Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fever is a complex and important nonspecific, host defense mechanism against infection. The generation of the heat necessary to increase body temperature may involve thermogenesis in brown adipose tissue. To investigate whether the febrile response to Escherichia coli peritonitis involves thermogenesis in brown adipose tissue, we assessed whole rat oxygen consumption and brown adipose tissue mitochondrial guanosine 5'-diphosphate binding. Non-lethal doses of E. coli, 1 x 10(6) to 1 x 10(8) colony forming units, induced a fever for greater than 8 h. In contrast, a dose of 1 x 10(9) colony forming units resulted in a progressive hypothermia culminating in death. A 48% increase in oxygen consumption (p less than 0.05) in E. coli-infected rats occurred almost immediately, preceded the development of the fever, and was sustained throughout the fever. There was a highly significant correlation (r = 0.736, p less than 0.01) between oxygen consumption and body temperature for both control and infected animals. Guanosine 5'-diphosphate binding assessed by multi-point Scatchard analysis of [3H]guanosine 5'-diphosphate binding to isolated mitochondria was increased by 45.4 +/- 7.3% at 1.75 h and by 31.9 +/- 9.0% at 3.5 h (p less than 0.05). The greater increase was during the rising phase of the fever. Unexpectedly, a lethal dose of 5 x 10(9) colony forming units of E. coli also increased guanosine 5'-diphosphate binding sites by 54.4 +/- 14.2% (p less than 0.05) despite a hypothermia of -1.71 +/- 0.29 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Escherichia coli peritonitis activates thermogenesis in brown adipose tissue: relationship to fever. 165 79

In this paper we report the development of the immunologically detected uncoupling protein (UCP) in brown adipose tissue during the perinatal period in the rat and its relationship with its functional activity expressed in terms of GDP-binding capacity, GDP-sensitive permeabilities and GDP-sensitive respiration. Immunologically detected UCP increased during the last 2 days of foetal life (under euthermic conditions) and after birth (after postnatal hypothermia) during the early suckling period, reaching its maximum value on day 10 after birth. This increase in UCP is accompanied by parallel increases in the GDP-binding capacity, GDP-sensitive permeabilities to protons and chloride ions and GDP-inhibitable respiration. During the suckling--weaning transition, there was a regression of the parameters related to the functional activity of the UCP (GDP-binding capacity and nucleotide-sensitive permeabilities and respiration) without changes in the immunologically detected UCP. These results suggest that the involution of this tissue in the rat commences in this period; the first parameters affected are those related to the functional activity of the UCP while the UCP is still present in its highest level. This seems to support the idea that, in this period of development of the rat, the UCP may exist in the brown fat mitochondria in a functional (unmasked) form and a non-functional (masked) form.
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PMID:Development of the uncoupling protein in the rat brown-adipose tissue during the perinatal period. Its relationship with the mitochondrial GDP-binding and GDP-sensitive ion permeabilities and respiration. 168 44

Experiments were carried out to test whether the ventromedial hypothalamus (VMH) is the site of a pathway that stimulates thermoregulatory heat production in brown adipose tissue (BAT). Adult Sprague-Dawley rats received bilateral 50 nl microinjections of colchicine solution into the VMH (0.1, 0.32, 1.0 or 3.2 micrograms per side). Beginning a day later, hyperphagia developed consistently with 0.32 microgram colchicine; and with higher doses there appeared the additional effect that for several days rats developed hypothermia when placed temporarily at 6 degrees C. The degree of hypothermia was limited by activation of nonshivering thermogenesis (NST) in BAT, as evidenced by increased shivering after propranolol injection to block NST, and by increased GDP binding measured in IBAT mitochondria after cold exposure. The findings suggest that chemical lesioning to induce the VMH hyperphagia syndrome does not produce an obligatory impairment of thermoregulation against cold unless the dose of neurotoxin and lesion area extends beyond that which underlies the overeating response. Furthermore, when tolerance to cold is thus compromised, the effect is not readily explained in terms of simply disconnecting a proposed stimulatory pathway from the VMH to BAT.
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PMID:Colchicine lesions of ventromedial hypothalamus: effects on regulatory thermogenesis in the rat. 273 41

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

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.
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PMID:Body temperature: an important determinant of severity of ischemic renal injury. 372 86

We investigated the effect of a beta 3-adrenergic agonist, Zeneca D7114, on thermoregulation in near-term lambs delivered by cesarean section. Lambs were delivered into a cool ambient temperature of 15 degrees C, and between 60 and 80 min of life were given an oral dose of Zeneca D7114 (10 mg.kg body weight-1) dissolved in 20 mL of milk, or milk alone. During the first 0.5 h of life colonic temperature decreased in all lambs, and then increased to plateau levels (39.6-40.4 degrees C) after 120-150 min of life, in 19 out of 23 lambs studied. In the remaining lambs, colonic temperature failed to return to normothermic values, plateauing at 34.3 degrees C. All control lambs were observed to shiver throughout the study, but after Zeneca D7114 treatment 7 out of 10 normothermic lambs stopped shivering, and plateau colonic temperature was 0.8 degree C higher. Hypothermic beta 3-agonist-treated lambs had significantly lower rates of heat production, breathing frequency, and plasma triiodothyronine and cortisol concentrations than normothermic lambs. the level of GDP binding and norepinephrine content of brown adipose tissue (BAT) sampled from hypothermic beta 3-agonist-treated lambs was significantly lower than in normothermic lambs. There was no difference in GDP binding in BAT between control and Zeneca D7114-treated groups, but the Hb content was higher in the latter group. It is concluded that administration of Zeneca D7114 to euthyroid lambs enhances their ability to thermoregulate and restore colonic temperature without altering the thermogenic activity of BAT. This response may be mediated by increasing blood flow to BAT and/or an improvement in the animal's thermal efficiency (i.e. decreased heat loss) due to a reduced reliance on shivering thermogenesis.
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PMID:Effect of beta 3-adrenergic agonist (Zeneca D7114) on thermoregulation in near-term lambs delivered by cesarean section. 882 86