“…Cold exposure for 3 week attenuated the decrease in rectal temperature following ACE. This result is consistent with previous studies [4,13,15]. The relative weight of IBAT to body weight was not increased by cold exposure for 3 week in the present study.…”
ABSTRACT. There are several benefits to a high-fat diet for animals exposed to cold, including improved tolerance to severe cold conditions and increased survival rates in cold environments. It is therefore of interest to examine whether animals exposed to cold will selectively consume lipids. We examined the intake of safflower oil (SO) by rats exposed to cold (4 ± 2°C) under a feeding condition in which the rats were given free access to SO. Rats exposed to cold consumed more SO than those housed at 25 ± 2°C. This finding suggests that rats prefer SO in a cold environment. There was no significant difference in the ratio of calories of SO ingested to that of matter (standard laboratory chow plus SO) ingested between rats exposed to cold and those at 25 ± 2°C. The high SO intake also affected cold tolerance and metabolite kinetics in the rats. Factors that affected the SO intake of rats exposed to cold are also discussed. KEY WORDS: cold exposure, cold tolerance, interscapular adipose tissue, rats, safflower oil.J. Vet. Med. Sci. 67 (7): [653][654][655][656][657][658] 2005 There are several benefits to a high-fat diet for animals exposed to cold, including improved tolerance to severe cold conditions and increased survival rates in cold environments [5,15,18]. Previous studies have examined diets that included a higher portion of lipid than standard diets. Thus, animals were forced to eat a high-fat diet to satisfy their energy needs and to obtain essential nutrients. However, whether animals prefer lipids in a cold environment has not been studied. It is therefore of interest to examine whether animals exposed to cold will selectively consume lipids. Safflower oil (SO) has often been used as a lipid in experiments related to diet [8, 20-22, 26, 27]. Thus, in the present study we examined the SO intake of rats exposed to cold (4 ± 2°C) under a free-feeding condition in which both SO and a standard laboratory chow were available ad libitum. We also measured rectal temperature upon acute cold exposure (ACE: -20°C in a cold room, 60 min) to evaluate the effect of ingestion of SO on cold tolerance of rats compared with rats not given SO [15]. Changes in the blood levels of glucose, nonesterified fatty acids (NEFA), and β-hydroxybutyrate caused by ACE were also measured to evaluate changes in the use of these substances by cold exposure [15]. The interscapular brown adipose tissue (IBAT) was weighed to assess its generation of heat [10,15].
MATERIALS AND METHODSMale Slc: Wistar rats 9 week of age (Japan SLC, Shizuoka, Japan) were divided into 4 groups with 2 rats per cage (Fig. 1). Two groups were housed at room temperature (25 ± 2°C) for 4 week and then exposed to cold (4 ± 2°C, using a cold room) for the following 3 week period. The 1st group served as controls exposed to the cold environment (CECNT), and the 2nd group had access to SO (CESO). The other 2 groups were fed at room temperature for 7 week.One group served as controls housed at room temperature (RTCNT), and the other group had access to SO (RTSO). A...
“…Cold exposure for 3 week attenuated the decrease in rectal temperature following ACE. This result is consistent with previous studies [4,13,15]. The relative weight of IBAT to body weight was not increased by cold exposure for 3 week in the present study.…”
ABSTRACT. There are several benefits to a high-fat diet for animals exposed to cold, including improved tolerance to severe cold conditions and increased survival rates in cold environments. It is therefore of interest to examine whether animals exposed to cold will selectively consume lipids. We examined the intake of safflower oil (SO) by rats exposed to cold (4 ± 2°C) under a feeding condition in which the rats were given free access to SO. Rats exposed to cold consumed more SO than those housed at 25 ± 2°C. This finding suggests that rats prefer SO in a cold environment. There was no significant difference in the ratio of calories of SO ingested to that of matter (standard laboratory chow plus SO) ingested between rats exposed to cold and those at 25 ± 2°C. The high SO intake also affected cold tolerance and metabolite kinetics in the rats. Factors that affected the SO intake of rats exposed to cold are also discussed. KEY WORDS: cold exposure, cold tolerance, interscapular adipose tissue, rats, safflower oil.J. Vet. Med. Sci. 67 (7): [653][654][655][656][657][658] 2005 There are several benefits to a high-fat diet for animals exposed to cold, including improved tolerance to severe cold conditions and increased survival rates in cold environments [5,15,18]. Previous studies have examined diets that included a higher portion of lipid than standard diets. Thus, animals were forced to eat a high-fat diet to satisfy their energy needs and to obtain essential nutrients. However, whether animals prefer lipids in a cold environment has not been studied. It is therefore of interest to examine whether animals exposed to cold will selectively consume lipids. Safflower oil (SO) has often been used as a lipid in experiments related to diet [8, 20-22, 26, 27]. Thus, in the present study we examined the SO intake of rats exposed to cold (4 ± 2°C) under a free-feeding condition in which both SO and a standard laboratory chow were available ad libitum. We also measured rectal temperature upon acute cold exposure (ACE: -20°C in a cold room, 60 min) to evaluate the effect of ingestion of SO on cold tolerance of rats compared with rats not given SO [15]. Changes in the blood levels of glucose, nonesterified fatty acids (NEFA), and β-hydroxybutyrate caused by ACE were also measured to evaluate changes in the use of these substances by cold exposure [15]. The interscapular brown adipose tissue (IBAT) was weighed to assess its generation of heat [10,15].
MATERIALS AND METHODSMale Slc: Wistar rats 9 week of age (Japan SLC, Shizuoka, Japan) were divided into 4 groups with 2 rats per cage (Fig. 1). Two groups were housed at room temperature (25 ± 2°C) for 4 week and then exposed to cold (4 ± 2°C, using a cold room) for the following 3 week period. The 1st group served as controls exposed to the cold environment (CECNT), and the 2nd group had access to SO (CESO). The other 2 groups were fed at room temperature for 7 week.One group served as controls housed at room temperature (RTCNT), and the other group had access to SO (RTSO). A...
“…ACTH (HELM and HULL, 1966) and glucagon (KUROSHIMA et al, 1978) cause BAT thermogenesis. In addition, hormones secreted from the adrenal glands, glucocorticoids (WUNNENBERG et al, 1974) and epinephrine (CoTTLE and CARLSON, 1956) were suggested to promote nonshivering thermogenesis.…”
The role of the sympathetic nervous system in l0-min cold (5°C)-or 2-min immobilization-induced thermogenesis in brown adipose tissue (BAT) was studied in warm(25°C)-acclimated rats. Both coldand immobilization-stresses increased heat production (M), interscapular brown adipose tissue temperature (Tbat), and colonic temperature (Tco1). Resulting from both stresses, the increase in Tbat was greater than that in Tco1, the differences (4Tbat) becoming approximately 0.48 and 0.46°C by the cold exposure and the immobilization, respectively. After sympathectomy, Tbat and 4Tbat did not change on immobilization but increased significantly on the cold exposure. 4Tbat was 0.31 °C in the sympathectomized rats at the end of the cold exposure period. Immobilization-induced BAT thermogenesis may be mainly controlled by the sympathetic nervous system. On the other hand coldinduced BAT thermogenesis seems to be controlled by certain hormonal factors as well as the sympathetic nervous system.
“…What was unexpectedly observed in rodents in the 1950s was that after a prolonged period in the cold, the animals ceased to shiver but retained an equally high metabolic rate (Sellers et al, 1954;Cottle and Carlson, 1956;Hart et al, 1956). This would allow for a more comfortable life in the cold.…”
SummaryAlterations in nonshivering thermogenesis are presently discussed as being both potentially causative of and able to counteract obesity. However, the necessity for mammals to defend their body temperature means that the ambient temperature profoundly affects the outcome and interpretation of metabolic experiments. An adequate understanding and assessment of nonshivering thermogenesis is therefore paramount for metabolic studies. Classical nonshivering thermogenesis is facultative, i.e. it is only activated when an animal acutely requires extra heat (switched on in minutes), and adaptive, i.e. it takes weeks for an increase in capacity to develop. Nonshivering thermogenesis is fully due to brown adipose tissue activity; adaptation corresponds to the recruitment of this tissue. Diet-induced thermogenesis is probably also facultative and adaptive and due to brown adipose tissue activity. Although all mammals respond to injected/infused norepinephrine (noradrenaline) with an increase in metabolism, in non-adapted mammals this increase mainly represents the response of organs not involved in nonshivering thermogenesis; only the increase after adaptation represents nonshivering thermogenesis. Thermogenesis (metabolism) should be expressed per animal, and not per body mass [not even to any power (0.75 or 0.66)]. A 'cold tolerance test' does not examine nonshivering thermogenesis capacity; rather it tests shivering capacity and endurance. For mice, normal animal house temperatures are markedly below thermoneutrality, and the mice therefore have a metabolic rate and food consumption about 1.5 times higher than their intrinsic requirements. Housing and examining mice at normal house temperatures carries a high risk of identifying false positives for intrinsic metabolic changes; in particular, mutations/treatments that affect the animal's insulation (fur, skin) may lead to such problems. Correspondingly, true alterations in intrinsic metabolic rate remain undetected when metabolism is examined at temperatures below thermoneutrality. Thus, experiments with animals kept and examined at thermoneutrality are likely to yield an improved possibility of identifying agents and genes important for human energy balance.
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