Biphasic brown fat temperature responses to hypothalamic stimulation in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R328-R337 ◽  
Author(s):  
A. J. Woods ◽  
M. J. Stock

Low-level electrical stimulation (monophasic square-wave pulses: 15 Hz, 7.0 microA, 0.5 ms) of the ventromedial hypothalamus (VMH) in anesthetized rats produced a decrease (phase 1) in interscapular brown adipose tissue (IBAT) temperature that was sustained for as long as the stimulus was applied (2-45 min). A rise in IBAT temperature (phase 2) occurred only after the stimulation had stopped. VMH stimulations ipsilateral and contralateral to a lateral hypothalamic (LH) lesion indicated that the phase 1 response required an intact LH, and denervation of IBAT showed that both phases required an intact sympathetic innervation. Central intracerebroventricular injections of amphetamine and dopamine produced decreases in IBAT temperature similar in magnitude to the phase 1 response to electrical stimulation of the VMH. This, as well as the observation that pimozide blocked phase 1, suggested that dopaminergic pathways were responsible for mediating the phase 1 decrease in IBAT temperature. The peripheral mechanisms responsible for phase 1 are unknown, but a vascular component might explain the unexpected decrease in IBAT temperature seen during sustained VMH stimulation.

1984 ◽  
Vol 247 (4) ◽  
pp. R650-R654 ◽  
Author(s):  
A. Niijima ◽  
F. Rohner-Jeanrenaud ◽  
B. Jeanrenaud

Previous studies have suggested the presence, in hypothalamic obesity, of an impairment of the energy-dissipating capacity of brown adipose tissue ascribed to a functional disconnection of the sympathetic innervation of this tissue. The following observations demonstrate, with electrophysiological techniques, the presence of a functional link between the ventromedial hypothalamic (VMH) area and the interscapular brown adipose tissue (IBAT) in the rat: the spontaneous activity of the efferent sympathetic nerves reaching the IBAT of normal rats was increased in response to an acute cold stimulus, whereas this increase failed to occur in nerves of VMH-lesioned rats studied 4–7 days after the lesions; and the spontaneous activity of the efferent sympathetic nerves of IBAT decreased rapidly (by greater than or equal to 80% within 30 min) after acute lesions of the VMH area. It is suggested that the VMH area plays a role in increasing the activity of the efferent sympathetic nerves of IBAT during an acute cold stimulus and that alone or in relationship with other, as yet undetermined, central nervous system sites, it has a tonic stimulatory effect on the final common pathways that innervate the IBAT via the efferent sympathetic nerves.


1996 ◽  
Vol 270 (3) ◽  
pp. R605-R613 ◽  
Author(s):  
A. J. Woods ◽  
M. J. Stock

Previous work has shown that low-level electrical stimulation of the ventromedial hypothalamus (VMH) in anesthetized rats produces a sustained decrease (phase 1) in interscapular brown adipose tissue (IBAT) temperature followed by a rise (phase 2) after the stimulus has stopped [Woods, A. J., and M. J. Stock. Am. J. Physiol. 266 (Regulatory, Integrative Comp. Physiol. 35): R328-R337, 1994]. In this study, rat oxygen consumption was found to decrease (24%) and then increase (74%) during phase 1 and 2, respectively. The effect of norepinephrine, alpha-adrenoceptor antagonists, substance P, and neuropeptide Y, with and/or without VMH stimulation, suggested that vasoconstriction was unlikely to account for the phase 1 decreases in thermogenesis and temperature. However, measurement with radio-labeled microspheres showed that IBAT capillary blood flow was reduced by 70% during phase 1, and this, plus a 50% decrease in blood oxygen extraction, indicated that phase 1 could be due to vasodilatation of arteriovenous anastomoses. It was postulated that phase 1 resulted from release of neuropeptides, such as substance P, causing diversion of arterial blood away from IBAT capillaries, thereby increasing convective heat loss and inhibiting heat production during phase 1.


Author(s):  
Clara Huesing ◽  
Rui Zhang ◽  
Sanjeev Gummadi ◽  
Nathan Lee ◽  
Emily Qualls‐Creekmore ◽  
...  

1994 ◽  
Vol 266 (2) ◽  
pp. R400-R404 ◽  
Author(s):  
A. Terao ◽  
M. Oikawa ◽  
M. Saito

To examine the effects of brain cytokines on the sympathetic nervous system, norepinephrine (NE) turnover in peripheral organs (spleen, lung, diaphragm, pancreas, heart, liver, kidney, and interscapular brown adipose tissue) was assessed after intraperitoneal or intracerbroventricular administrations of human recombinant interleukin (IL)-1 beta and IL-6 in rats. An intraperitoneal injection of IL-1 (1 microgram/rat) accelerated NE turnover in the spleen, lung, diaphragm, and pancreas without appreciable effects in other organs examined. When IL-1 was injected intracerebroventricularly at much lower doses (1-100 ng/rat), a dose-dependent increase in NE turnover was observed in the spleen, lung, diaphragm, and pancreas. IL-6 did not affect NE turnover in every organ examined, even when it was given at much higher doses, 100 micrograms/rat and 100 ng/rat for intraperitoneal and intracerebroventricular injections, respectively. In contrast to tissue NE turnover, plasma corticosterone level was increased after the administration of IL-6 as well as IL-1, regardless of the site of administration. These results suggest that central IL-1, but not IL-6, increases sympathetic nerve activity in some specific organs, whereas both cytokines are effective for adrenocortical activation. A possible role of the sympathetic nervous system in physiological and immune responses to central IL-1 was discussed.


1988 ◽  
Vol 254 (5) ◽  
pp. R821-R827 ◽  
Author(s):  
T. Yoshida ◽  
G. A. Bray

To study diurnal differences in norepinephrine turnover, groups of rats were housed in rooms with alternating 12 h light and 12 h dark where half the animals were in a normal light cycle and half were in a reversed light cycle. Norepinephrine turnover was measured in all groups beginning at 1000 by inhibition of tyrosine hydroxylase. When rats are fed ad libitum, the turnover of norepinephrine in interscapular brown adipose tissue and heart was significantly higher in the normal cycle than in the reversed cycle. In addition, there was an interaction between the turnover of norepinephrine and the feeding and lighting schedules. When animals were adapted to eating from 0700 to 1900, the turnover of norepinephrine was somewhat faster when the animals ate in the reversed cycle than when they ate in the normal cycle. Conversely, when the feeding schedule was reversed and animals ate between 1900 and 0700, the turnover of norepinephrine in the absence of food was slightly slower in the animals eating in the reversed cycle than in those eating in the light cycle. This interaction between lighting and food intake observed in both male and female rats was abolished by ventromedial hypothalamic lesions. These data suggest that food intake and lighting conditions interact as controllers of the sympathetic nervous system and that these interactions are modulated by the ventromedial hypothalamus.


1985 ◽  
Vol 248 (1) ◽  
pp. E20-E25 ◽  
Author(s):  
M. Saito ◽  
Y. Minokoshi ◽  
T. Shimazu

The interscapular brown adipose tissue (IBAT) from obese rats with lesions of the ventromedial hypothalamus (VMH) was approximately 5 times heavier than those from controls. This hypertrophy of IBAT was associated with a marked enlargement of constituent adipocytes and their apparent transformation from multiloculated structure of lipid droplets into the uniloculated structure. The rate of fatty acid synthesis in IBAT of the obese rats was less than one-tenth of that in control rats and approximated the value in white adipose tissue (WAT) when they were starved for 24 h. When rats were fed, the synthetic rate was increased, but the lipogenic response of IBAT in the obese rats was much greater than that in controls, the extent of the response being comparable to that of WAT. The IBAT temperature rose rapidly on electrical stimulation of the sympathetic nerves to the tissue in control rats, whereas the temperature response was reduced markedly in the obese rats. It was suggested that thermogenesis in BAT was impaired in obese rats with VMH lesions by decreasing triglyceride turnover in BAT, probably due to dysfunction of the sympathetic nervous system and a consequent transformation of BAT into WAT.


1987 ◽  
Vol 65 (6) ◽  
pp. 1299-1303 ◽  
Author(s):  
Kyoko Imai-Matsumura ◽  
Teruo Nakayama

This study was performed to investigate central efferent mechanisms for brown adipose tissue thermogenesis. In unanesthetized rats, the effects of local anesthesia of the ventromedial hypothalamus, anterior hypothalamus, and lateral hypothalamus were observed on the brown adipose tissue thermogenesis induced by preoptic cooling. Rats had a thermode, thermocouple, and bilateral injection cannulae chronically implanted in the hypothalamus and a thermocouple beneath the interscapular brown adipose tissue. The experiments were done at an ambient temperature of 24–25 °C. Preoptic cooling increased brown adipose tissue and colonic temperatures without shivering. Injecting lidocaine bilaterally into the ventromedial hypothalamus during preoptic cooling reduced brown adipose tissue temperature (Tbat). The mean maximum decrease of Tbat was 0.51 ± 0.26 °C and occurred 5–8 min after lidocaine injection. When lidocaine was injected into the anterior hypothalamus, Tbat increased. The mean maximum increase of Tbat was 0.85 ± 0.29 °C and occurred 4–9 min after lidocaine injection. In the lateral hypothalamus, lidocaine had no effect on Tbat∙Tbat was not influenced by injection of saline into the ventromedial, anterior, or lateral hypothalamus. The efferent pathway from preoptic to brown adipose tissue may thus traverse the medial part of hypothalamus. The ventromedial hypothalamus facilititates and anterior hypothalamus inhibits brown adipose tissue thermogenesis induced by preoptic cooling.


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