测VLDLR基因对血糖、胰岛素、稳态模型胰岛素抵抗指数（HOMA-IR）、甘油三酯（TG）、胆固醇（TC）、脂蛋白脂酶（LPL）活性及主动脉粥样斑块的影响。结果: rAAV-0组大鼠骨骼肌、主动脉、脂肪VLDLR mRNA及蛋白水平低于正常组,VLDLR治疗组VLDLR mRNA及蛋白水平较rAAV-0组有不同程度增加。VLDLR治疗后4、8周的TG及4、8、12周的TC明显降低（P＜0.05）,8周HOMA-IR明显降低(P＜0.05),LPL活性明显增强(P＜0.05),主动脉内膜损伤减轻。结论: 增加VLDLR基因表达对改善2型糖尿病大鼠脂代谢紊乱效果显著,并可在此基础上减轻主动脉粥样斑块程度。     

Site specific effects of acute exercise on muscle and adipose tissue metabolism in sedentary female rats

The effects of endurance exercise on muscle, and adipose tissue metabolism were investigated. Female lean Zucker rats swam for two hours at high intensity. Three groups were examined: pre-exercise control (C), exercised (E) and 24 hours post-exercise (E-24). Exercise increased fat cell lipolysis in the inguinal depot (p less than 0.05) while no effect was detected in the parametrial depot. In contrast, parametrial pad lipoprotein lipase (LPL) activity decreased after exercise with 24 hours post-exercise values being reduced below E and C rats (p less than 0.05). Gastrocnemius LPL activity remained unchanged during exercise while heart LPL increased, E having higher values than C and E-24 (p less than 0.05). Gastrocnemius, but not heart, citrate synthase activity increased with exercise, with E-24 values increased compared to E and C (p less than 0.05). These results demonstrate that adipose tissue's response to exercise is site specific, and suggests a distinct physiological role for different adipose depots. Muscle LPL and citrate synthase activities were modified differently for gastrocnemius and heart, confirming the distinct metabolic response to exercise of these two muscles.     

Metrnl在肥胖小鼠模型中的表达

目的:探讨肥胖对小鼠各组织中Metrnl表达的影响。方法:高脂饮食4个月诱导小鼠肥胖,实时定量PCR与免疫组织化学法检测正常饮食与高脂饮食小鼠肝、骨骼肌、肾、结肠及脂肪组织中Metrnl mRNA与蛋白的表达。结果:高脂饮食增加了小鼠的体质量和白色脂肪量。同时,高脂饮食显著增加了白色脂肪组织Metrnl mRNA与蛋白的水平,但未增加肝、骨骼肌、肾、结肠组织中Metrnl的表达。结论:肥胖特异性增加脂肪组织中Metrnl的表达,从而形成"肥胖-脂肪组织上调Metrnl表达-代谢改善"的反馈调节通路。     

Dietary effects on glycogen and lipoprotein lipase activity in skeletal muscle in man

The influence of short-term adaptation to a fat and protein enriched diet (F+P) and a carbohydrate enriched diet (CHO) on skeletal muscle lipoprotein lipase (LPL) activity and muscle glycogen levels was evaluated in 7 males. Muscle biopsies were taken from the m. vastus lateralis after an uncontrolled, mixed diet (M), after a 3 day F+P diet preceded by intense exercise, and after a 3 day CHO diet. After the F+P diet glycogen concentration was 55% that of the M diet while LPL activity increased by 21% (n. s.). After the CHO diet glycogen levels increased by 82% and LPL activity decreased by 55% compared to the M diet (p<0.01). The changes in LPL after the CHO diet were related to the changes in glycogen concentration (r = 0.98, p<0.01). LPL activity in the control situation was directly related to percent slow twitch (ST) muscle fibre type (r = 0.95, p<0.01). The results suggest that the uptake of fat from the circulation may be actively regulated by the muscle as a function of intramuscular substrate availability and that this regulation may be related to muscle fibre type composition.     

Effects of diet composition on food intake and carcass composition in rats

Since most of the weight-reduced obese humans are in a protein deficit state, this study was designed to examine whether a high protein diet (HP) enhances the restoration of lean body mass and facilitates the maintenance of weight loss. Obesity in rats was produced by 16 weeks of high fat diet (HF) feeding. In the 17th week, all HF-fed obese rats were fed a limited amount of control diet to normalize their body weights, but they still had more body fat content. The HF-fed rats were then divided into subgroups with different diets offered for 5 weeks: HP, HF or chow diet. A control group was fed the chow diet throughout the study. HP feeding maintained normal body weight and carcass composition in weight-reduced obese rats by reducing feeding efficiency levels to within normal ranges. Weight-reduced rats fed a chow diet, however, had more fat mass than controls and HF feeding stimulated weight gain again. Therefore, a HP diet has a higher probability of enhancing weight loss maintenance in weight-reduced obese subjects than does a usual well-balanced diet.