PubMed HealthSearch

Biomedical subjects

B A Horwitz

Publications and source records attributed to B A Horwitz.

At least 19 recordsLinked to original sources

Effect of cold on serum substrate and glycogen concentration in young and old Fischer 344 rats.

This investigation evaluated the hypothesis that the age-related decline in cold-induced thermogenesis observed in male (F344) rats is associated with altered substrate concentrations of glucose, lactate, and/or liver and muscle glycogen. Body mass-independent O2 consumption, core temperature, and serum glucose and lactate concentrations were measured at rest and during 4 h of exposure to 5 degrees C in male F344 rats ages 6, 12, and 26 months. At the end of the 4-h cold exposure, liver, soleus, and gastrocnemius tissues were removed, frozen, and analyzed for glycogen concentration and/or citrate synthase activity. Core temperature decreased during cold exposure and was consistently less in the 26-month versus the 6- and 12-month rats. There were no significant differences between the 6- and 12-month-old rats with respect to cold-induced O2 consumption, but measures were significantly lower in the 26-month-old rats. During cold exposure, serum lactate and glucose concentrations increased in the 26-month-old animals compared to those in the 6- and 12-month-old rats, while liver glycogen concentrations decreased in all groups, and gastrocnemius glycogen contents decreased in the 12- and 26-month-old rats. Citrate synthase specific activity (mumol.[min.microgram.protein] -1) did not differ with age. These data suggest that carbohydrate availability (as measured by serum glucose and muscle glycogen) is not a limiting factor in the attenuated cold-exposed thermogenic response of the 26-month-old male F344 rat. However, it appears that the 26-month-old rat may have a diminished capacity to fully oxidize carbohydrate during cold exposure.

Aging

The gene encoding rat liver glycogen phosphorylase contains multiple polyadenylation signal sequences.

RNA blot analysis of rat liver and adipose tissues detected two glycogen phosphorylase (GP)-encoding transcripts. The polymerase chain reaction was used to characterize the 3'-noncoding region of the gene (L-GP) encoding liver-GP (L-GP) from the lean Zucker rat (Fa/Fa). Three distinct classes of colinear cDNA clones were identified by nucleotide (nt) sequence analysis, demonstrating that the L-GP gene contains at least three functional polyadenylation sites. The predominant L-GP transcript was generated by polyadenylation 130 nt 3' from the end of the coding region. A previously uncharacterized L-GP transcript is generated by polyadenylation at 346 nt 3' of the first polyadenylation site. Polyadenylation site selection does not appear to be regulated in a tissue-specific fashion. The relative steady-state L-GP mRNA levels in the different types of adipose tissues were comparable to, or exceeded transcript levels in liver.

Adipose Tissue

Effect of photoperiod on body weight and food intake of obese and lean Zucker rats.

Although the rat is usually not considered to be sensitive to photoperiod, under some experimental conditions photoperiod responses are unmasked. In addition, we have observed photoperiod-induced changes in body weight gain in lean and obese Zucker rats. In this experiment, body mass, food intake, body composition, brown adipose tissue (BAT) thermogenic state, and blood concentrations of corticosterone, insulin, and glucose were evaluated under one of two lighting conditions: a short (10 h light: 14 h dark) or a long (14 h light: 10 h dark) photoperiod. Plasma corticosterone and glucose concentrations measured under fasting conditions were unaffected by photoperiod in either genotype. The amount of BAT mitochondrial protein isolated was less in long photoperiod rats. BAT mitochondrial GDP binding was unaffected by photoperiod in the lean rats, but tended to be lower in long photoperiod obese rats than in short photoperiod obese rats. Although, photoperiod had no effect on daily food intake of rats exposed to the short versus long photoperiod, body mass was heaviest in obese rats raised in long photoperiod. Plasma insulin was increased in both lean and obese rats in long photoperiod. In addition, fat storage appeared to shift to internal depots in the lean rats exposed to long photoperiod. Our data demonstrate that photoperiod does have an effect on male Zucker rats with respect to body weight and fat distribution, with the obese rats being more sensitive to changes in photoperiod than the lean rats.

Adipose Tissue, Brown

Animal models of obesity: genetic aspects.

Among the candidate genes that have been reviewed herein, adipsin, calcitonin, cholecystokin, Gi alpha and Gs subunits of G proteins, insulin I and II, and lipoprotein lipase have all been mapped to specific chromosomes in mouse or rat or both. In none of these cases is the chromosomal location syntenic with murine obesity genes db (on chromosome 4), or ob (on chromosome 6). Thus, all of these genes that code for metabolic modulators that are altered in obese animals but not in lean animals can be ruled out as possible loci of the primary genetic defect, at least for the murine models of obesity. In the case of neuropeptide Y, growth hormone, glucose transporter GLUT-4, the insulin receptor, and glyceraldehyde-3-phosphate dehydrogenase, chromosomal mapping has not yet been reported. However, in each of these cases, the evidence available strongly argues against any one of these physiologic modulators as the likely site of the primary defect for any one of the obesity mutations. Rather, in all of these cases, regardless of whether or not the gene has been mapped, the evidence suggests that posttranscriptional and/or post-translational processes are involved in bringing about the specific alterations in level or activity of the protein product that is seen in the obese animal. Often hormonal regulation is invoked as a possible explanation for the changes observed in gene expression. The hormones most commonly identified as having a mediating effect on the particular metabolic pathways involved are insulin and/or the adrenal glucocorticoids. Since in each of the obese mutants, circulating amounts of these hormones are elevated, severely so in the case of insulin, it would not be surprising to find that they influence the levels and activities of many protein products involved in a variety of central nervous system and peripheral metabolic pathways. Glucocorticoids are known to exert direct effects on gene expression; however, with respect to adipsin gene expression, a direct effect has not been found. Furthermore, insulin itself has been considered as a candidate for the genetic lesion in these animals and has been ruled out by chromosomal localization. Thus, while it may certainly prove to be the case that both insulin and glucocorticoids affect these systems in some way, their effects appear to be indirect. The work by Platt and colleagues in transgenic mice provides the first evidence of signal transduction between an obese mutant allele and the promoter sequence for a gene that shows significantly altered expression in the obese animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals

Exercise decreases fat selection in female rats during weight cycling.

Weight cycling (weight loss and regain) increases fat intake in rats allowed to self-select a diet from protein, carbohydrate, and fat sources. This study reports the effects of exercise on macronutrient self-selection. Female Sprague-Dawley rats (5 mo old) self-selected their diet. After 3 wk, rats were assigned to one of the following three groups: ad libitum fed sedentary (Con), sedentary food restricted to 40% Con intake (R-Sed), or treadmill exercised (20 m/min, 1 h/day, 6 day/wk) food restricted to 40% Con intake (R-Ex). Food restriction was for 3 wk followed by 5 wk of refeeding. This was repeated for a second cycle. During restriction, body weight decreased by 30% in R-Sed and by 33% in R-Ex than in R-Sed, fat regain was greater in R-Sed. By week 3 of refeeding, total caloric consumption did not differ. However, fat selection increased in R-Sed (56% kcal) vs. R-Ex (30%) and Con (35%). Fat selection in R-Sed increased further during cycle 2 (73% kcal). Resting oxygen consumption decreased during food restriction in R-Sed and R-Ex. After refeeding, resting metabolic rate in R-Ex was significantly greater than in R-Sed. In conclusion, weight cycling increases dietary fat selection and adiposity. Exercise mitigates this effect.

Adipose Tissue

The effects of 2-deoxy-D-glucose and sympathetic denervation of brown fat GDP binding in Sprague-Dawley rats.

Central administration of 2-deoxy-D-glucose (2-DG) decreases brown fat thermogenesis. This effect is suggested to be mediated via a central control mechanism. Our study was designed to determine the importance of the sympathetic nervous system in the response of brown fat to intraperitoneal (i.p.) injection of 2-DG. Unilateral denervation of interscapular brown adipose tissue (IBAT) was performed on male Sprague-Dawley rats (300 g body weight). Nine days after surgery, rats were injected i.p. with either saline vehicle (0.9% sodium chloride) or 2-DG (360 mg/kg wt) and then killed one hour later. Sympathetic denervation resulted in 50% decreases in total IBAT protein and in mitochondrial protein recovered. In the denervated lobes, mitochondrial GDP binding (expressed as nmol/mg mitochondrial protein and as total activity recovered) was decreased to 36% and 18%, respectively. Injection of 2-DG did not change mitochondrial protein content in either the innervated or denervated IBAT. In the innervated lobes, 2-DG significantly lowered GDP binding to 55% of that in saline-treated animals, whether expressed per mg mitochondrial protein or as total recovered activity. In contrast, 2-DG did not further decrease GDP binding in the denervated lobes. In conclusion, the effects of i.p. injection of 2-DG on brown fat thermogenesis (as evidenced by GDP binding) appear to be primarily mediated via the sympathetic nervous system.

Adipose Tissue, Brown

Induction of Trichoderma sporulation by nanosecond laser pulses: evidence against cryptochrome cycling.

An important question in the study of photoreceptor action in morphogenesis is whether the chromophore is unidirectionally photobleached, or whether it is recycled, allowing each receptor molecule to be counted more than once. The common soil fungus Trichoderma harzianum grows vegetatively in the dark and sporulates in response to a pulse of blue or UV-A light. Colonies were grown at 26 degrees C, transferred to 3 degrees C, illuminated with non-saturating light, and then put back at 26 degrees C to sporulate. The fluence-response curves for photoinduction in the cold and at 26 degrees C were identical, indicating that there are no enzymatic transduction processes during irradiation. Regions of the perimeter of dark-grown colonies were given single pulses (maximum duration, 30 ns) at 355 nm with a neodymium laser. We obtained a complete fluence-response curve for the laser pulses, which agreed with data for irradiations in the second to minute range. Photoinduction at 3 degrees C, and validity of Bunsen-Roscoe reciprocity from nanoseconds to minutes, support the hypothesis that the inductive event is a simple first-order photobleaching reaction.

Cold Temperature

Neuronal activity in hypothalamic nuclei of obese and lean Zucker rats.

Central neural activity was assessed by measuring relative cytochrome oxidase (CO) activity in the ventromedial nucleus (VMN; thermogenesis regulation), the parvocellular paraventricular nucleus (PVN; feeding regulation), and the magnocellular PVN (secretion of vasopressin and oxytocin) in 10 age-matched pairs of 39- to 42-day-old Zucker rats. When obese (fa/fa) were compared to lean (Fa/Fa) rats, relative CO activity was significantly lower (approximately 10 percent) in the VMN and parvocellular PVN, but not in the magnocellular PVN. Cell diameters did not differ. To determine if there were corresponding differences in levels or release of hypothalamic monoamines, we compared 7 pairs of 90- to 94-day-old lean (Fa/?) and obese (fa/fa) rats at rest and after 2 h of 9 degrees C. Tissue punches from frozen PVN, VMN, and preoptic area (the latter being a site of thermosensitive units modulating VMN output) were assayed. In obese vs. lean noncold-exposed rats, we observed lower concentrations of: 5-hydroxyindoleacetic acid (5HIAA; metabolite of serotonin, 5HT) in the VMN; 3-methoxy-4-hydroxyphenylglycol (MHPG; metabolite of norepinephrine, NE) and NE + MHPG (index of total NE) in the preoptic area; and 3,4-dihydroxyphenylacetic acid (DOPAC; metabolite of dopamine, DA) in the PVN. Additionally, in the VMN, cold exposure resulted in: elevated concentrations of MHPG and MHPG + NE in both lean and obese rats; elevated concentrations of 5HT, 5HIAA, and 5HT + 5HIAA in obese rats, with no significant changes in these variables in lean animals; decreased ratio of 5HIAA/5HT in obese rats and increased ratio in leans. In the preoptic region, cold exposure led to increased concentrations of MHPG, NE + MHPG, 5HT, and 5HT + 5HIAA in obese but not lean rats. In the PVN, 5HT concentrations were increased in cold-exposed obese but not lean rats. Our data support the hypothesis that neuronal activity in obese rats differs from that of lean rats at rest and during cold exposure and suggest that several monoamine systems play a role in such differences.

Adipose Tissue, Brown

Thermogenic responses of younger and older rats to cold exposure: comparison of two strains.

Oxygen consumption and colonic temperatures at rest and during 6 hours at 6 degrees C, body composition, adipose tissue cellularity, and the binding of guanosine 5'-diphosphate (GDP) to isolated brown fat mitochondria were measured in younger (12 months) and older (24 months) male Fischer 344 (F344) and Osborne-Mendel (O-M) rats. The rates of resting mass-independent oxygen consumption, the total cold-induced oxygen consumption expressed as body mass-independent (L.kg body mass-.67) or as lean body mass-independent (L.kg lean body mass-.67) did not differ among the four groups. Although the absolute (g) and the percentage of carcass mass as lean body tissue did not differ within the strains, these measures were significantly greater in the younger and older O-M rats compared to the F344 counterparts. In contrast, cold-exposed O-M rats showed significantly greater total specific GDP binding to isolated brown fat mitochondria than did the O-M animals (an index of brown fat thermogenic capacity); GDP binding did not differ between 12 and 24 months in either strain except when expressed in terms of body mass to the 0.67 power. In general, the results presented here showed no significant age-related loss in oxygen consumption in either strain. However, there did appear to be strain-related differences in brown fat mitochondrial GDP binding, and body composition.

Adipose Tissue

Effect of gender on the response to a high fat diet in aging Fischer 344 rats.

The purpose of this study was to describe the effects of high fat (HF) and low fat (LF) diets in male and female Fischer 344 (F344) rats ages 5, 23 and 27 mo. Rats were fed the diet for 3 mo, and then resting metabolic rate, body composition and adipose tissue cellularity were evaluated. Although body mass was greater in rats fed the HF diet, this difference was due to a rapid increase in mass within the first 2 wk. There was no difference in the rate of body mass gain after this period. Resting mass-independent metabolic rate did not significantly differ due to age, diet or gender. In general, percentage fat mass was greater in rats fed the HF diet and in female than in male rats in both diet groups. However, lean body mass (%) was not altered due to diet or age. Cell number of the retroperitoneal depot increased with age and diet between 5 and 23 mo of age in both male and female rats. There was no effect of age, diet or gender on retroperitoneal cell size or gonadal cell number and size. These data suggest that age, gender and diet do not significantly alter the ability of F344 rats to regulate body composition or fat cell proliferation.

Adipose Tissue

Maternal brown fat metabolism returns to control level by four weeks postweaning in rats.

We studied body composition, white and brown adipose tissue cellularity, lipoprotein lipase activity and metabolic enzyme activity in three groups of rats: nonpregnant controls, lactating dams and nonlactating dams (i.e., dams not permitted to suckle their young). Nine to 11 rats in each group were killed on d 12 postpartum (study d 34) and on d 40 postpartum (study d 62). During lactation, brown fat citrate synthase, beta-hydroxyacylCoA dehydrogenase (HOAD) and lipoprotein lipase activities were significantly lower in the lactating than in the nonlactating dams or virgin controls. Although the nonlactating dams had their pups removed within 24 h after delivery, by d 12 postpartum citrate synthase and HOAD activities were significantly lower than those of nonpregnant controls. By the end of the study there were no differences among the three groups except in the case of HOAD. HOAD activity in the lactation group was significantly lower than in the nonlactation group. White fat cell number in the parametrial depot was significantly increased in the nonlactation groups by d 12 postpartum. In the lactation group, increased white fat cell number in this depot was detectable at d 40 postpartum, when carcass fat stores and fat cells had been repleted. These results demonstrate that both lactating and nonlactating dams undergo cellular hyperplasia, at least in the parametrial depot. This may predispose them to obesity. Also, decreased brown fat metabolism in the nonlactating dams may be contributing to their significantly greater carcass fat content at d 12 postpartum.

3-Hydroxyacyl CoA Dehydrogenases

Hyperprolactinemia prevents short photoperiod-induced changes in brown fat.

Previous studies demonstrated that short photoperiod exposure significantly decreases circulating prolactin levels. The present study investigated the possibility that concomitant changes in brown fat tissue mass, protein content, thermogenic capacity, and carcass composition are dependent on this change in prolactin levels. Male golden (Syrian) hamsters were sham operated and exposed to a short (10L:14D) or long (14L:10D) photoperiod. A third group was implanted with exogenous pituitaries under the right kidney capsule and exposed to a short photoperiod. In experiment I, 4 wk of short- vs. long-photoperiod exposure did not result in significant changes in circulating prolactin levels, nor was there an increase in brown fat mass, protein content, or thermogenic capacity. Four weeks of short-photoperiod exposure did significantly increase carcass lipid content. However, this increase did not occur in hamsters exposed to 4 wk of short photoperiod but made hyperprolactinemic (implanted with two exogenous pituitaries). Ten weeks of short photoperiod significantly reduced circulating prolactin levels. Concomitantly, brown fat mass, protein content, and thermogenic capacity, as well as carcass fat, were increased. These short-photoperiod-induced changes were not observed in similarly exposed hamsters that were made hyperprolactinemic via two implanted pituitaries. In experiment II, similar changes in brown fat and body composition occurred in sham-operated hamsters exposed to 10 wk of short photoperiod. These changes were prevented in hamsters exposed to 10 wk of short photoperiod but made hyperprolactinemic via only one implanted pituitary. These results suggest that decreased prolactin is a necessary condition for the increased brown fat mass, protein content, and thermogenic capacity that occurs when golden hamsters are exposed to short photoperiod.

Adipose Tissue, Brown

Prolactin stimulates food intake in a dose-dependent manner.

Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Adipose Tissue

Prolactin stimulates food intake in the absence of ovarian progesterone.

Increases in serum estrogen inhibit food intake. Conversely, progesterone stimulates food intake, probably via its antiestrogenic action. We have reported that elevated serum prolactin also stimulates food intake in female rats. It is unclear whether this effect is mediated through elevated levels of progesterone. The present study investigated the effects of prolactin on food intake and brown fat activity in the absence of progesterone. Female Osborne-Mendel rats were assigned to one of six groups: sham operated (Sham, n = 10), ovariectomized (OVX, n = 10), OVX + low estrogen (EL, n = 11), OVX + EL + prolactin (PIT, n = 9), OVX + high estrogen (EH, n = 10), and OVX + EH + PIT (n = 8). Estrogen levels were elevated by Silastic implants. Prolactin levels were elevated through pituitary transplants placed under the kidney capsule. Nine days postsurgery, food intake was significantly higher in OVX vs. Sham rats. Estrogen-treated rats (OVX + EL and OVX + EH) had significantly suppressed food intake values compared with both Sham and OVX animals. Finally, hyperprolactinemic rats (OVX + EL + PIT and OVX + EH + PIT) ate significantly more food than did estrogen-treated rats without pituitary explants. Despite the hyperphagia, no significant differences in brown fat GDP binding were observed. These data indicate that prolactin stimulates food intake in the absence of ovarian progesterone.

Adipose Tissue, Brown

Regional blood flow of exercise-trained younger and older cold-exposed rats.

O2 consumption (thermogenesis) and regional blood flows (measured using radioactively labeled microspheres) were evaluated in younger (12 mo) and older (24 mo) sedentary and exercised male Fischer 344 (F-344) rats. These variables were measured at rest and during exposure to 6 degrees C. Exercise-trained rats were run on a motor-driven treadmill 5 days/wk, 1 h/day, at 20 m/min for 6 mo. Resting rates of O2 consumption did not differ with age or exercise training. However, thermogenesis during cold exposure was significantly greater in the older exercised rats than in the other three groups. This difference did not reflect a greater contribution from brown fat as indicated by the fact that total blood flow to the brown fat depots during cold exposure was not greater in the older exercised vs. the other rat groups. Neither exercise training nor age had a significant effect on specific resting blood flow (expressed as ml.min-1.g tissue mass-1) to most of the organs measured, including heart, kidney, brown fat, white fat, and skeletal muscle. The notable exception to this was in the spleen of the older sedentary animals where flow was diminished compared with that in the older exercised animals. We conclude that aging, between 12 and 24 mo of age, and/or exercise training have only a minor effect on regional blood flow of F-344 rats during rest or cold exposure and that the enhanced thermogenesis seen in cold-exposed older exercised vs. sedentary F-344 rats cannot be explained by a greater contribution from brown fat.

Aging

Effect of age and gender on thermoregulation.

Previous investigations have shown that during cold exposure 24-mo-old male Fischer 344 (F344) rats do not thermoregulate as well as do 12-mo-old animals. To determine if this deficiency also occurs in female rats, we measured oxygen consumption (thermogenesis) and colonic temperature of male and female rats 5, 23, and 27 mo of age at rest and during 6 h of exposure to 6 degrees C. In addition, nonshivering thermogenesis (NST) was evaluated from the capacity of brown adipose tissue (BAT) mitochondria isolated from cold-exposed rats to bind guanosine 5'-diphosphate (GDP). Neither age nor gender had a significant effect on resting or cold-exposed oxygen consumption expressed on a mass-independent basis (l/kg body mass0.67) or on a lean body mass independent basis (l/kg lean body mass0.67). The drop in colonic temperature in response to cold was greater in the male rats. However, females exhibited increased BAT mass and relatively constant GDP binding with advancing age, whereas males showed decreased mass and GDP binding. Although the data suggest greater NST capacity in the female rats, rates of cold-induced oxygen consumption were similar in older female vs. male rats. Taken together, our data indicate that gender has a significant impact on thermoregulation and that, under the cold exposure conditions of the study, this effect involves differential heat conservation rather than heat production.

Acclimatization

Cold- and norepinephrine-induced thermogenesis in younger and older Fischer 344 rats.

Older rats exposed to low environmental temperatures show attenuated thermogenesis. However, the mechanisms responsible for this attenuation are not clear. This investigation evaluated the possibility that reduced nonshivering thermogenic capacity is associated with this attenuation. O2 consumption was measured in male Fischer 344 rats ages 7 and 24 mo at thermoneutrality (26 degrees C), during exposure to cold (6 degrees C) for 2 h, and during norepinephrine (NE) infusion (an in vivo measure of nonshivering thermogenesis). In addition, the binding of GDP to isolated mitochondria of brown fat, an in vitro estimate of nonshivering thermogenesis, was also measured. Resting mass-independent O2 consumption (ml.min-1.g body mass -0.67) was not different between the two age groups. However, mass-independent O2 consumption was significantly greater in the younger vs. older rats during 2 h of cold exposure (younger, 2.86 +/- 0.19 l/kg body mass 0.67; older, 2.39 +/- 0.10 l/kg body mass 0.67) and during 20 min of maximum NE infusion (younger, 410.4 +/- 15.1 ml/kg body mass)] was greater in younger than ml/kg body mass 0.67). Brown fat mass [absolute (g) as well as relative (g tissue/kg body mass)] was greater in younger than in older rats. Furthermore, younger rats had significantly greater binding of GDP to isolated mitochondria of brown fat than did the older rats. This effect was true whether the data were expressed as nanomoles bound per milligram mitochondrial protein (32% lower in older rats), bound nanomoles recovered (57% lower), or bound picogram per kilogram body mass 0.67 (59% lower).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown

Cold-induced thermogenesis in younger and older Fischer 344 rats following exercise training.

The inability of old rats to maintain body temperature during cold exposure has been well documented. This study evaluated the effect of exercise on the rates of cold-induced O2 consumption and the contribution of nonshivering thermogenesis (NST) to these rates. Younger (12 mo) and older (24 mo) male Fischer 344 (F344) rats were divided into exercised and sedentary groups. Exercised rats were run on a motor-driven treadmill 60 min/day, at 19-24 m/min, 5 days/wk for 6 mo. At the conclusion of the 6-mo training period, O2 consumption of all four groups was measured at thermoneutrality (26 degrees C) and during 6 h of exposure to 6 degrees C. Rectal temperatures were recorded before and after cold exposure. NST was estimated from the ability of isolated brown fat mitochondria to bind guanosine 5'-diphosphate (GDP). Core temperature of older sedentary rats fell 5.1 +/- 0.4 degrees C after cold exposure (36.3 +/- 0.3 vs. 31.2 +/- 0.8 degrees C). Exercise training in older animals prevented this fall from occurring (36.4 +/- 0.2 vs. 35.3 +/- 0.3 degrees C). Core temperatures of cold-exposed younger exercised and sedentary rats did not differ from thermoneutral values. Exercise did not alter the rates of resting body mass-independent (ml.min-1.kg body mass-0.67) O2 consumption in younger or older rats. However, body mass-independent and lean body mass (LBM)-independent (ml.min-1.g LBM-0.67) cold-induced O2 consumptions of older exercised rats were significantly elevated relative to those of older sedentary animals. This effect of exercise was not seen in younger rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue