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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of substrate cycles in metabolic control was first indicated over ten years ago, but the recent interest in such cycles has developed from the direct demonstration by isotopic techniques of their existence in various tissues. I propose that substrate cycles form part of a logical series of biochemical mechanisms that exist to increase the sensitivity of non-equilibrium reactions to changes in concentrations of metabolic regulators. The possible importance of such cycles for provision of precise metabolic regulation in the tissues of the normal subject and the trained athlete is proposed. Furthermore, cycling may provide a mechanism by which hormones can change the magnitude of response in a tissue to a given metabolic signal, without interfering in the biochemistry of the basic control mechanism. It is, however, possible to extend the role of cycling to heat generation and thus to controlled energy loss by an organism. Heat generation by substrate cycles may be important as an acute mechanism for maintaining the body temperature in man in response to a sudden decrease in the environmental temperature; alcoholic hypothermia would be explained by inhibition of substrate cycling in the liver, and accidental hypothermia in the elderly could be explained by decreased capacity of substrate cycles with age. If heat generated by the cycles is rapidly lost to the environment, the expenditure of energy to maintain this heat loss could explain, in part, the physiological phenomena of the thermic response to food and the oxygen debt which is always observed after exercise. Finally, the energy expended in these ways could be part of a general biochemical mechanism for maintenance of the correct body weight; a decrease in the capacity of substrate cycles might be one factor involved in the development of obesity.
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PMID:Substrate cycles: their metabolic, energetic and thermic consequences in man. 15 56

1. The capacity ofr thermoregulation and thermogenesis in lean and genetically obese (ob/ob) mice has been investigated. 2. At 4 degrees C ob/ob mice rapidly die of hypothermia, because of a reduced capacity for cold-induced thermogenesis, but the animals are able to survive if previously adapted to 12 degrees C. 3. At all environmental temperatures between 30 degrees C and 10 degrees C the body temperature of ob/ob mice is 2.0-2.5 degrees C below that of lean animals. This may be due to a lower "setting" for body temperature. 4. At 34 degrees C the oxygen consumption of obese mice is greater than that of the lean animals while at 30 degrees C it is similar. When the environmental temperature is below 30 degrees C the oxygen consumption of the lean mice is greater. The obese animals therefore expend less energy on thermoregulatory thermogenesis. 5. The capacity for non-shivering thermogenesis was measured in lean and obese mice by investigating the effect of an injection of L-nor-adrenaline (1000 microgram/kg body weight) on the metabolic rate at 31 degrees C. Non-shivering thermogenesis was reduced by one-half in the obese animals. 6. One cause of the obesity of the ob/ob mouse is its high metabolic efficiency. We suggest that this high metabolic efficiency is due, at least in part, to less energy being expended on thermoregulatory thermogenesis.
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PMID:Thermoregulation and non-shivering thermogenesis in the genetically obese (ob/ob) mouse. 56 45

1. Thermoregulation and non-shivering thermogenesis have been studied in the genetically diabetic obese (db/db) mouse. 2. At all environmental temperatures between 33 and 10 degrees C the body temperature of the diabetic mice was lower than that of the normal littermates, the difference varying from 1.1 degrees C at 33 degrees C to 4.5 degrees C at 10 degrees C. 3. At 4 degrees C the diabetic mice rapidly died (3.2h) of hypothermia while the normal mice maintained their body temperature within the normal range. 4. At 23 degrees C the diabetic animals exhibited a diurnal rhythm in body temperature which was similar in both phase and amplitude to the controls, but at every point throughout the 24h cycle the temperature of the mutants was lower by 1--2 degrees C. 5. The resting metabolic rate at thermoneutrality (33 degrees C) was higher per whole animal for the diabetics than for the normals. However, at temperatures below thermoneutrality the converse was observed; between 30 and 4 degrees C the RMR of the mutants was lower than the controls by approximately 25%. 6. The capacity for non-shivering thermogenesis in diabetic mice was only one-half that found in normal animals. 7. The diabetic mouse has abnormalities in thermoregulation and non-shivering thermogenesis which are similar to those found in the genetically obese (ob/ob) mouse. It is concluded that the high metabolic efficiency of the diabetic mouse, like that of the ob/ob mouse, can be explained by a reduced energy expenditure on thermoregulatory thermogenesis; this may represent a primary mechanism for the operation of the "thirfty genotype" associated with obesity and diabetes.
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PMID:Thermoregulation in the diabetic-obese (db/db) mouse. The role of non-shivering thermogenesis in energy balance. 57 63

Changes of colonic temperature were investigated to examine a mechanism of hypothermia in the obese rats which received subcutaneous administration of intermediate type-insulin (8 U/day) for 8 weeks. Although diurnal rhythmicity of colonic temperature levels was maintained similarly with those of vehicle-injected controls, the overall colonic temperature levels were significantly lowered in insulin-treated animals. In the condition of cold exposure at 5 degrees C, colonic temperature levels of insulin-treated animals were immediately and significantly decreased at 60 minutes after the start of cold exposure. The data obtained herein demonstrated that hyperinsulinemia accompanying with hyperphagia should be profoundly involved in hypothermia, observed in various experimental models of obesity.
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PMID:Hypothermia in insulin-treated obese rats. 163 26

With the combination of a noninvasive saturation measurement and plethysmography, pulse oximetry has become an important monitoring method for peripheral perfusion and oxygen supply. Indications for pulse oximetry is practically every anaesthesia especially in geriatric patients and patients with one-lung-anaesthesia, obesity, asthma and emphysema. Pulse oximetry has proved its worth in the transport of emergency patients. Sources of error are a bad perfusion at the site of measurement (hypotension, hypothermia), dyshaemoglobinaemia (Met-carboxy-haemoglobin) and interference of colours (dark skin, intravenous colours, high light intensity). Accuracy of response of most currently available pulse oximeters lies between 2-3% (SD) with oxygen saturations between 80-100%. Deviations increase at lower oxygen saturations. Pulse oximetry will soon be regarded as minimal monitoring standard worldwide together with the ECG, blood pressure, pulse and respiratory monitoring.
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PMID:[The importance of pulse oximetry for anesthesia]. 204 38

2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol, hydrochloride (JO 1017) is a novel antidepressant drug. Its biochemical and pharmacological properties were investigated in mice, rats, dogs, rabbits and guinea pigs. In vitro, it selectively inhibited serotonin uptake and had a high affinity for the 3H-paroxetine and 3H-imipramine binding sites. Biochemical studies demonstrated the lack of MAO-A and MAO-B inhibition and the absence of marked affinity for muscarinic, histaminic or other conventional brain receptors. Chronic treatment with JO 1017 induced a decrease in the Bmax values for imipramine sites but did not modify the Bmax for beta-adrenergic and 5-HT2 receptors. The neuropsychopharmacological profile of JO 1017 is characterized by a decrease of the immobility times in behavioural despair tests with mice, a decrease of the escape failures in the rat learned helplessness test, a strong potentiation of L-5-HT P-induced head-twitches in mice and an antagonism of reserpine-induced ptosis in rabbits. It weakly antagonized oxotremorine-induced hypothermia and did not influence the hypothermia induced by apomorphine. In contrast to most other antidepressants, a high dose of JO 1017 induced hypermotility in mice placed in an activity meter without producing stereotyped behaviour and group toxicity. Unlike tricyclic antidepressants, JO 1017 was devoid of severe cardiotoxicity in guinea pigs and had no central anticholinergic nor antihistaminic properties. These results suggest that JO 1017 is a selective serotonin uptake inhibitor with a high safety margin. JO 1017 may have a potential clinical utility both in the treatment of depression and for indications where serotonin transmission is involved, e.g., anxiety, panic attack, obsessive compulsive disorder, obesity and alcohol consumption.
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PMID:Biochemical and pharmacological evaluation of the novel antidepressant and serotonin uptake inhibitor 2-(3,4-Dichlorobenzyl)-2-dimethylamino-1-propanol hydrochloride. 216 3

The anti-obesity drug fenfluramine, promotes loss of weight by reducing food intake; however, there is controversy as to whether the drug can also elevate expenditure of energy. Resting consumption of oxygen (VO2) was measured in conscious rats to determine whether the injection of fenfluramine increased metabolic rate and whether prior fasting, or ambient temperature altered the response. Regardless of whether the rats were fed or had been fasted for 22 hr, in a thermoneutral environment (28 degrees C), the intraperitoneal injection of dl-fenfluramine (20 mg/kg) caused a raised oxygen consumption. This elevation was sustained to the end of the 60-min period of measurement after the injection, at which point the colonic temperature was found to be increased. This metabolic response to fenfluramine was largely attenuated when the drug was administered at 23 degrees C, and the colonic temperature of the rats was decreased by 60 min after the injection. At 4 degrees C, the injection of fenfluramine inhibited thermogenesis against cold, the oxygen consumption fell and the rats exhibited hypothermia. It was concluded that fenfluramine can increase the metabolic rate, but that this effect is not conditional on associated food intake, as has been reported. Rather, the ambient temperature governs whether stimulation or inhibition of thermogenesis will be evoked. These metabolic effects of fenfluramine explain, in part, its divergent effects on body temperature, reported previously.
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PMID:Ambient temperature modulation of fenfluramine-induced thermogenesis in the rat. 232 33

Many of the disturbances which characterize adult C57BL/6 ob/ob mice, including obesity, hypometabolism and hypothermia could arise from reduced circulating levels of thyrotropin and thyroid hormones. In the present study, measurement of these hormones in ad libitum-fed obese and lean mice housed at 22 degrees C revealed that mutant mice had levels of TSH equal to those of their ?/+ siblings, while total T4 and T3 concentrations were slightly higher than those of lean controls. The hormonal responses of obese mice to overnight food deprivation or to meal ingestion were also similar to those of lean control mice. Males of both phenotypes typically had higher TSH, T4 and T3 concentrations than did females, and in male mice the circulating levels of each hormone were much more responsive to the feeding condition. The present data are consistent with recent reports of defective target tissue responses and impaired hormone deiodination rather than depressed pituitary-thyroid hormone levels in accounting for the metabolic disturbances which characterize ob/ob mice.
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PMID:Thyroid hormone responses to feeding in ob/ob mice. 280 44

Mice treated with glutamate in the neonatal period are known to develop into stunted obese adults, despite hypophagia. Our objective was to find out whether brown adipose tissue (BAT) thermogenic function might be abnormal in the glutamate-obese mouse. At 10 wk of age, group-housed glutamate-obese mice exhibited nocturnal and early diurnal torpor, i.e., they thermoregulated at a lower than normal body temperature. When exposed to 4 degrees C, they died in hypothermia within 24 h. They could adapt to living at 14 degrees C for up to 1 wk but failed to adjust their food intake sufficiently to maintain their body weight. Their fat stores were, nevertheless, conserved. BAT was present in increased amounts in glutamate-obese mice. Its thermogenic activity (as assessed by the level of mitochondrial GDP binding) was normal (male mice) or reduced (female mice). A normal thermogenic responsiveness of BAT to cold occurred. The thermogenic response of BAT to a cafeteria diet was normal (male mice) or reduced (female mice). Serum corticosterone concentration was increased in both male and female glutamate-treated mice particularly in the cold. We conclude that the high metabolic efficiency and obesity of the glutamate-obese mouse are principally a consequence of its maintenance of a hypothermic torpid state for more than 50% of the time. An additional deficit in energy expenditure in female, but not male, glutamate-obese mice is associated with suppressed responsiveness of the thermogenic function of BAT to diet and may account for the greater degree of obesity in female than in male glutamate-treated mice.
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PMID:Brown adipose tissue thermogenesis, torpor, and obesity of glutamate-treated mice. 287 42

Measurements were made of cytochrome c oxidase activity and the GDP-binding capacity of mitochondria in brown adipose tissue of genetically obese mice and wild-type siblings, to estimate the thermogenic capacity of the tissue. The binding capacity was decreased in ad libitum fed obese animals compared with wild-type animals. Limited feeding of obese animals to restrict their body weight caused a large increase in the binding capacity of the tissue, which was greater than that in wild-type animals fed either ad limitum or on a limited diet. The decreased binding capacity of brown adipose tissue mitochondria in obese mice appears to be a consequence of ad libitum feeding and therefore not a cause of the obesity. Limit feeding of obese animals also corrected their characteristic hypothermia at low ambient temperature. The large increase in the thermogenic capacity of brown adipose tissue in obese animals, induced by limited feeding, may account for the vital improvement of their thermoregulation. However, close similarities were found between obesity hypothermia and hypothermia induced in wild-type animals by restraint. It is suggested that changes in posture caused by obesity, resulting in increased loss of body heat, may be important in the development of obesity hypothermia. Obese animals fed less than wild-type grained more weight than wild-type animals, indicating that the high thermogenic capacity of their brown adipose tissue did not function to regulate their calorie intake.
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PMID:Influence of restricted food intake on brown adipose tissue function in genetically obese mice (genotype, ob/ob). 298 19


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