Angiotensin II regulates oxygen consumption

2002 ◽  
Vol 282 (2) ◽  
pp. R445-R453 ◽  
Author(s):  
Lisa Cassis ◽  
Marc Helton ◽  
Vicki English ◽  
Gerome Burke
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Energy Expenditure ◽  
Water Intake ◽  
Systolic Pressure ◽  
Ang Ii ◽  
Exposure Energy ◽  
Rebound Increase

Previous studies demonstrated that angiotensin II (ANG II) decreases body weight. This study examined whether ANG II regulates body weight through energy expenditure. Acute ANG II administration decreased oxygen consumption. To determine whether this effect was maintained, rats were infused with ANG II or saline for 14 days. Oxygen consumption was transiently decreased on day 1 of ANG II infusion; however, body weight and food intake were reduced for 14 days. In pair-feeding studies, reductions in food intake accounted for 63% of the effect of ANG II on body weight but did not influence systolic pressure, water intake, or oxygen consumption. With 28 days of ANG II infusion, differences in body weight between ANG II and control rats were of greater magnitude. An initial decrease in oxygen consumption was followed by a rebound increase. Coadministration of losartan prevented the effect of ANG II on body weight, food intake, blood pressure, and water intake. However, losartan only partially prevented ANG II reductions in oxygen consumption. These results demonstrate that ANG II transiently decreases oxygen consumption through mechanisms unrelated to food intake. With chronic ANG II exposure, energy expenditure may contribute to sustained reductions in body weight.

Effect of intracerebroventricular angiotensin II on body weight and food intake in adult rats

2004 ◽  
Vol 287 (2) ◽  
pp. R422-R428 ◽  
Author(s):  
James P. Porter ◽  
Kristen R. Potratz
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Water Intake ◽  
Time Course ◽  
Uncoupling Protein ◽  
Ang Ii ◽  
Adult Rats ◽  
Brown Adipose ◽  
Increase Water Consumption

We recently reported that intracerebroventricular infusions of ANG II decreased food intake and increased energy expenditure in young rats. The aim of the present study was to determine if intracerebroventricular ANG II has similar effects in adult rats. The time course of the effect was also investigated with the idea that at earlier time points, a potential role for increased hypothalamic expression of corticotropin-releasing hormone (CRH) in the anorexia could be established. Finally, the contribution of ANG II-induced water drinking to the decrease in food intake was directly investigated. Rats received intracerebroventricular saline or ANG II using osmotic minipumps. Food intake, water intake, and body weight were measured daily. Experiments were terminated 2, 5, or 11 days after the beginning of the infusions. ANG II (∼ 32 ng·kg−1·min−1) produced a transient decrease in food intake that lasted for 4–5 days although body weight continued to be decreased for the entire experiment most likely due to increased energy expenditure as evidenced by increased uncoupling protein-1 mRNA expression in brown adipose tissue. At 11 and 5 days, the expression of CRH mRNA was decreased. At 2 days, CRH expression was not suppressed even though body weight was decreased. The decrease in food intake and body weight was identical whether or not rats were allowed to increase water consumption. These data suggest that in adult rats ANG II acts within the brain to affect food intake and energy expenditure in a manner that is not related to water intake.

Intracerebroventricular losartan inhibits postprandial drinking in sheep

1997 ◽  
Vol 272 (4) ◽  
pp. R1055-R1059 ◽  
Author(s):  
M. Mathai ◽  
M. D. Evered ◽  
M. J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Fluid Balance ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Drinking Response ◽  
Dependent Mechanism

We investigated the contribution of brain angiotensinergic mechanisms to postprandial drinking in sheep. Sheep in fluid balance were given 0.8 kg chaff for 30 min, and water intake was measured for the next hour. Intracerebroventricular infusion of the AT1 type angiotensin II (ANG II) receptor blocker losartan (1 mg/h) reduced postprandial drinking by approximately 70% (n = 7, P < 0.01) but did not affect food intake. The same losartan dose given intravenously had little or no effect on prandial drinking. Feeding increased Na+ concentrations in plasma and cerebrospinal fluid (CSF; n = 5, P < 0.05). Intracerebroventricular losartan (1 mg/h) inhibited the drinking responses to intracarotid infusion of ANG II (0.8 microg/min for 30 min, n = 4, P < 0.01) and to intracerebroventricular infusion of 0.5 M NaCl (1 ml/h for 1 h, n = 5, P < 0.05) but had no effect on drinking responses to intravenous infusion of 4 M NaCl (1.3 ml/min for 30 min). These findings indicate that a brain ANG II-dependent mechanism is involved in postprandial drinking in sheep. They suggest also that the mechanism by which increasing CSF Na+ causes thirst involves brain ANG II and is different from the mechanism subserving the drinking response to changes in blood Na+.

Abstract 082: Chronic Angiotensin-(1-7) Attenuates the Development of Obesity in Mice by Enhancing Energy Expenditure

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Amy C Arnold ◽  
Charlene Finney ◽  
Italo Biaggioni
Keyword(s):  
Insulin Resistance ◽  
Oxygen Consumption ◽  
Energy Expenditure ◽  
Water Intake ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
High Fat ◽  
Angiotensin System ◽  
Obesity In Mice

Activation of the renin-angiotensin system, and in particular angiotensin (Ang) II, is observed in obese patients and closely correlates with insulin resistance. Obesity is also associated with deficiency of Ang-(1-7), a vasodilatory peptide that mitigates Ang II actions. Accumulating evidence suggests that Ang-(1-7) has direct positive metabolic effects including reducing adiposity and reversing whole-body glucose intolerance and insulin resistance in animal models of cardiometabolic syndrome. In this study, we tested the hypothesis that chronic Ang-(1-7) administration would prevent high fat diet-induced obesity in mice, and determined potential mechanisms underlying this effect. To test this hypothesis, adult male C57BL/6J mice received a 12-week systemic infusion of Ang-(1-7) (400 ng/kg/min; n=7) or saline (n=6) via subcutaneous osmotic mini-pumps. Immediately following mini-pump implantation, mice were placed on a 60% high fat diet, with body mass measured weekly. Body composition (mq10 nuclear magnetic resonance analyzer), food and water intake, and energy expenditure (indirect calorimetry) were measured during the last week of treatment. Ang-(1-7) attenuated high fat diet-induced weight gain [39.7±1.3 Ang-(1-7) vs. 43.9±0.7 g saline at 12 weeks; p=0.023) and adiposity [32±1 Ang-(1-7) vs. 29±1% saline; p=0.050). The reduced gain in body weight following Ang-(1-7) was associated with increased average energy expenditure [0.55±0.02 Ang-(1-7) vs. 0.42±0.06 kcal/hour saline, p=0.038] and oxygen consumption [1.84±0.07 Ang-(1-7) vs. 1.39±0.23 ml/min saline, p=0.049] during the dark cycle, with no effect on locomotor activity. A similar trend for Ang-(1-7) to increase energy expenditure and oxygen consumption was observed during the light cycle. There were no significant differences in food or water intake following chronic Ang-(1-7) versus saline infusion. These findings suggest that targeting of Ang-(1-7) may be a novel strategy to prevent the development of obesity by enhancing energy expenditure, and further highlight the importance of the renin-angiotensin system in metabolic regulation.

Behavior of sheep drinking ethanol solution

1995 ◽  
Vol 268 (6) ◽  
pp. R1526-R1532 ◽  
Author(s):  
J. R. Blair-West ◽  
D. R. Deam ◽  
D. A. Denton ◽  
E. Tarjan ◽  
R. S. Weisinger
Keyword(s):  
Body Weight ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Ethanol Solution ◽  
Ethanol Intake ◽  
Chronic Ethanol ◽  
Ang Ii ◽  
Water Drinking ◽  
Drinking Ethanol

Sheep that were habituated to drinking 10% (vol/vol) ethanol solution instead of water were subjected to proven thirst stimuli to study the effect of chronic ethanol intake on brain mechanisms subserving thirst. Sheep that had not previously drunk 10% ethanol were also tested. All sheep were trained to press a pedal that delivered 50 ml/press of fluid (either 10% ethanol or water) into a drinking cup. In some experiments, fluids were presented in bins. All animals had access to only one fluid at a time. Five ethanol-drinking sheep appeared healthy and maintained body weight over 18 mo. They always preferred water to 10% ethanol. The intracerebroventricular (icv) infusion of angiotensin II (ANG II) at 3.8 micrograms/h for 2 h increased ethanol intake from 15 +/- 10 to 200 +/- 55 ml in the 1st h, but 2,850 +/- 320 ml of water was drunk in the 2nd h. The icv infusion of 500 mM NaCl had a similar effect. After fluid deprivation for 22 or 46 h, ethanol intake in 1 h of access was only 280 +/- 40 and 400 +/- 90 ml, respectively, and 24-h intake was not increased. Water-drinking sheep drank 1,300 +/- 195 ml of water in 1 h after 22-h water deprivation, and 24-h intake was 1.5 times normal. The icv infusion of ANG II in these sheep increased water intake in 1 h from 10 +/- 10 to 1,630 +/- 250 ml and intake of 10% ethanol to only 310 +/- 60 ml. In conclusion, sheep accept 10% ethanol as a substitute for water for daily drinking.(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of angiotensin II in water intake of genetically polydipsic mice

1991 ◽  
Vol 260 (6) ◽  
pp. R1152-R1158 ◽  
Author(s):  
T. Katafuchi ◽  
Y. Hattori ◽  
I. Nagatomo ◽  
K. Koizumi ◽  
E. Silverstein
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Dark Period ◽  
Plasma Renin ◽  
Ang Ii ◽  
Arterial Blood ◽  
Daily Water Intake ◽  
Reduced Drinking

The involvement of angiotensin II (ANG II) in the genetic polydipsia of the STR/N strain of mice was investigated. Daily water intake of the polydipsic inbred STR/N of both sexes ranged between five and eight times that of nonpolydipsic controls: STR/1N, a mutant of the STR/N, and Swiss-Webster (S/W) mice. Nevertheless the diurnal pattern of drinking was maintained in the STR/N. There was no difference in daily food intake, arterial blood pressure, and plasma renin activity among the three groups. Drinking responses to 48 h of water deprivation were not significantly different between the polydipsic mice and their control groups. Captopril, an angiotensin I converting-enzyme inhibitor, injected subcutaneously just before the dark period, reduced drinking for 6 h in the polydipsic strain only. Food intake of all three groups of mice was not affected. Similarly the ANG II antagonist saralasin, [Sar1,-Ile8]ANG II, injected into the lateral cerebroventricle just before the dark period, significantly reduced water intake for 6 h after injection in the polydipsic mice only. Intracerebroventricular injection of ANG II increased drinking in the nondeprived controls but not in the polydipsic mice. These findings suggest that the polydipsia in the STR/N mice may involve, at least in part, the ANG II system in the brain.

scholarly journals Central angiotensin II has catabolic action at white and brown adipose tissue

2011 ◽  
Vol 301 (6) ◽  
pp. E1081-E1091 ◽  
Author(s):  
Annette D. de Kloet ◽  
Eric G. Krause ◽  
Karen A. Scott ◽  
Michelle T. Foster ◽  
James P. Herman ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Angiotensin Ii ◽  
Energy Balance ◽  
Food Intake ◽  
Adrenergic Receptor ◽  
Receptor Expression ◽  
Ang Ii ◽  
Sympathetic Activation ◽  
Brown Adipose

Considerable evidence implicates the renin-angiotensin system (RAS) in the regulation of energy balance. To evaluate the role of the RAS in the central nervous system regulation of energy balance, we used osmotic minipumps to chronically administer angiotensin II (Ang II; icv; 0.7 ng/min for 24 days) to adult male Long-Evans rats, resulting in reduced food intake, body weight gain, and adiposity. The decrease in body weight and adiposity occurred relative to both ad libitum- and pair-fed controls, implying that reduced food intake in and of itself does not underlie all of these effects. Consistent with this, rats administered Ang II had increased whole body heat production and oxygen consumption. Additionally, chronic icv Ang II increased uncoupling protein-1 and β3-adrenergic receptor expression in brown adipose tissue and β3-adrenergic receptor expression in white adipose tissue, which is suggestive of enhanced sympathetic activation and thermogenesis. Chronic icv Ang II also increased hypothalamic agouti-related peptide and decreased hypothalamic proopiomelanocortin expression, consistent with a state of energy deficit. Moreover, chronic icv Ang II increased the anorectic corticotrophin- and thyroid-releasing hormones within the hypothalamus. These results suggest that Ang II acts in the brain to promote negative energy balance and that contributing mechanisms include an alteration in the hypothalamic circuits regulating energy balance, a decrease in food intake, an increase in energy expenditure, and an increase in sympathetic activation of brown and white adipose tissue.

scholarly journals Severe protein deficiency induces hepatic expression and systemic level of FGF21 but inhibits its hypothalamic expression in growing rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joanna Moro ◽  
Catherine Chaumontet ◽  
Patrick C. Even ◽  
Anne Blais ◽  
Julien Piedcoq ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Dietary Protein ◽  
Protein Deficiency ◽  
Protein Diet ◽  
Growing Rats ◽  
Low Protein ◽  
Protein Diets

AbstractTo study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and to assess the role of FGF21 in the adaptation to a low protein diet. Thirty-six weanling rats were fed diets containing 3%, 5%, 8%, 12%, 15% and 20% protein for three weeks. Body weight, food intake, energy expenditure and metabolic parameters were followed throughout this period. The very low-protein diets (3% and 5%) induced a large decrease in body weight gain and an increase in energy intake relative to body mass. No gain in fat mass was observed because energy expenditure increased in proportion to energy intake. As expected, Fgf21 expression in the liver and plasma FGF21 increased with low-protein diets, but Fgf21 expression in the hypothalamus decreased. Under low protein diets (3% and 5%), the increase in liver Fgf21 and the decrease of Fgf21 in the hypothalamus induced an increase in energy expenditure and the decrease in the satiety signal responsible for hyperphagia. Our results highlight that when dietary protein decreases below 8%, the liver detects the low protein diet and responds by activating synthesis and secretion of FGF21 in order to activate an endocrine signal that induces metabolic adaptation. The hypothalamus, in comparison, responds to protein deficiency when dietary protein decreases below 5%.

scholarly journals Susceptibility to diet induced obesity at thermoneutral conditions is independent of UCP1

2021 ◽  
Author(s):  
Sebastian Dieckmann ◽  
Akim Strohmeyer ◽  
Monja Willershaeuser ◽  
Stefanie Maurer ◽  
Wolfgang Wurst ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Knockout Mice ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Exon 2 ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Knockout Model

Objective Activation of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) upon cold stimulation leads to substantial increase in energy expenditure to defend body temperature. Increases in energy expenditure after a high caloric food intake, termed diet-induced thermogenesis, are also attributed to BAT. These properties render BAT a potential target to combat diet-induced obesity. However, studies investigating the role of UCP1 to protect against diet-induced obesity are controversial and rely on the phenotyping of a single constitutive UCP1-knockout model. To address this issue, we generated a novel UCP1-knockout model by Cre-mediated deletion of Exon 2 in the UCP1 gene. We studied the effect of constitutive UCP1 knockout on metabolism and the development of diet-induced obesity. Methods UCP1 knockout and wildtype mice were housed at 30°C and fed a control diet for 4-weeks followed by 8-weeks of high-fat diet. Body weight and food intake were monitored continuously over the course of the study and indirect calorimetry was used to determine energy expenditure during both feeding periods. Results Based on Western blot analysis, thermal imaging and noradrenaline test, we confirmed the lack of functional UCP1 in knockout mice. However, body weight gain, food intake and energy expenditure were not affected by deletion of UCP1 gene function during both feeding periods. Conclusion Conclusively, we show that UCP1 does not protect against diet-induced obesity at thermoneutrality. Further we introduce a novel UCP1-KO mouse enabling the generation of conditional UCP1-knockout mice to scrutinize the contribution of UCP1 to energy metabolism in different cell types or life stages.

scholarly journals Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Positive Energy ◽  
Chow Diet ◽  
Chromatin Regulator ◽  
Positive Energy Balance ◽  
The Impact ◽  
Deficient Mice

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.

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