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Leptin, the product of the human homologue of the ob gene, which is defective in the obese (ob/ob) mouse, may be a humoral regulator of human adiposity. Plasma leptin concentrations were measured by RIA in 19 normal weight [body mass index (BMI) = 24.5 +/- 0.6 kg/m2] and 19 overweight to obese (BMI = 34.7 +/- 1.2 kg/m2) nondiabetic postmenopausal women on sequential controlled weight-maintaining diets containing 31%, 23%, and 14% of energy as fat, each for 4-6 weeks. Thereafter, the subjects ate a very low fat diet (< 15%) ad libitum; plasma leptin and insulin concentrations, BMI, percent body fat (%BF), and resting energy expenditure were determined after 6 and 8 months. Absolute and adiposity-corrected plasma leptin levels were higher in overweight/obese women (37.7 +/- 3.5 ng/mL; 1.01 +/- 0.07 ng.mL-1.%BF-1) than in normal weight women (16.9 +/- 2.2 ng/mL; 0.57 +/- 0.06 ng.mL-1.%BF-1, both P < 0.005 vs. obese), but were not different between the 31%, 23%, and 14% fat diets when body weight was stable. Plasma leptin was highly correlated with BMI (r = 0.81, P < 0.0001), %BF (r = 0.80, P < 0.0001), and fasting plasma insulin (r = 0.61, P < 0.0001). After 8 months on the ad libitum low fat diet, the women had lost an average of 6.9 +/- 1.0% of body mass (-2.0 +/- 0.3 kg/m2, P < 0.0001). In 15 subjects who lost more than 7% of body mass (-12.3 +/- 1.0%), plasma leptin concentrations decreased (-9.6 +/- 1.9 ng/mL, P < 0.0005), and the decrease of plasma leptin per change of adiposity (delta leptin/delta %BF) was greater in overweight/obese women (3.6 +/- 0.5) than in normal weight women (0.9 +/- 0.4, P < 0.01 vs. obese). In 18 other subjects who lost less than 7% of body mass (-2.7 +/- 0.6%), plasma leptin was unchanged (+1.4 +/- 1.4 ng/mL). Overall, the change of plasma leptin was significantly correlated with change of BMI (r = 0.43, P < 0.02), the change of %BF (r = 0.49, P < 0.005), the change of resting energy expenditure (r = 0.40, P < 0.02), and with the change of plasma insulin independently of changes of body adiposity (r = 0.45, P < 0.01). We conclude that plasma leptin concentrations are: 1) not affected by dietary fat content per se; 2) highly correlated with BMI, %BF, and plasma insulin in both overweight/obese and normal weight women; 3) decreased in parallel with plasma insulin after sustained weight loss; and 4) decreased more in overweight/obese than in normal weight women.

Attenuated regulatory thermogenesis in genetically obese (fa/fa) Zucker rats involves an impaired capacity to increase sympathetic drive to brown adipose tissue in response to dietary stimuli. Young, growing lean rats fed a low protein diet reduce energetic efficiency to compensate for elevated energy intake; however, it is not known if obese rats adapt similarly to chronic protein restriction by decreasing energetic efficiency and whether this would be accompanied by increased brown adipose tissue thermogenic capacity. Lean (Fa/Fa) and obese Zucker rats were either protein-restricted (protein 8% of total energy) or fed a control diet (21% protein) starting at age 5 wk. At 9 wk, oxygen consumption (VO2) was measured in response to an intubated meal of mixed macronutrient composition. Mass-adjusted food intake (i.e., food intake/body weight 0.67) was greater in protein-restricted than in control lean rats, but not different due to diet in obese rats. Mass-adjusted brown adipose tissue uncoupling protein levels were more than 100% greater in protein-restricted vs. control lean rats, but not different between protein-restricted and control obese rats. The uncoupling protein level was not significantly different in control lean vs. obese rats. Energetic efficiency was 40% lower in protein-restricted vs. control lean, but not different in obese rats; however, the efficiency of protein utilization was significantly greater in obese protein-restricted than in obese control rats. Meal-induced energy expenditure (VO2) did not differ significantly due to diet or genotype. In conclusion, protein restriction led to overfeeding in lean rats which appeared to enhance brown adipose tissue thermogenic capacity and decrease energetic efficiency. Protein efficiency increased to more than two times its original value in obese (fa/fa) rats, but otherwise no metabolic accommodation in the capacity for regulatory thermogenesis was observed in this genotype.

Adipose tissue was obtained from six women undergoing liposuction twice at 6-mo intervals. Samples obtained bilaterally from abdomen, inner thigh, and outer thigh had fatty acids quantified by gas chromatography. There were no important differences between sides or over time. The saturates 14:0, 16:0, 18:0, and 20:0 were higher in abdominal adipose than in outer thigh (P < 0.002 for all); 16:1 and 18:1 omega 9 were lower in abdomen vs outer thigh (P < 0.01), whereas 18:1 omega 7 and 20:1 omega 9 were unchanged. Polyunsaturates 18:2 omega 6, 20:3 omega 6, and 20:4 omega 6 were higher in outer thigh than in abdomen (P < 0.06), and inner thigh values were intermediate. These changes in fatty acid composition resulted in lower mean triglyceride melting points from abdomen to inner thigh to outer thigh, and suggest that temperature may influence the selection process determining the variation in adipose fatty acid composition with anatomical location. Because the site-specific differences included essential fatty acids, selective uptake as well as potential differences in in situ fatty acid modification are indicated.

The existence of a restriction fragment length polymorphism (RFLP) closely linked to the fatty locus between the Zucker (Z) and Brown Norway (BN) rat strains allows evaluation of early effects of the fatty (fa) gene using offspring of back-crosses (N2) between F1 females and Zucker obese males. We examined several metabolic characteristics of N2 animals to determine if these hybrid animals exhibited similar characteristics of the obese syndrome to those of Zucker rats. Females from crosses of obese male Zucker (fa/fa) and lean female BN (+/+) rats were back-crossed to their sires, resulting in twelve N2 litters. At 9 weeks of age, liver, spleen, interscapular brown fat (IBAT), and gonadal, retroperitoneal (RP), and inguinal fat depots were removed and weighed. Samples of the RP depot were analyzed for cell size and number. Obese N2 rats were hyperphagic, with body weights in the range of those of obese Zucker rats. Obese N2 rats were also hyperinsulinemic [mean +/- SEM, microU/ml: females, 7.9 +/- 0.6 vs. 82.1 +/- 8.4 (lean vs. obese); males, 10.5 +/- 1.6 vs. 128.5 +/- 13.4 (lean vs. obese)] and mildly hyperglycemic [mean +/- SEM, mg/dl: females, 104.1 +/- 2.0 vs. 139.0 +/- 14.7 (lean vs. obese); males, 100.9 +/- 2.6 vs. 132.0 +/- 2.8 (lean vs. obese) p < or = 0.05]. White fat depots in obese rats were 3 to 7 times heavier than those in lean rats; adipocyte numbers in RP depots were 50% greater in obese than in lean rats; and cell size was more than 3 times larger. IBAT, liver, and spleen were also heavier in obese vs. lean rats, while tail lengths were shorter. Percent lean carcass mass and % carcass protein were about 30% greater in lean vs. obese rats, while % carcass fat in obese rats was 5 times greater than that of lean rats. Thus, phenotypic expression of the fa gene in ZBN hybrid animals, with approximately 25% of their genetic background coming from the BN strain, appears to be similar to that in Zucker rats. Given the similarity of phenotypic expression of the fa gene between the Zucker strain and ZBN hybrids, it is plausible to consider using ZBN hybrids for studies of early manifestations of fa gene action prior to onset of detectable obesity.

Wide ranges in weight and fat gain in response to high-fat diets have been reported in rats. This study measured epinephrine-stimulated lipolysis in adipose tissue of normal weight, 3-mo-old, female Sprague-Dawley rats as a metabolic predictor of "efficient gain" before feeding them a high-fat (84% kcal) diet for 11 wk. Subcutaneous (inguinal) adipose tissue (1-1.5 g) was excised, and the glycerol release was measured after incubation with 0, 10(-7), 10(-5), and 10(-3) M epinephrine. Differences in gain efficiency explained much of the variation in lipid (r = 0.78) and weight (r = 0.83) gain. Low glycerol release by 10(-5) and 10(-3) M epinephrine was significantly correlated to high final fat accumulation. Low and high quartiles based on glycerol release were not different in numbers of adipocytes or food intake but were significantly different in gain efficiency (P = 0.011), final weight (P = 0.036), carcass lipid (P = 0.033), and carcass lean mass (P = 0.017). In conclusion, female Sprague-Dawley rats are preferentially predisposed to efficiency of adipose accumulation on a high-fat diet. This tendency is negatively correlated in the preobese state to the lipolytic response to epinephrine of subcutaneous adipose tissue in vitro.

The effect of a high fat diet in stimulating adipocyte proliferation, as measured by the incorporation of [3H]-thymidine into fat cell DNA, was studied in 22-month-old female Sprague-Dawley rats. Rats were fed a low fat (n = 10) or a high fat diet (n = 9) for a total of six days. On days 4 and 5 of dietary manipulation, rats were injected with 80 microCi/100 g body weight of [3H]-thymidine. Rats were continued on their respective diets for one more day, starved for 72 h and then refed a stock diet for three weeks in order to increase turnover of stroma cells, thus diluting the specific activity of stromal DNA with minimal effect on specific activity of fat cell DNA. The diet groups did not differ significantly with respect to body masses, food intake, parametrial (PARA) and retroperitoneal (RP) depot masses, cell number or cell size. The specific activity of DNA in both PARA and RP depots was greater in the adipocyte than in the stromavascular fraction. Specific activity of fat cells was significantly greater from rats fed the high fat than the low fat diet in both PARA and RP depots. Radioautography of adipose tissue confirmed that there was a greater percentage of adipocyte nuclei labeled in the rats fed the high fat diet. Also, there were few labeled nuclei found in stroma cells. In conclusion, older female rats increased adipocyte proliferation when fed a high fat diet.

It has been reported previously that lateral hypothalamic (LH) lesions alter body composition including reducing adipocyte cellularity in lean and obese Zucker rats. The present experiment was designed to determine whether these alterations in body composition and adipose cell number are secondary to the reduced energy consumption of LH-lesioned rats or to a direct effect of the hypothalamic lesion. Groups of lean and obese Zucker rats, sustaining lesions of the lateral hypothalamus at 10 wk of age, maintained body weight at 72% that of nonlesioned controls until killed at 32 wk. Pair-feeding nonlesioned rats to the intakes of lean and obese LH-lesioned rats produced a reduction in adipocyte number similar to that caused by lesions. However, neither the lean nor obese LH-lesioned rats displayed an increase in cell number when fed a palatable diet that markedly increased carcass lipids. This finding suggests that adipocyte number may be constrained in LH-lesioned rats. These and further observations that 1) lean control rats maintained a higher body weight than the LH-lesioned rats to which they were pair fed and 2) in obese rats, food restriction further reduced protein deposition and elevated plasma insulin relative to comparably fed LH-lesioned obese rats suggest that the LH syndrome is mimicked by simple food restriction.

Obese and lean Zucker rats received bilateral electrolytic lesions of the lateral hypothalamus (LH) at 10 wk of age; control obese and lean rats were sham lesioned. After lesioning the body weights of both obese and lean animals were first reduced and then maintained until being killed (32 wk) at a stable percentage of the nonlesioned control levels (74.5 and 78.3%, respectively). Carcass analysis revealed that the adipose tissue mass was significantly lowered by LH lesions in both the obese and lean animals. Percent carcass fat of lesioned lean rats was less than that of controls (15.0 vs. 23.5%) due to the presence of slightly, but not significantly, smaller and fewer adipocytes. Though absolute levels of fat were likewise lowered in obese rats, their percent carcass fat remained at control levels (52.0 vs. 53.0%) due to equivalent decreases in other body compartments. In the lesioned rats the reduced levels of adipose tissue were associated with a significant reduction in adipocyte number; adipocyte size was unchanged. It is concluded that the lateral hypothalamus of obese Zucker rats participates in the regulation of body weight in the same manner as in lean rats. The differences noted in percent carcass fat between LH lesioned lean and obese Zucker rats are apparently related to the obese animal's known propensity to sequester energy in the form of lipid.

Obese and lean alloxan-diabetic rats were given daily injections of insulin for 9 days. Plasma glucose and insulin concentrations were not different between the two genotypes given comparable amounts of insulin. Carcass fat and epididymal and retroperitoneal fat pad weights increased as the dose of insulin was increased. At each of four doses, fatties had larger fat cells, bigger pads, and more body fat than lean rats. Adipose lipoprotein lipase (LPL) activity per pad or per fat cell was increased by insulin. Except for the lowest dose of insulin, LPL activity was higher in obese rats than in lean rats. LPL activity per cell and cell size were highly correlated. However, when differences in cell size were corrected for, no significant effect of genotype existed. Cardiac LPL activities were different between the two genotypes only in nondiabetic rats. These results suggested that both insulin and some other genetic factors were important in elevating adipose LPL activities and thus fat deposition in obese Zucker rats.

Golden-mantled ground squirrels undergo marked fattening and fat depletion during the prehibernatory and hibernatory phases, respectively, of their annual body weight cycle. Fat regulation was studied by surgical removal (lipectomy) of most of the inguinal-subcutaneous, retroperitoneal, and parametrial fat depots from female squirrels during the weight-gain phase of the annual cycle. Seven weeks after surgery, body weights of lipectomized (Lipx) and Sham-Lipx squirrels were equivalent, although white adipose tissue was not completely recovered in Lipx animals. Lipoprotein lipase (LPL) activity was markedly elevated in subcutaneous adipose tissue of Lipx squirrels, but not in other depots. Plasma triglyceride (TG) levels also were higher in Lipx squirrels 7 weeks after surgery. Changes in LPL activity and plasma TG may contribute to body mass and lipid restoration following lipectomy.

Five-week-old male, Osborne-Mendel rats were fed a control (CON) or high fat diet (HF) (18 and 68% calories as fat, respectively). At 15 weeks of age HF rats weighed more and had a greater percent body fat than CON rats. Half the rats in each diet group were then exercised for 6 weeks on a treadmill. During exercise, food intake was unaffected in both diet groups, while body weight gain was reduced only in HF rats compared to sedentary rats. Exercise lowered fat gain and decreased lipoprotein lipase (LPL) activity in all rats, reduced in vivo lipogenesis in CON rats, and attenuated the development of obesity in HF rats. Following exercise, rats were kept inactive (i.e., detrained) for 2 weeks. Detraining increased food intake, weight gain, fat deposition and LPL activity in comparison to sedentary rats. In CON detrained rats lipogenesis returned to sedentary levels; in all detrained rats retroperitoneal fat cell number increased over that found in exercised rats. Thus, HF feeding induced obesity while exercise attenuated its development. Exercise-induced effects were not long lasting as they were reversed within 2 weeks of exercise termination as evidenced by a rapid increase in food intake, weight gain and lipogenesis.

To determine whether hyperglycemia in the obese hyperglycemic (ob/ob) mouse is related to enhanced activity of the pancreatic beta cell, streptozotocin (175 mg/kg) was injected into lean and ob/ob mice at 8 wk of age. The influence of this injection upon glucose metabolism, adipose cellularity, pancreatic morphology and immunoreactive insulin (IRI) release from isolated pancreatic islets was measured. The plasma glucose levels before and after an oral glucose load were elevated in lean and decreased in ob/ob mice 2 wk after treatment with streptozotocin. By 5 wk after this treatment, a reduced pancreatic islet size, beta cell number and a decreased pancreatic islet IRI release were present in both lean and ob/ob mice. At this time, plasma glucose was still elevated in lean, but depressed in ob/ob mice and the insulin responsiveness in muscle and adipocytes was unchanged. Hyperglycemia abates in the ob/ob mouse as hypersecretion of insulin is diminished, but these observations may not be directly related, since streptozotocin affects key metabolic activities of the livers as well as the pancreatic beta cell. The progression of obesity and status of adipose cellularity are not directly related to hyper-insulinemia, since they are not altered following streptozotocin treatment.

The genetically obese adult Zucker rat (fafa) exhibits reduced thermogenesis when stimulated by physiological agents (cold, catecholamines). Recent evidence suggests that this thermogenic defect may be important in the manifestation of the animal's obesity and that it reflects a reduced thermogenic contribution from brown adipose tissue, the major nonshivering thermogenic site in many mammals. The present study describes the effects of the obese genotype on brown (and white) adipocyte size, number, and lipid content and tissue lipoprotein lipase (LPL) activity. In the obese rats, brown fat depots were increased in mass. This increase could be accounted for by brown fat hypertrophy (due primarily to an increase in the amount of triglyceride present in each cell) rather than hyperplasia (there being no increase in the number of brown fat cells). In addition, unlike the situation in white fat, the brown fat from the obese rats did not exhibit higher LPL activity than did the brown fat from their lean littermates. This absence of an increased capacity for triglyceride uptake, coupled with the greater amount of triglyceride per brown adipocyte, is consistent with a reduction of triglyceride oxidation (and, thus, heat production) in the cells from the obese (v the lean) rats.

The development of spontaneous activity was studied in obese and lean Zucker rats. Rats were given access to activity wheels for 3 hr/day before weaning and for 24 hr/day after weaning. Zucker obese rats are less active than lean rats. This decreased activity occurs at weaning and follows the onset of hyperphagia and obesity. At 8 wk of age exercised lean and obese rats have less total fat and fewer adipocytes than their appropriate controls. Adipose cell size is decreased only in exercised lean rats. When rats are exercised until 8 wk of age and then confined until 6 mo of age, body weight and fat is elevated in these formerly active rats compared to control rats. Adipose cell number is permanently decreased only in formerly active lean rats. Exercise has no long-term effect in decreasing cell number in obese rats.

Ten-week-old lean and obese Zucker rats were sham lesioned or received bilateral, electrolytic lesions of the lateral hypothalamus (LH). They were maintained on a wet mash diet until killing at 15 or 32 wk of age; control lean and obese rats were also killed at 6 and 10 wk. Body composition analyses were performed and adipocyte cellularity of epididymal, retroperitoneal, and subcutaneous depots were calculated. Changes in body composition of LH-lesioned rats, though similar in the two genotypes on an absolute basis, differed on a percentage basis due to the extreme adiposity of the obese rats. Retarded development of protein depots in both lesioned lean and obese rats was apparent at 15 but not 32 wk. Relative to genotypic controls, lesioned lean and obese rats had smaller adipose depots by 32 wk due to decreased adipocyte size in lean rats and reduced adipocyte number in the obese. This genotype-specific response was probably due to the chronic hyperplasia of adipocytes unique to the obese rats. This distinctive developmental pattern of the epididymal depot is discussed.

Obese and lean Zucker rats, 7 wk old, were swim trained or kept sedentary. Another group of obese rats was food restricted and exercised. Half the rats were killed after training for 8 wk, the remainder were retired and killed after an additional 8 wk. Neither treatment decreased adipocyte size in obese rats. Although basal lipolysis per cell was elevated in obese rats, their adipocytes were insensitive to epinephrine at 15 and 23 wk of age. Exercise training did not affect lipolysis. At all ages, adipose lipoprotein lipase (LPL) capacity was higher in obese relative to lean rats. In obese rats, swim training and exercise plus food restriction increased adipose and gastrocnemius LPL activity and depressed plasma insulin and triglyceride levels. All effects of exercise were transient. Thus, exercise training improved some of the metabolic disturbances in the Zucker obese rat but did not normalize adipocyte size, LPL activity, or lipolysis.

Adult rats of various strains became obese when they were fed a highly palatable diet for several months. Analysis of their adipose tissue morphology revealed increases in both adipocyte size and number in most depots. Reintroduction of an ordinary chow diet to such animals precipitated a period of weight loss during which only mean adipocyte size returned to normal. Adipocyte number remained at the elevated level achieved during the period of weight gain. Thus, transient dietary obesity in rats results in a persistent obesity of a purely hyperplastic, nonhypertrophic form. Furthermore, the persistence of the cell number increase suggests that it is the result of proliferation or differentiation rather than of only an increase in the lipid content of a pool of very small and normally undetected adipocytes. An analysis of adipose tissue morphology changes during the course of diet-induced weight gain suggests that the achievement of some specific mean adipocyte size triggers the events that culminate in adipocyte number increase. What mechanisms may link adipocyte size to the formation of new adipocytes remains unknown.

Ad libitum fed golden-mantled ground squirrels undergo marked annual fluctuations in body mass; during the first cycle, peak and trough masses were approximately 291 and approximately 192 g, respectively. Peak masses were significantly higher (9%) during the second than the first cycle, reflecting a 15% increase in fat-free dry mass and a 12% increase in lipid reserves. The reduction in body mass during the weight loss phase was almost entirely due to an 84% decrease in total lipid reserves and reflected a decrease in adipocyte size but not number. All measured fat depots decreased at similar rates, and there was no evidence of preferential utilization or sparing of individual depots. Fat cell size decreased progressively in each depot during the transition from peak to trough masses and did not vary among the several depots at any stage of annual cycle. Adipocyte number increased in parametrial and retroperitoneal depots but not in the subcutaneous fat between the first and second body mass peaks; fat cell size in these two depots decreased by 28 and 20%, respectively, from the first to the second peak in body mass. Reduced lipid filling of adipocytes at the second peak mass, concomitant with adipocyte hyperplasia, suggests that total lipid mass, not simply fat cell size, is regulated during the annual body mass cycle. Maturation of the subcutaneous fat depot before the initial entry into hibernation may be adaptive in providing insulation during dormancy.

Male golden-mantled ground squirrels subjected to surgical removal of substantial portions of inguinal, retroperitoneal, and epididymal adipose tissue [lipectomy (Lipx)] or to sham lipectomy (Sham) during the early prehibernatory fattening phase did not differ in body mass 4 mo later at the time of their annual body weight peaks. Body mass restoration by Lipx squirrels was achieved without compensatory increases in food intake. There was little or no regeneration of epididymal adipose tissue, complete regeneration of the retroperitoneal depot, and an increase in mass of subcutaneous fat of Lipx animals. Epididymal and retroperitoneal adipocytes were equivalent in size in Sham and Lipx squirrels; adipocytes in subcutaneous fat were 20% larger in Lipx than in Sham animals. Generation of the annual body mass cycle of this ground squirrel involves active regulation of the lipid mass.

Seven-week-old female lean and obese Zucker rats were swim trained or kept sedentary for 8 wk. Another group of obese rats was exercised plus food restricted. During exercise training, obese and lean rats ate more but gained less body weight than sedentary controls. Exercise favorably altered body composition, adipose cellularity, and plasma insulin of the obese rat. Exercise plus food restriction more dramatically affected body composition and adipose cellularity but was no more effective in depressing hyperinsulinemia than exercise alone. Following 8 wk of retirement, dorsal fat cell number remained depressed to formerly exercised obese rats whereas adipose cellularity in other depots, body composition, and plasma insulin were similar to control levels. Thus, exercise delayed but did not prevent the full development of obesity in the Zucker rat. Food restriction along with exercise resulted in more permanent effects on adipose cellularity than exercise alone but stunted muscle and skeletal growth.

Glucose oxidation and incorporation into lipid were measured in epididymal adipose tissues and isolated adipose cells of normal and hypophysectomized rats in an effort to determine whether the acute hypoglycemic effect of a systemic growth hormone (GH) injection was related to alterations in the glucose metabolism of adipose tissue. The rats were fed rat chow or a high sucrose diet and received 100 mug GH intraperitoneally 30 minutes or three and one-half hours before sacrifice. Hypophysectomized rats showed a lower plasma glucose as compared with normal rats on both diets. Thirty minutes after a GH injection there was a further decrease of the plasma glucose which, however, was not present in those rats receiving GH three and one-half hours before sacrifice. Adipose tissues from hypophysectomized rats fed the high sucrose diet showed a blunted insulin sensitivity as compared with normal rats on a similar diet. The insulin sensitivity of these tissues was further decreased 30 minutes after a GH injection. Basal glucose metabolism of isolated adipocytes from hypophysectomized rats, as compared with normal rats, was depressed if they were fed rat chow, was at normal levels if they were fed the high sucrose diet and was increased if they were fed the sucrose diet and received triiodothyronine and cortisone supplements. No manipulations of diet or hormonal treatments made the isolated adipocyte from hypophysectomized rats sensitive to insulin either 30 minutes or three and one-half hours after a GH injection. Since basal glucose utilization is not enhanced by GH injection and both the blunted insulin sensitivity of adipose tissue and the absent insulin sensitivity of adipopocytes would be expected to produce hyperglycemia rather than hypoglycemia, it is concluded that immediate systemic effects of a GH injection on carbohydrate metabolism are not related to changes in glucose metabolism of the peripheral adipose tissues.

Thirteen-week-old male, Osborne-Mendel rats were exercised for 6 weeks on a motorized treadmill. Exercise depressed weight gain and cumulative light cycle food intake while cumulative dark cycle and 24-hour total food intake were unaffected. Rats in sedentary and exercise groups were killed 24 hours after the last bout of exercise to assess the effects of chronic exercise and at 48, 60, 72, and 84 hours to determine the effects of exercise termination. Compared to sedentary controls, exercise decreased plasma insulin, epididymal and retroperitoneal depot weight and cell size, and retroperitoneal lipoprotein lipase (LPL) activity. Forty-eight hours after exercise, plasma insulin concentration increased to sedentary levels. By 60 hours, dark cycle food intake was increased above and adipose LPL activity was comparable to sedentary levels. At 84 hours postexercise termination, dark cycle food intake, plasma triglyceride, and epididymal LPL activity per depot and per cell were significantly greater than sedentary values. Exercise termination resulted in a preparatory response for rapid lipid deposition probably arising from increased food intake, plasma insulin, and enhanced LPL activity within 84 hours following termination of exercise.