Renal contribution to thermolability in rats: role of renal nerves.
BACKGROUND
Body temperature is closely regulated via the integration of a number of mechanisms, the study of which has been greatly assisted by the exploitation of comparative physiology. Previous studies have demonstrated that chronic renal failure patients have significantly lower body temperatures than healthy subjects when artifacts from circadian changes were taken into consideration. We hypothesize that the blunting of renal sensory neurons after kidney partial ablation may contribute to the lack of suppression of sympathetic efferent outflow towards BAT, modifying the glucose metabolism signaling pathway, UCP 1 expression and liver mitocondrial respiratory chain activity.


METHODS
To evaluate the influence of renal mass reduction, renal denervation and chronic deafferentation by capsaicin on thermoregulation, glucose metabolism, UCP1 expression and liver mitocondrial respiration, was used respectively, the blocking of heat dissipation by thermoneutral body water immersion, the oxygen consumption by Clark-type electrode, and western blot method.


RESULTS
The study confirmed that, following 5/6 nephrectomy, the basal core temperature of rats was significantly lower than that of control animals when maintained in a thermoneutral body water immersion recipient, as compared to controls. Additionally, we demonstrated that exposure of bilateral renal denervated or of renal chronic capsaicin-treated rats to a similar experimental protocol results in a fast and high rise in rectal temperature response, and this is associated with a significant increase in the basal serine phosphorylation and protein levels of Akt and protein levels of UCP1. This was observed despite unchanged liver mitochondria respiratory control and ADP/O ratios in 5/6 Nx, as well as DNx, when compared to control mitochondria.


CONCLUSIONS
Speculatively, it may be suggested that one of the renal sensory nerve signal defects associated with decreased kidney energy generation, induced by kidney ablation, may result in an inability to control the body temperature.
Lutaif
Nelson A
NA
Departamento de Clínica Médica, Laboratório de Metabolismo Hidro-Salino, Núcleo de Medicina e Cirurgia Experimental, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, 13083-592 Campinas, SP, Brazil
Rocha
Eduardo M
EM
Veloso
Lício A
LA
Bento
Leda M
LM
Gontijo
José A R
JA
D002001:Adipose Tissue, Brown / Q000378:metabolism; D000818:Animals; D001833:Body Temperature Regulation / Q000502:physiology*; D002211:Capsaicin; D002395:Catecholamines / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D007668:Kidney / Q000294:innervation* / Q000502:physiology*; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D009392:Nephrectomy; D010101:Oxygen Consumption; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011984:Sensory Receptor Cells / Q000502:physiology; D015398:Signal Transduction; D013562:Sympathectomy; D013563:Sympathectomy, Chemical; D000071256:Uncoupling Protein 1
D002395:Catecholamines; D055504:Insulin Receptor Substrate Proteins; D007473:Ion Channels; C526296:Irs1 protein, rat; D024101:Mitochondrial Proteins; C000604373:Ucp1 protein, rat; D000071256:Uncoupling Protein 1; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D019950:Mitogen-Activated Protein Kinase 1; D005947:Glucose; D002211:Capsaicin