Metabolic responses to fasting and refeeding in lean and genetically obese rats

1983 ◽  
Vol 244 (5) ◽  
pp. R615-R620 ◽  
Author(s):  
N. J. Rothwell ◽  
M. E. Saville ◽  
M. J. Stock
Keyword(s):  
Nervous System ◽  
Oxygen Consumption ◽  
Sympathetic Nervous System ◽  
Metabolic Rate ◽  
Zucker Rats ◽  
Sprague Dawley ◽  
Mixed Composition ◽  
Obese Rats ◽  
Single Meal ◽  
Sympathetic Nervous

Injection of norepinephrine (NE) (25 micrograms/100 g body wt) caused a similar rise in metabolic rate in lean and obese (fa/fa) Zucker rats, but 3-day fasting suppressed the response in lean rats and enhanced the rise in obese mutants. Triiodothyronine (T3) injection (10 micrograms/100 g body wt) caused a significantly greater rise in oxygen consumption (Vo2) in obese than lean rats, but the response was attenuated by fasting in all animals. The thermic response to a single meal of either mixed composition, carbohydrate, or protein (40 kJ) was much smaller in obese rats than lean, but the response to the mixed nutrient meal was similar for all rats after a 3-day fast. Refeeding 3-day fasted lean rats with a single carbohydrate meal (40 kJ) caused a rise in plasma T3 levels after 3 h and a delayed increase in metabolic rate 24 h later. Injection of NE instead of refeeding caused a similar delayed rise in metabolic rate. Carbohydrate refeeding had no effect on plasma T3 levels or oxygen consumption in 3-day fasted obese Zuckers, but injection of NE did produce a significant increase in metabolic rate after 24 h. Refeeding 3-day fasted rats with protein (40 kJ) caused a rise in oxygen consumption 24 h later in lean animals but had no effect in obese animals. The data from lean Zucker rats confirm previous findings in Sprague-Dawley rats and suggest that the thermic response to refeeding involves a complex interaction between the sympathetic nervous system and thyroid hormones. Obese Zuckers responded normally to NE and T3, indicating that their reduced thermogenesis after food may be due to insensitivity to nutrient availability or an inability to activate the sympathetic nervous system.

scholarly journals Change in activity of the sympathetic nervous system in diet-induced obese rats

2000 ◽  
Vol 15 (6) ◽  
pp. 635 ◽  
Author(s):  
So Young Park ◽  
Yeon Je Lee ◽  
Yong Woon Kim ◽  
Hyeong Jin Kim ◽  
Kyung Oh Doh ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Obese Rats ◽  
Sympathetic Nervous

scholarly journals Role of the renin-angiotensin system in cardiac hypertrophy induced in rats by hyperthyroidism

1997 ◽  
Vol 273 (2) ◽  
pp. H593-H599 ◽  
Author(s):  
H. Kobori ◽  
A. Ichihara ◽  
H. Suzuki ◽  
T. Takenaka ◽  
Y. Miyashita ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Renin Angiotensin System ◽  
Sympathetic Denervation ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sympathetic Nervous

This study was conducted to examine whether the renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy without involving the sympathetic nervous system. Sprague-Dawley rats were divided into control-innervated, control-denervated, hyperthyroid-innervated, and hyperthyroid-denervated groups using intraperitoneal injections of thyroxine and 6-hydroxydopamine. After 8 wk, the heart-to-body weight ratio increased in hyperthyroid groups (63%), and this increase was only partially inhibited by sympathetic denervation. Radioimmunoassays and reverse transcription-polymerase chain reaction revealed increased cardiac levels of renin (33%) and angiotensin II (53%) and enhanced cardiac expression of renin mRNA (225%) in the hyperthyroid groups. These increases were unaffected by sympathetic denervation or 24-h bilateral nephrectomy. In addition, losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced cardiac hypertrophy. These results suggest that thyroid hormone activates the cardiac renin-angiotensin system without involving the sympathetic nervous system or the circulating renin-angiotensin system; the activated renin-angiotensin system contributes to cardiac hypertrophy in hyperthyroidism.

Lack of Influence of the Sympathetic Nervous System on the Calorigenic Response to Thyroxine

1957 ◽  
Vol 188 (3) ◽  
pp. 503-506 ◽  
Author(s):  
A. Surtshin ◽  
James K. Cordonnier ◽  
S. Lang
Keyword(s):  
Nervous System ◽  
Oxygen Consumption ◽  
Sympathetic Nervous System ◽  
Significant Rise ◽  
Published Data ◽  
Physiological Effects ◽  
Concurrent Administration ◽  
Rate Of Oxygen Consumption ◽  
Sympathetic Nervous ◽  
Adrenergic Blocking

Normal rats as well as thyroparathyroidectomized rats concurrently given thyroxine and an adrenergic blocking dose of Dibenzyline show the expected rise in rate of oxygen consumption. After bilateral adrenal demedullation the resting rate of oxygen consumption is not significantly different from normal, and injection of a large dose of thyroxine either with or without concurrent administration of adrenergic blocking doses of Dibenzyline is followed by a significant rise in the rate of oxygen consumption. Our data and other pertinent published data lend support neither to the claim that the calorigenic effect of exogenous thyroxine is dependent upon the presence of normally acting adrenal medullary hormones nor to the claim that the metabolic changes of thyrotoxicosis are due to the physiological effects of epinephrine and norepinephrine as augmented by the thyroid hormones.

Vascular angiotensin and the sympathetic nervous system: do they interact?

1994 ◽  
Vol 267 (1) ◽  
pp. H187-H194 ◽  
Author(s):  
K. F. Hilgers ◽  
R. Veelken ◽  
I. Kreppner ◽  
D. Ganten ◽  
F. C. Luft ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Nerve Stimulation ◽  
High Performance ◽  
Spontaneously Hypertensive Rat ◽  
Pressor Response ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Sympathetic Nervous

We tested the hypothesis that local vascular formation of angiotensin (ANG) II and the sympathetic nervous system potentiate each other. Isolated rat hindquarters were perfused with an artificial medium, and ANG I and II release was measured by high-performance liquid chromatography and radioimmunoassay. Electrical stimulation of the lumbar sympathetic chain (0.5, 2, and 8 Hz) did not affect vascular ANG release in Sprague-Dawley (SD) rats. Hypertensive, ren-2 transgenic (TG+) rat hindquarters released significantly more ANG I (110 +/- 19 vs. 65 +/- 21 fmol/30 min in SD rats) and ANG II (235 +/- 22 vs. 140 +/- 30 fmol/30 min); however, nerve stimulation did not alter ANG release in TG+ rats. Captopril inhibited vascular ANG II release by 90%, but neither captopril nor ANG II receptor blockade by losartan affected the pressor response to nerve stimulation in SD and TG+ rats. Isoproterenol failed to increase either vascular ANG release or pressor response to nerve stimulation in SD or spontaneously hypertensive rat hindquarters. Exogenous renin, which increased vascular ANG release approximately 100-fold, prolonged the pressor responses to nerve stimulation. We conclude that the vascular renin-ANG system does not interact with the sympathetic nervous system locally. However, high concentrations of ANG II, which can be induced by circulation-derived renin, may prolong the duration of sympathetic nerve-induced vasoconstriction.

scholarly journals Development of temperature regulation in newborn reindeer

Rangifer ◽  
1981 ◽  
Vol 1 (1) ◽  
pp. 29 ◽  
Author(s):  
R. Hissa ◽  
S. Saarela ◽  
M. Nieminen
Keyword(s):  
Nervous System ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Metabolic Rate ◽  
Heat Production ◽  
Temperature Regulation ◽  
Rangifer Tarandus ◽  
Normal Body Temperature ◽  
Newborn Calves ◽  
Sympathetic Nervous

<p>Development of temperature regulation was investigated by determining the ability of newborn reindeer calves (Rangifer tarandus tarandus) to maintain a normal body temperature when exposed to an incrementially decreasing ambient temperature. Newborn calves (1 day old) can maintain their body temperature even at -15 &deg;C. They can increase their metabolic rate five- to sixfold. Heat production is primarily stimulated by the sympathetic nervous system. The response to exogenous administration of noradrenaline and propranolol was investigated.</p><p>Poronvasan l&aring;mmons&aring;&aring;telyn syntym&aring;nj&aring;lkeinen kehittyminen.</p><p>Abstract in Finnish / Yhteenveto: Vastasyntyneiden poronvasojen kylmansietoa ja lammonsaatelya tutkittiin toukokuussa 1981 Inarin Kaamasessa Paliskuntain yhdistyksen koetarhassa. Tutkittavat vasat olivat 1-10 vuorokauden ikaisia. Vasa asetettiin j&aring;&aring;hdytett&aring;va&aring;n mittauskammioon. Sen aineenvaihdunta, lampotilat niin ihon eri kohdista kuin perasuolesta, lihasvarina ja sydanfrekvenssi rekisteroitiin jatkuvasti. Tulosten mukaan naytt&aring;a silt&aring; kuin 1 vuorokauden ikaiselle vasalle -15 &deg;C olisi ehdoton alaraja l&aring;mpotilan s&aring;&aring;telyssa. Se kykeni kohottamaan hapenkulutusta talloin 5-kertaisesti. Lihasvarinan merkitys on vahainen verrattuna kemialliseen l&aring;mmontuottoon kylmassa. Tama voitiin osoittaa injisoimalla vasaan sympaattisen hermoston valittajaainetta noradrenaliinia.</p><p>Temperaturreguleringens utvikling hos nyf&oslash;dte reinkalver.</p><p>Abstract in Norwegian / Sammendrag: Temperaturreguleringens utvikling er studert ved &aring; bestemme nyf&oslash;dte reinkalvers evne til &aring; opprettholde normal kroppstemperatur under p&aring;virkning av gradvis synkende omgivelsestemperatur. Nyf&oslash;dte kalver (1 d&oslash;gn gamle) kan opprettholde sin kroppstemperatur selv ved -15 &deg;C. De kan &oslash;ke sin omsetningshastighet fem til seks ganger. I starten er varmeproduksjonen stimulert av det sympatiske nervesystem. Virkningen av tilf&oslash;rt noradrenalin og propranolol ble studert og skjelving synes &aring; spille bare en mindre rolle umiddelbart etter f&oslash;dselen.</p>

Oxygen consumption after massive sympathetic nervous system discharge

1989 ◽  
Vol 256 (3) ◽  
pp. E345-E351 ◽  
Author(s):  
S. A. Lang ◽  
M. B. Maron ◽  
S. A. Signs
Keyword(s):  
Nervous System ◽  
Oxygen Consumption ◽  
Sympathetic Nervous System ◽  
Plasma Concentrations ◽  
Neurogenic Pulmonary Edema ◽  
O2 Consumption ◽  
Anesthetized Dogs ◽  
Sympathetic Nervous ◽  
O2 Supply ◽  
Alpha Chloralose

We evaluated the possibility that massive, sympathetic nervous system (SNS) activation [as may precede the development of neurogenic pulmonary edema (NPE)] increases O2 demand. O2 consumption (VO2) and plasma concentrations of the calorigenic agents, epinephrine (EPI) and norepinephrine (NE) were measured in alpha-chloralose-anesthetized dogs under control conditions and for 3 h after the administration of either 1) intracisternal (ic) veratrine to activate the SNS, 2) intravenous (iv) veratrine, 3) ic saline, or 4) ic veratrine, after clamping the adrenal blood vessels. VO2 increased 31.7 +/- 3.6% (SE), and EPI and NE increased to, respectively, 30,853 +/- 8,347 and 8,176 +/- 2,104 pg/ml in the ic veratrine group. No increases in VO2 and EPI and attenuated increases in NE were observed in the ic veratrine animals with clamped adrenals. No significant increases in VO2 or catecholamine concentrations were observed after ic saline or iv veratrine administration. These data suggest that the elevated VO2 may have been mediated by adrenal catecholamines and that an increased metabolic rate may complicate the ability of patients with severe NPE to balance O2 supply with demand.

Corticotropin-releasing factor: Effects on the sympathetic nervous system and oxygen consumption

Life Sciences ◽  
1982 ◽  
Vol 30 (2) ◽  
pp. 207-210 ◽  
Author(s):  
Marvin R. Brown ◽  
Laurel A. Fisher ◽  
Jean Rivier ◽  
Joachim Spiess ◽  
Catherine Rivier ◽  
...  
Keyword(s):  
Nervous System ◽  
Oxygen Consumption ◽  
Sympathetic Nervous System ◽  
Corticotropin Releasing Factor ◽  
Sympathetic Nervous

scholarly journals Hyperinsulinemic rats are normotensive but sensitized to angiotensin II

2008 ◽  
Vol 294 (4) ◽  
pp. R1240-R1247 ◽  
Author(s):  
Maria E. Johansson ◽  
Irene J. Andersson ◽  
Camilla Alexanderson ◽  
Ole Skøtt ◽  
Agneta Holmäng ◽  
...  
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Vascular Function ◽  
Ex Vivo ◽  
Sprague Dawley ◽  
Angiotensin Ii Receptor ◽  
Air Jet ◽  
Important Interaction ◽  
Sympathetic Nervous

The effect of insulin on blood pressure (BP) is debated, and an involvement of an activated renin-angiotensin aldosterone system (RAAS) has been suggested. We studied the effect of chronic insulin infusion on telemetry BP and assessed sympathetic activity and dependence of the RAAS. Female Sprague-Dawley rats received insulin (2 units/day, INS group, n = 12) or insulin combined with losartan (30 mg·kg−1·day−1, INS+LOS group, n = 10), the angiotensin II receptor antagonist, for 6 wk. Losartan-treated (LOS group, n = 10) and untreated rats served as controls ( n = 11). We used telemetry to measure BP and heart rate (HR), and acute ganglion blockade and air-jet stress to investigate possible control of BP by the sympathetic nervous system. In addition, we used myograph technique to study vascular function ex vivo. The INS and INS+LOS groups developed euglycemic hyperinsulinemia. Insulin did not affect BP but increased HR (27 beats/min on average). Ganglion blockade reduced mean arterial pressure (MAP) similarly in all groups. Air-jet stress did not increase sympathetic reactivity but rather revealed possible blunting of the stress response in hyperinsulinemia. Chronic losartan markedly reduced 24-h-MAP in the INS+LOS group (−38 ± 1 mmHg P < 0.001) compared with the LOS group (−18 ± 1 mmHg, P ≤ 0.05). While insulin did not affect vascular function per se, losartan improved endothelial function in the aorta of insulin-treated rats. Our results raise doubt regarding the role of hyperinsulinemia in hypertension. Moreover, we found no evidence that insulin affects sympathetic nervous system activity. However, chronic losartan treatment revealed an important interaction between insulin and RAAS in BP control.

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