Increase In Brown Adipose Tissue Temperature Research Articles

EEG arousal, sympathetic activity, and brown adipose tissue thermogenesis after conditioned taste aversion

Conditioned taste aversion was induced in rats by pairing saccharin with intraperitoneal LiCl injection. Animals injected with NaCl served as controls. After evaluating the preference levels for saccharin in rats of both groups, the animals were anesthetized with urethane and the duration of EEG desynchronization, firing rate of sympathetic nerves innervating interscapular brown adipose tissue (BAT), and temperature of the same tissues were recorded, before and after oral stimulation with saccharin or water. The EEG desynchronization was longer in conditioned rats after stimulation with saccharin. Firing rate of sympathetic nerves was higher in conditioned rats after presentation of saccharin. BAT temperature, decreased in conditioned rats after saccharin stimulus, was unchanged in the three other conditions. In a second experiment temperature and firing rate of sympathetic nerves of BAT were recorded after oral presentation of water or saccharin in rats treated as in the first experiment and injected with the α 1-adrenergic blocker prazosin. As in the first experiment, saccharin presentation in conditioned animals enhanced the neural sympathetic activity, whereas differently from the first experiment it increased BAT temperature. No changes were found in the same measurements in the three other conditions. The drop in interscapular BAT temperature found in the first experiment, an unexpected finding, probably depends on the use of lithium as unconditioned stimulus, because LiCl interacting with adrenergic receptors changes the two-phase response, normally seen in interscapular BAT after increased sympathetic activity, in a single-phase response.

HETEROGENOUS ACTIVITY OF BRL 35135, A β3‐ADRENOCEPTOR AGONIST, IN THERMOGENESIS AND INCREASED BLOOD FLOW IN BROWN ADIPOSE TISSUE IN ANAESTHETIZED RATS

1. The effects of BRL 35135, a beta 3-adrenergic agonist, on body temperature and regional blood flow in brown adipose tissue (BAT) were simultaneously recorded in anaesthetized rats and compared to isoproterenol. 2. BRL 35135 at doses of 0.1 and 1 micrograms/kg (i.v.) induced dose-dependent increases in BAT temperature with minimal effects on systemic diastolic blood pressure (DBP), heart rate (HR) and BAT blood flow. 3. The thermogenic effect of BRL 35135 at a dose of 10 micrograms/kg (i.v.) was smaller than that at a dose of 1 microgram/kg, and was accompanied by a marked increase in BAT blood flow. 4. Isoproterenol at doses of 0.01-1 microgram/kg (i.v.) dose-dependently increased HR and BAT blood flow and decreased DBP. It did not affect BAT temperature. 5. These findings indicate that unlike isoproterenol, BRL 35135, at the lower doses, selectively causes thermogenesis in BAT which was detectable as changes in BAT temperature, and that the vasodilator effect in BAT is not as sensitive as the thermogenic effect of beta 3-adrenergic agonists.

Involvement of nitric oxide in noradrenaline-induced increase in blood flow through brown adipose tissue

N ω-nitro- L -arginine methyl ester ( L -NAME) (80 mg), a NO synthase blocker, completely abolished noradrenaline (NA)-induced increase in blood flow through brown adipose tissue (BAT) in the urethan-anesthetized rat. L -NAME suppressed NA-induced increase in blood flow dose-dependently. L -arginine (80 mg), but not D -arginine (80 mg), reversed the inhibitory effect of L -NAME (0.8 mg). NA-induced increase in BAT temperature was also decreased by L -NAME. These results suggest that nitric oxide mediates NA-induced increase in BAT blood flow.

Effects of the α1-adrenergic agonist cirazoline on locomotion and brown adipose tissue thermogenesis in the rat

Anorexia is induced by injection of α1-adrenergic receptor agonists into the hypothalamic paraventricular nucleus (PVN) in rats. Of the agonists tested to date, cirazoline is the most potent when administered either into the PVN or systemically. The present experiments assess the effects of systemically administered cirazoline, at doses that suppress food intake, on dopamine and norepinephrine systems as evident in locomotion and stereotypy and in the induction of brown adipose tissue (BAT) thermogenesis. In Experiment 1, adult male rats were treated with either vehicle (0) or 0.05, 0.1, 0.2 or 0.4 mg/kg cirazoline (IP) prior to 30 minutes assessment of horizontal and vertical locomotion and stereotypy in Omnitech activity chambers. Horizontal activity and sterotypy were significantly suppressed at 0.05 mg/kg cirazoline but these effects waned at higher cirazoline doses. In Experiment 2, interscapular BAT temperature in adult male rats was monitored for 30 minutes after injection (IP) of either vehicle or 0.4 mg/kg cirazoline. Cirazoline, at 0.4 mg/kg did not influence BAT temperature whereas a positive control treatment (phenylpropanolamine: 40 mg/kg) rapidly increased BAT temperature during a 15 minute period after injection. These results suggest that cirazoline-induced anorexia is not the result of competing motor responses and that this drug, at a dose that produces maximal suppression of feeding, does not alter BAT thermogenesis.

Response of brown adipose tissue to electrical stimulation of hypothalamic centres in intact and adrenalectomized Zucker rats.

Electrical stimulation of the ventromedial nucleus of the hypothalamus (VMN) increased brown adipose tissue (BAT) temperature in lean and obese Zucker rats, whereas stimulation of the paraventricular nucleus (PVN) was without effect in either genotype, before or after adrenalectomy. The prolonged duration of the increase in BAT temperature in the obese (fa/fa) rat observed after VMN stimulation was normalized after adrenalectomy.

Hypothalamic control of brown adipose tissue in Zucker lean and obese rats. Effect of electrical stimulation of the ventromedial nucleus and other hypothalamic centres

Electrophysiological stimulation of the hypothalamic ventromedial nucleus (VMN) resulted in an increase in interscapular brown adipose tissue (BAT) temperature in both lean and obese ( fa/fa) rats. Graded stimulations resulted in progressively larger temperature increases in both lean and obese ( fa/fa) groups. Both intraperitoneal injection of propranolol and surgical denervation (but not sham denervation) abolished the increase in BAT temperature following VMN stimulation, in both lean and obese ( fa/fa) groups. Electrical stimulation of the supraoptic region, and certain anterior hypothalamic regions also resulted in increases in BAT temperature of lean and obese ( fa/fa) rats, but stimulation of the dorsomedial nucleus and regions of the lateral hypothalamus did not affect BAT temperature. All hypothalamic regions capable of activating BAT gave a similar maximum rise in temperature for a given stimulus in lean and obese ( fa/fa) rats. These results suggest that the efferent sympathetic pathway from the VMN and other hypothalamic regions of BAT is normal in the obese ( fa/fa) rat.

Brown adipose tissue thermogenesis induced by low level electrical stimulation of hypothalamus in rats

Brown adipose tissue (BAT) is an energy dissipating form of adipose tissue implicated in non-shivering thermogenesis as well as diet-induced thermogenesis. In the present study, in vivo interscapular BAT (IBAT) temperature was recorded prior to and following low level electrical stimulation (a 30 sec train of 60 Hz, 100 μA 0.5 msec isolated pulses) of various hypothalamic regions in rats. Significant increases in IBAT temperature were observed after stimulation of the anterior, medial preoptic, paraventricular and dorsomedial hypothalamus but not after stimulation of either ventromedial or caudal hypothalamus. For positive sites, IBAT temperature typically increased at 3–4 minutes following stimulation, peaked at 7–8 minutes after stimulation and declined at 20 minutes after stimulation. Although alterations in diet-induced thermogenesis have been reported after ventromedial hypothalamic lesions, the increases in BAT temperature noted in the present study suggest that inhibitory fibers that course through the paraventricular hypothalamus may form part of the central nervous system control of brown adipose tissue thermogenesis induced by overfeeding.