Escherichia coli peritonitis activates thermogenesis in brown adipose tissue: relationship to fever.

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)