Core temperature is regulated, although at a lower temperature, in rats exposed to hypergravic fields

1. In rats acclimated to 23 degrees C (RT rats) or 5 degrees C (CA rats), core temperature (Tc), tail temperature (Tt) and oxygen consumption (VO2) were measured during exposure to a hypergravic field. 2. Rats were exposed for 5.5 h to a 3 g field while ambient temperature (Ta) was varied. For the first 2 h, Ta was 25 degrees C; then Ta was raised to 34 degrees C for 1.5 h. During this period of warm exposure, Tc increased 4 degrees C in both RT and CA rats. Finally, Ta was returned to 25 degrees C for 2 h, and Tc decreased toward the levels measured prior to warm exposure. 3. In a second experiment at 3 g, RT and CA rats were exposed to cold (12 degrees C) after two hours at 25 degrees C. During the one hour cold exposure, Tc fell 1.5 degrees C in RT and 0.5 degree C in CA rats. After cold exposure, when ambient temperature was again 25 degrees C, Tc of RT and CA rats returned toward the levels measured prior to the thermal disturbance. 4. Rats appear to regulate their temperature, albeit at a lower level, in a 3 g field.     

Shivering and nonshivering thermogenesis in exercised cold-deacclimated rats

Norepinephrine (NE)-induced increase in oxygen consumption (VO2) and colonic temperature (Tc) was greater in cold-acclimated rats housed at 4 degrees C for 4 weeks (CA) than warm-acclimated controls housed at 24 degrees C for 4 weeks (WA). On the other hand, shivering activity measured at 4 degrees C was less in CA than in WA, while propranolol administration eliminated the difference between these two groups by enhancing shivering in CA. Wet weight and protein content of interscapular brown adipose tissue (IBAT) were greater in CA than in WA. Following cold acclimation, CA were deacclimated at 24 degrees C for 5 weeks. During deacclimation, half of this latter group were forced to run (15 m.min-1 for 1 h) every day (CD-T) while the remaining rats remained sedentary (CD-S). Shivering activity assessed at 4 degrees C 4 weeks after commencing cold deacclimation was significantly less in CD-T than in CD-S and the difference disappeared following propranolol injection. VO2 and Tc responses to NE injection measured 1, 2 and 5 weeks after commencing cold deacclimation did not differ between CD-S and CD-T. Although IBAT weight was lighter in CD-T than in CD-S, its total protein content was not different between the latter two groups of rats. These results suggest that a greater degree of NE-independent nonshivering thermogenesis (NST) is retained in rats that are exercised during the process of deacclimation as compared with animals that are sedentary. This difference in NST would not seem to be directly related to BAT thermogenic capacity.     

Influence of cold exposure on liver amino acid metabolism enzymes of the rat

The activities of alanine, aspartate and branched-chain amino acid transaminases, glutamate dehydrogenase, glutamine synthetase and adenylate deaminase have been studied in liver of male rats exposed [12 hours at 4 degrees C] or acclimated [15 days at 4 degrees C] to cold temperature. Cold temperature induced an increase of the activities of glutamate dehydrogenase and alanine and aspartate transaminases both in cold-exposed and cold-acclimated animals; adenylate deaminase activity diminished after 15-day cold acclimation. There were not significant changes induced by cold temperature in the activities of the other two enzymes studied. These results agree with a possible direct implication of amino acid utilization by the liver in the context of the overall thermogenic response to cold temperature.     

Interaction between exercise training and cold acclimation in rats

Five groups of 10 rats were used. Group A included sedentary rats kept at 24 degrees C, group B exercised-trained rats and group C rats exposed at -15 degrees C for 2 h every day and kept at 24 degrees C for the remaining time. These 3 groups were kept on this regimen for 10 weeks. In addition group D was acclimated to cold (2 h.d-1 at -15 degrees C) for 6 weeks and subsequently deacclimated at 24 degrees C for 4 weeks. Group E was also acclimated to cold for 6 weeks and during the deacclimation, at 24 degrees C period which lasted 4 weeks, the animals were exercised 2 h per day. Following the 10 week experimental period all animals were sacrificed and DNA and protein content of the IBAT as well as its total mass were measured. The results show significant increases in the cold adapted group. Exercise training which had no effect on brown adipose tissue IBAT at room temperature, caused an accelerated reduction in weight, DNA and protein content of the BAT in rats previously acclimated to cold. In spite of this, the thermogenic response to noradrenaline was significantly enhanced in the group which exercised during the deacclimation period. It is suggested that tissues other than IBAT may explain this enhanced heat production capacity.     

Differential metabolic capacity of mice selected for magnitude of swim stress-induced analgesia.

Maximum oxygen consumption (Vo(2)) elicited by swimming in 20 degrees C water or by exposure to -2.5 degrees C in helium-oxygen (Helox) atmosphere is higher in mice selected for low (LA) than for high (HA) stress-induced analgesia (SIA) produced by swimming. However, this line difference is greater with respect to swim- than to cold-elicited Vo(2). To study the relationship between the analgesic and thermogenic mechanisms, we acclimated HA and LA mice to 5 degrees C or to daily swimming at 20 or 32 degrees C. Next, the acclimated mice were exposed to a Helox test at -2.5 degrees C and to a swim test at 20 degrees C to compare Vo(2) and hypothermia (DeltaT). Cold acclimation raised Vo(2) and decreased DeltaT. These effects were similar in both lines in the Helox test but were smaller in the HA than in the LA line in the swim test. HA and LA mice acclimated to 20 or 32 degrees C swims increased Vo(2) and decreased DeltaT elicited by swimming, but only HA mice acclimated to 20 degrees C swims increased Vo(2) and decreased DeltaT in the Helox test. We conclude that the between-line difference in swim Vo(2) results from a stronger modulation of thermogenic capacities of HA mice by a swim stress-related mechanism, resulting in SIA. We suggest that the predisposition to SIA observed in laboratory as well as wild animals may significantly affect both the results of laboratory measurements of Vo(2) and the interpretation of its intra- and interspecific variation.     

Parallel measurements of heat production and thermogenin content in brown fat cells during cold acclimation of rats

The maximum thermogenic capacity of brown fat cells from control and cold acclimated rats was measured using a continuous-flow microcalorimetric system, The content of the 32.000 D, brown fat specific protein, thermogenin, was measured in the cells used for heat production measurements by competitive ELISA. The ratio between the maximal thermogenic capacity and the amount ofthermogenin for control and cold acclimated rats was compared. It was found that the ratio between the two parameters decreased during cold acclimation due to a decrease in maximal thermogenic capacity and an increase in the amount ofthermogenin, indicating regulation of heat production either at thermogenin or receptor level.     

The effect of progressive hypoxia on respiration in the dogfish (scyliorhinus canicula) at different seasonal temperatures.

1. Dogfish were acclimated to 7, 12 or 17 degrees C and exposed to progressive hypoxia at the temperature to which they had been acclimated. During normoxia, the Q10 values for oxygen uptake, heart rate, cardiac output and respiratory frequency over the full 10 degrees C range were: 2.1, 2.1, 2.1 and 2.5 respectively. Increased acclimation temperature had no effect on cardiac stroke volume or systemic vascular resistance, although there was a decrease in branchial vascular resistance, pHa and pHv. 2. Progressive hypoxia had no effect on heart rate or oxygen uptake at 7 degrees C, whereas at 12 degrees C and 17 degrees C there was bradycardia, and a reduction in O2 uptake, with the critical oxygen tension for both variables being higher at the higher temperature. Cardiac stroke volume increased during hypoxia at each temperature, such that cardiac output did not change significantly at 12 and 17 degrees C. Neither pHa nor pHv changed significantly during hypoxia at any of the three temperatures. 3. The influence of acclimation temperatures on experimental results from poikilotherms is pointed out. Previously-published results show quantitative differences. 4. The significance of the present results with respect to the functioning and location of oxygen receptors is discussed. It is argued that as the metabolic demand and critical oxygen tension of the whole animal are increased at high acclimation temperatures the same must be the case with the oxygen receptor. This would raise the stimulation threshold and could account for the bradycardia seen during hypoxia becoming manifest at higher values of PI,O2, Pa,O2 and Pv,O2 as the acclimation temperature is raised.     

Ventilatory and metabolic responses to cold and hypoxia in intact and carotid body-denervated rats.

The effects of hypoxia on thermoregulation and ventilatory control were studied in conscious rats before and after carotid denervation (CD). Measurements of metabolic rate (VO2), ventilation (V), shivering intensity (SI), and colonic temperature (Tc) were made in groups of eight rats subjected to three protocols. In protocols 1 and 2, at ambient temperature (Ta) of 25 and 5 degrees C, respectively, rats were exposed to normoxia and hypoxia [inspired O2 fraction (FIO2) 0.13-0.11]. In protocol 3, Ta was decreased from 25 to 5 degrees C in 30-min steps of 5 degrees C. Recordings were made in normoxia and hypoxia (FIO2 0.12). The results show that in both intact and CD rats 1) in normoxia, cold exposure increased VO2, V, and SI, and these increases were proportional to the decrease in Ta; 2) hypoxia induced only a transient decrease in SI, and, for a given Ta, VO2 was reduced whereas V and SI were increased; and 3) in CD rats, V increased less during cold exposure in both normoxia and hypoxia; VO2 and Tc were more depressed during hypoxia. It is concluded that 1) the interaction between Ta and FIO2 in the control of V is partly dependent on the carotid body afferents, 2) shivering thermogenesis may be transiently affected by hypoxia independently of the carotid body afferents, and 3) nonshivering thermogenesis may be directly inhibited by hypoxia, especially during cold exposure.     

Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Cold-adapted (CA) rats, unlike non-adapted (NA) ones, give exaggerated metabolic response to acute cold exposure, with paradoxical "overshoot" core temperature (Tc) rise in the cold, and they also give enhanced hyperthermia to central injection of prostaglandin E1 (PGE1). The adaptation-dependent differences might be explained either by the high thermogenic capacity of peripheral tissues in CA rats or by differences in the central processing of regulatory signals. If high tissue metabolism sufficiently explains the extreme responses of CA animals, other hypermetabolic states (with high resting metabolic rate, RMR), e.g. hyperthyroidism, should also be accompanied by enhanced reactions. In the present study thermoregulatory responses to acute cold exposure or to PGE1 were compared in hypermetabolic CA, similarly hypermetabolic thyroxine-treated (T4) and control non-hypermetabolic NA rats (mean RMR = 8.12, 8.47 and 6.03 W kg(-1), respectively). Cold exposure was followed by paradoxical core temperature (Tc) rise of 0.5 to 0.7 degrees C only in CA rats, but by Tc fall (0.8 to 2.1 degrees C) in NA and T4 animals. Identical central stimuli (PGE1) induced larger elevations of Tc and metabolic rate in CA rats than in similarly hypermetabolic T4 or in non-hypermetabolic NA animals (mean Tc rise of 1.9 degrees C in CA vs. 0.9 degrees C in T4 and 1.0 degrees C in NA rats). Vasodilatation thresholds were also similar in NA and T4, but lowered in CA animals. A hypermetabolic status, per se, does not seem to explain the enhanced thermoregulatory responsiveness of CA animals, adaptation-induced central regulatory changes may be more important for the "overshoot" phenomenon.     

Behavioral thermoregulation in Hemigrapsus nudus,the amphibious purple shore crab

The thermoregulatory behavior of Hemigrapsus nudus, the amphibious purple shore crab, was examined in both aquatic and aerial environments. Crabs warmed and cooled more rapidly in water than in air. Acclimation in water of 16 degrees C (summer temperatures) raised the critical thermal maximum temperature (CTMax); acclimation in water of 10 degrees C (winter temperatures) lowered the critical thermal minimum temperature (CTMin). The changes occurred in both water and air. However, these survival regimes did not reflect the thermal preferences of the animals. In water, the thermal preference of crabs acclimated to 16 degrees C was 14.6 degrees C, and they avoided water warmer than 25.5 degrees C. These values were significantly lower than those of the crabs acclimated to 10 degrees C; these animals demonstrated temperature preferences for water that was 17 degrees C, and they avoided water that was warmer than 26.9 degrees C. This temperature preference was also exhibited in air, where 10 degrees C acclimated crabs exited from under rocks at a temperature that was 3.2 degrees C higher than that at which the 16 degrees C acclimated animals responded. This behavioral pattern was possibly due to a decreased thermal tolerance of 16 degrees C acclimated crabs, related with the molting process. H. nudus was better able to survive prolonged exposure to cold temperatures than to warm temperatures, and there was a trend towards lower exit temperatures with the lower acclimation (10 degrees C) temperature. Using a complex series of behaviors, the crabs were able to precisely control body temperature independent of the medium, by shuttling between air and water. The time spent in either air or water was influenced more strongly by the temperature than by the medium. In the field, this species may experience ranges in temperatures of up to 20 degrees C; however, it is able to utilize thermal microhabitats underneath rocks to maintain its body temperature within fairly narrow limits.     

Effects of thermal acclimation on nervous conduction and muscle contraction in the frog Rana temporaria

The effects of season and acclimation temperature on the latency of the leg withdrawal reflex and three of its components have been studied: conduction velocity in the sciatic nerve, spinal conduction time, and contraction time of gastrocnemius muscle. The latency of the leg withdrawal reflex was markedly shortened by cold acclimation: the reaction times were at 6 degrees C 1.54 s in 4 degrees C acclimated and 3.97 s in 24 degrees C acclimated winter frogs. Also, the temperature dependence of the reflex latency was reduced by cold acclimation. Thus, frogs acclimated to cold responded to external stimuli in cold more rapidly than warm-acclimated ones. This cold adaptation of the reflex could not be explained by changes in its studied components. These made up only one-tenth of the reflex response time, and either did not show significant cold acclimation (muscle contraction and spinal conduction times in summer) or showed inverse acclimation, especially when measured at high temperatures (i.e. conduction velocities were reduced by acclimation to cold). Thus, the cold acclimation of the reflex response probably resides in the sensory component of the response. The inverse temperature adaptation response of conduction velocities may reflect a reduced ion permeability across cellular membranes in cold which decreases metabolic energy expenditure during inactive periods.     

Deer mouse aerobic performance across altitudes: effects of developmental history and temperature acclimation

Aerobic physiology at high altitudes has been studied in many animals. Prior work on laboratory-bred deer mice (a species with a wide altitudinal range) showed depression of aerobic capacity at high altitude, even after acclimation. However, wild deer mice show no reduction in thermogenic performance at high altitude, and performance limits seem to be due to physiological and anatomical adjustments to environmental temperature and not to oxygen availability. We asked whether across-altitude performance differences exist in deer mice after accounting for temperature acclimation (approximately 5 degrees and 20 degrees -25 degrees C) and prenatal and neonatal development altitude (340 vs. 3,800 m). We measured maximal thermogenic oxygen consumption (VO2sum) in cold exposure and ran mice on a treadmill to elicit maximal exercise oxygen consumption (VO2max). We found a 10% reduction in VO2max at 3,800 m compared with that at 340 m; thus, the mice were able to compensate for most of the 37% reduction in oxygen availability at the higher altitude. Development altitude did not affect VO2max. There was no effect of test altitude or development altitude on VO2sum in warm-acclimated animals, but both test and development altitude strongly affected VO2sum in cold-acclimated mice, and compensation for hypoxia at 3,800 m was considerably less than that for exercise.     

Effects of acclimation temperature on thermal tolerance and membrane phospholipid composition in the fruit fly Drosophila melanogaster

Adaptative responses of ectothermic organisms to thermal variation typically involve the reorganization of membrane glycerophospholipids (GPLs) to maintain membrane function. We investigated how acclimation at 15, 20 and 25 degrees C during preimaginal development influences the thermal tolerance and the composition of membrane GPLs in adult Drosophila melanogaster. Long-term cold survival was significantly improved by low acclimation temperature. After 60 h at 0 degrees C, more than 80% of the 15 degrees C-acclimated flies survived while none of the 25 degrees C-acclimated flies survived. Cold shock tolerance (1h at subzero temperatures) was also slightly better in the cold acclimated flies. LT50 shifted down by ca 1.5 degrees C in 15 degrees C-acclimated flies in comparison to those acclimated at 25 degrees C. In contrast, heat tolerance was not influenced by acclimation temperature. Low temperature acclimation was associated with the increase in proportion of ethanolamine (from 52.7% to 58.5% in 25 degrees C-acclimated versus 15 degrees C-acclimated flies, respectively) at the expense of choline in GPLs. Relatively small, but statistically significant changes in lipid molecular composition were observed with decreasing acclimation temperature. In particular, the proportions of glycerophosphoethanolamines with linoleic acid (18:2) at the sn-2 position increased. No overall change in the degree of fatty acid unsaturation was observed. Thus, cold tolerance but not heat tolerance was influenced by preimaginal acclimation temperature and correlated with the changes in GPL composition in membranes of adult D. melanogaster.     

The after-effects of temperature and irradiance during early growth of winter oilseed rape (Brassica napus L. var. oleifera, cv. Górczański) seedlings on the progress of their cold acclimation

Experiments performed under controlled conditions showed that level of PPFD (photosynthetic photon flux density) during early seedlings growth (preceding cold acclimation at +2 °C) was not the key factor for the development of frost resistance. It did not modify the beneficial effects of prehardening (Rapacz 1997, in this issue) at moderately low (+12 °C) day temperature. Now I have shown that the increase of PPFD may replace to some extent prehardening in the development of frost resistance. It was particularly seen in non-prehardened plants, which had been grown under warm-day (+20 °C) conditions. Prehardening performed under controlled conditions, as well as seedlings growth under natural autumn conditions in the field, allowed to maintain a high net-photosynthesis rate at chilling temperatures. A net-photosynthesis rate during cold acclimation at +2 °C corresponded well with higher frost resistance. As a result, seedlings non subjected to prehardening and grown before cold acclimation under low PPFD acclimated better, if the cold treatment was applied only at nights (+20/2 °C day/night). Only under such conditions the photosynthetic rate was sufficiently high to allow plants to reach a higher level of frost resistance. All other plants acclimated better when they were exposed to the hardening temperature continuously during days and nights (+2/2 °C day/night).     

The effects of acclimation temperature on pituitary and plasma beta-endorphin in rats at 32.5 degrees C

Endocrine and thermoregulatory responses were studied in male rats exposed to heat (32.5 +/- 0.1 degrees C) from acclimation temperatures of either 24.5 +/- 0.1 degrees C or 29.2 +/- 0.1 degrees C. After 1 hr in the heat, evaporative water loss and tail skin temperature changes in the 24.5 degrees C acclimated rats were greater than in the 29.2 degrees C acclimated rats; both groups displayed similar changes in metabolic rate and rectal temperature. At the respective acclimation temperatures, 29.2 degrees C rats displayed lowered plasma thyroid hormones, elevated beta-endorphin-like immunoreactivity (beta-END-LI) in the plasma, neurointermediate and anterior lobes of the pituitary gland, and no change in plasma corticosterone levels compared to 24.5 degrees C rats. After exposure to 32.5 degrees C for 1 hr, both groups of rats maintained similar plasma corticosterone levels; however, only the 24.5 degrees C group increased plasma thyroxine and beta-END-LI. These data suggest that beta-endorphin may be involved in body temperature regulation during acclimation to elevated environmental temperatures.     

Thermogenic capabilities of the opossum Monodelphis domestica when warm and cold acclimated: similarities between American and Australian marsupials

1. Monodelphis domestica is a small marsupial mammal from South America. Its thermogenic abilities in the cold were determined when the opossums were both warm (WA) and cold (CA) acclimated. Maximum heat production of M. domestica was obtained at low temperatures in helium-oxygen. 2. Basal metabolic rate (BMR) in the WA animals was 3.2 W/kg and mean body temperature was 32.6 degrees C at 30 degrees C. These values were lower than those generally reported for marsupials. Nevertheless, these M. domestica showed considerable metabolic expansibility in response to cold. Sustained (summit) metabolism was 8-9 times BMR, while peak metabolism was 11-13 times BMR. These maximum values were equal to, or above, those expected in small placentals. 3. Cold acclimation altered the thermal responses of M. domestica, particularly in warm TaS. However, summit metabolism was not significantly increased; nor did M. domestica show a significant thermogenic response to noradrenaline, which in many small placentals elicits non-shivering thermogenesis. The thermoregulatory responses of this American marsupial were, in most aspects, similar to those of Australian marsupials. This suggests that the considerable thermoregulatory abilities of marsupials are of some antiquity.     

Effects of hypoxia and cold acclimation on thermoregulation in the rat.

The effects of hypoxia (inspired O2 fraction = 0.12) on thermoregulation and on the different sources of thermogenesis were studied in rats before and after periods of 1-4 wk of cold acclimation. Measurements of metabolic rate (VO2) and body temperature (Tb) were made at 5-min intervals, and shivering activity was recorded continuously in groups of rats subjected to three protocols. In protocol 1, rats were exposed to normoxia to an ambient temperature (Ta) of 5 degrees C for 2 h. In protocol 2, at Ta of 5 degrees C, rats were exposed for 30 min to normoxia, then for 45 min to hypoxia, and finally for 30 min to normoxia. In protocol 3, in the non-cold-acclimated (NCA) rats, Ta was decreased from 30 to 5 degrees C in steps of 5 degrees C and of 30-min duration while in cold-acclimated (CA) rats at 5 degrees C for 4-wk, Ta was increased from 5 to 30 degrees C in steps of 5 degrees C and of 30-min duration. Recordings were made in normoxia and in hypoxia on different days in the same animals. The results showed that 1) in NCA rats, cold exposure in normoxia induced increases in VO2 and shivering that were proportional to the decrease in Ta; 2) in CA rats in normoxia, for a given Ta, VO2 and Tb were higher than in NCA rats, whereas shivering was generally lower; and 3) in both NCA and CA rats, hypoxia induced a transient decrease in shivering and a sustained decrease in nonshivering thermogenesis associated with a marked decrease in Tb that was about the same in NCA and CA rats. We speculate that hypoxia acts on Tb control to produce a general inhibition of thermogenesis. Nonshivering thermogenesis is markedly sensitive to hypoxia, especially demonstrable in CA rats; a recovery or even an increase in shivering can compensate for the decrease in nonshivering thermogenesis.     

The effect of cold acclimation and deacclimation on cold tolerance,trehalose and free amino acid levels in Sitophilus granarius and Cryptolestes ferrugineus (Coleoptera)

Canadian and French laboratory strains of Sitophilus granarius (L.) and Cryptolestes ferrugineus (Stephens) were cold acclimated by placing adults at 15, 10 and 5 degrees C successively for 2wk at each temperature before deacclimating them for 1wk at 30 degrees C. Unacclimated S. granarius had an LT(50) (lethal time for 50% of the population) of 12days at 0 degrees C compared with 40days after the full cold acclimation. At -10 degrees C, unacclimated C. ferrugineus had an LT(50) of 1.4days compared with 24days after the full acclimation. Cold acclimation was lost within a week after returning insects to 30 degrees C. Trehalose, as well as the amino acids proline, asparagine, glutamic acid and lysine were higher in cold acclimated insects for both species. For S. granarius, glutamine was higher in cold acclimated insects and isoleucine, ethanolamine and phosphoethanolamine, a precursor of phospholipids, were lower in cold acclimated insects. For C. ferrugineus, alanine, aspartic acid, threonine, valine, isoleucine, leucine, phenylalanine and phosphoethanolamine were higher in cold acclimated insects. For both species tyrosine was lower in cold acclimated insects. There were small but significant differences between Canadian and French strains of S. granarius, with the Canadian strain being more cold hardy and having higher levels of trehalose. There were small but significant differences between male and female S. granarius, with males being more cold hardy and having higher levels of proline, asparagine and glutamic acid. In conclusion, high levels of trehalose and proline were correlated with cold tolerance, as seen in several other insects. However, correlation does not prove that these compounds are responsible for cold tolerance, and we outline further tests that could demonstrate a causal relationship between trehalose and proline and cold tolerance.     

Attenuated response to cold of brown adipose tissue of mice made obese with gold thioglucose

In a first study, mice made obese with gold thioglucose became hypothermic when exposed to 4 degrees C. In a second study, lean mice and mice made obese with gold thioglucose (dynamic phase) were acclimated to 14 degrees C for up to 2 weeks and their brown adipose tissue was studied. The cold-induced increase in thyroxine 5'-deiodinase activity was initially slightly smaller in obese mice, but by 24 h and 2 weeks in the cold the activity of thyroxine 5'-deiodinase was the same in lean and obese mice. Unexpectedly, the elevated activity of 5'-deiodinase returned to the low level seen in warm-acclimated mice in both lean and obese mice after 2 weeks of cold acclimation. In gold thioglucose obese mice, a progressive cold-induced increase in the binding of guanosine diphosphate to isolated mitochondria, an index of both acute thermogenic activation and a long-term increase in uncoupling protein concentration, paralleled that seen in normal lean mice and remained at a high level after 2 weeks in the cold, although still remaining slightly lower than normal. It is not clear how a high level of mitochondrial GDP binding is maintained in cold-acclimated mice at the same time as a low level of thyroxine 5'-deiodinase activity when both are believed to be controlled by the sympathetic nervous system. We conclude that the gold thioglucose obese mouse can activate its brown adipose tissue fairly normally when it is exposed to cold, but that some attenuation of this process may contribute to the impaired survival of this mouse at low temperatures.     

The effects of temperature- and oxygen-acclimation on phospholipids of goldfish (Carassius auratus L.) brain microsomes

Brain microsome phospholipids and their acyl groups, from temperature and oxygen acclimated goldfish, were investigated. At the lower acclimation temperature (5C) the proportion of ethanolamine- to choline-glycerophosphatides (GPE/GPC) was increased, and the proportion of phosphatidal ethanolamine value decreased. A rise in the n-6/n-3 fatty acyl group also occurred in cold acclimation. Irrespective of acclimation temperature, 25 degrees C or 5 degrees C, a partial replacement of GPC by GPE occurred when the concentration of oxygen was increased; conversely the GPE/GPC ratio decreased at the hypoxic level. The plasmalogen GPE content increased as the oxygen concentration was raised. A rise in the n-6/n-3 ratio, for ethanolamine glycerophosphatides and phosphatidyl choline, occurred when the oxygen concentration was increased (hypoxia to hyperoxia). It is concluded that the lipid alterations associated with thermal acclimation are, in part, attributable to the concomitant change in oxygen concentration.