Ethnic differences in sympathetic nervous system-mediated energy expenditure

1991 ◽  
Vol 261 (6) ◽  
pp. E789-E794 ◽  
Author(s):  
M. F. Saad ◽  
S. A. Alger ◽  
F. Zurlo ◽  
J. B. Young ◽  
C. Bogardus ◽  
...  
Keyword(s):  
Nervous System ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Fat Mass ◽  
Weight Maintenance ◽  
Resting Metabolic Rate ◽  
Fat Free Mass ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous ◽  
The Impact

The impact of sympathetic nervous system (SNS) activity on energy expenditure (EE) was evaluated in nondiabetic Caucasian and Pima Indian men while on a weight-maintenance diet using two approaches as follows. 1) The relationship between 24-h EE, measured in a respiratory chamber, and 24-h urinary norepinephrine was studied in 36 Caucasians [32 +/- 8 (SD) yr, 95 +/- 41 kg, 22 +/- 13% fat] and 33 Pimas (29 +/- 6 yr, 103 +/- 28 kg, 30 +/- 9% fat). There was no difference between the two groups in 24-h EE (2,422 vs. 2,523 kcal/24 h) and in urinary norepinephrine (28 vs. 31 micrograms/24 h), even after adjusting for body size and composition. Twenty-four-hour EE correlated significantly with 24-h urinary norepinephrine in Caucasians (r = 0.78, P less than 0.001) but not in Pimas (r = 0.03), independent of fat-free mass (FFM), fat mass, and age. 2) The effect of beta-adrenoceptor blockade with propranolol (120 micrograms/kg FFM bolus and 1.2 micrograms.kg FFM-1.min-1 for 45 min) on the resting metabolic rate (RMR) was evaluated in 36 Caucasians (30 +/- 6 yr, 103 +/- 36 kg, 25 +/- 11% fat) and 32 Pimas (28 +/- 6 yr, 100 +/- 34 kg, 27 +/- 10% fat). The RMR was similar in the two groups (2,052 vs. 1,973 kcal/24 h) even after adjustment for FFM, fat mass, and age and dropped significantly after propranolol infusion in Caucasians (-3.9%, P less than 0.001) but not in Pimas (-0.8%, P = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical sympathectomy alters regulation of body weight during prolonged ICV leptin infusion

2003 ◽  
Vol 284 (4) ◽  
pp. E778-E787 ◽  
Author(s):  
Robert L. Dobbins ◽  
Lidia S. Szczepaniak ◽  
Weiguo Zhang ◽  
J. Denis McGarry
Keyword(s):  
Physical Activity ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Chemical Sympathectomy ◽  
Sympathetic Nervous

To assess the importance of the sympathetic nervous system in regulating body weight during prolonged leptin infusion, we evaluated food intake, body weight, and physical activity in conscious, unrestrained rats. Initial studies illustrated that prolonged intracerebroventricular (ICV) infusion of leptin enhanced substrate oxidation so that adipose tissue lipid stores were completely ablated, and muscle triglyceride and liver glycogen stores were depleted. After neonatal chemical sympathectomy, changes in weight and food intake were compared in groups of sympathectomized (SYM) and control (CON) adult animals during ICV infusion of leptin. CON animals lost 60 ± 9 g over 10 days vs. 25 ± 3 g in the SYM animals when food intake was matched between the two groups. Greater weight loss despite similar energy intake points to an important role of the sympathetic nervous system in stimulating energy expenditure during ICV leptin infusion by increasing the resting metabolic rate, since no differences in physical activity were observed between CON and SYM groups. In conclusion, activation of the SNS by leptin increases energy expenditure by augmenting the resting metabolic rate.

Neurovascular Role of Sympathetic Nervous System and Beta-Adrenoceptor Polymorphisms in Obesity and Hypertension

2008 ◽  
Vol 4 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Kazuko Masuo ◽  
Gavin Lambert ◽  
Hiromi Rakugi ◽  
Toshio Ogihara ◽  
Murray Esler
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Beta Adrenoceptor ◽  
Sympathetic Nervous

scholarly journals Beta-Adrenoceptor Modulation in a Case of Pure Autonomic Failure

1992 ◽  
Vol 19 (1) ◽  
pp. 80-83
Author(s):  
Sergio Perna ◽  
Rocco Leone ◽  
Maria Jussie Farace ◽  
Vincenzo Brescia-Morra ◽  
Giuseppe Campanella ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Autonomic Dysfunction ◽  
Autonomic Failure ◽  
Plasma Catecholamines ◽  
Pure Autonomic Failure ◽  
Beta Adrenoceptor ◽  
The Poor ◽  
Sympathetic Nervous ◽  
Isoproterenol Infusion

ABSTRACT:In a patient with pure autonomic failure, exercise did not modify beta-adrenoceptor density, probably due to an insufficient increase in plasma catecholamines. Isoproterenol infusion increased the number of beta-adrenoceptor by only 17%. Since in control subjects an increased beta-adrenoceptor level was found, following both physical stress and isoproterenol infusion, we suggest that the lack of increased beta-adrenoceptor levels may contribute to the poor circulatory adjustments observed in autonomic dysfunction during activities involving the sympathetic nervous system.

scholarly journals Roles of Beta2- and Beta3-Adrenoceptor Polymorphisms in Hypertension and Metabolic Syndrome

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Kazuko Masuo
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Vascular Reactivity ◽  
Resting Metabolic Rate ◽  
Sympathetic Nervous ◽  
Obesity Hypertension ◽  
Sympathetic Nerve Activation

Hypertension, diabetes mellitus (especially type 2 diabetes mellitus), metabolic syndrome and obesity are rapidly growing public health problems. Sympathetic nerve activation is observed in obesity, hypertension and diabetes mellitus, which have strong genetic as well as environmental determinants. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity have been mainly mediated via the 2- and 3-adrenergic receptors in humans. Further, 2-adrenoceptors importantly influence vascular reactivity and may regulate blood pressure. Genetic polymorphistns of the -adrenoceptor gene have been shown to alter the function of several adrenoceptor subtypes and thus to modify the response to catecholamine. 2-adrenoceptor polymorphisms (Arg16Gly, Gln27Glu, and Thr164Ile) have been studied in relation to hypertension. Genetic variations in the 3-adrenoceptor (i.e. Try64Arg variant) are also associated with both obesity and hypertension. However, the precise relationships of the polymorphisms of 2- and 3-adrenoceptor genes with sympathetic nervous system activity, hypertension, and metabolic syndrome have not been fully clarified. This paper will discuss the current topics involving the influence of the sympathetic nervous system and 2- and 3- adrenoceptor polymorphisms in hypertension and metabolic syndrome.

scholarly journals Role of leptin in energy expenditure: the hypothalamic perspective

2017 ◽  
Vol 312 (6) ◽  
pp. R938-R947 ◽  
Author(s):  
R. Pandit ◽  
S. Beerens ◽  
R. A. H. Adan
Keyword(s):  
Nervous System ◽  
Energy Expenditure ◽  
Sympathetic Nervous System ◽  
Cardiovascular System ◽  
Ventromedial Hypothalamus ◽  
Leptin Signaling ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Sympathetic Nervous

The adipocyte-derived hormone leptin is a peripheral signal that informs the brain about the metabolic status of an organism. Although traditionally viewed as an appetite-suppressing hormone, studies in the past decade have highlighted the role of leptin in energy expenditure. Leptin has been shown to increase energy expenditure in particular through its effects on the cardiovascular system and brown adipose tissue (BAT) thermogenesis via the hypothalamus. The current review summarizes the role of leptin signaling in various hypothalamic nuclei and its effects on the sympathetic nervous system to influence blood pressure, heart rate, and BAT thermogenesis. Specifically, the role of leptin signaling on three different hypothalamic nuclei, the dorsomedial hypothalamus, the ventromedial hypothalamus, and the arcuate nucleus, is reviewed. It is known that all of these brain regions influence the sympathetic nervous system activity and thereby regulate BAT thermogenesis and the cardiovascular system. Thus the current work focuses on how leptin signaling in specific neuronal populations within these hypothalamic nuclei influences certain aspects of energy expenditure.

scholarly journals Metabolic Adaptations to Weight Loss: Relative Changes in Resting Metabolic Rate and Energy Expenditure for Physical Activity and Association With Weight Loss Maintenance

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 526-526
Author(s):  
Rachel Silver ◽  
Sai Das ◽  
Michael Lowe ◽  
Susan Roberts
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Linear Regression ◽  
Energy Expenditure ◽  
Metabolic Rate ◽  
Fat Mass ◽  
Weight Regain ◽  
Resting Metabolic Rate ◽  
Fat Free Mass ◽  
The Mean

Abstract Objectives There is persistent controversy over the extent to which different components of energy expenditure disproportionately decrease after weight loss and contribute to weight regain through decreased energy requirements. We conducted a secondary analysis of the CALERIE I study to test the hypothesis that decreased resting metabolic rate (RMR) and energy expenditure for physical activity (EEPA) after a 6-month calorie restriction intervention would predict weight regain at 12 months, with a greater decrease in RMR than EEPA. Methods Participants (n = 46) received all food and energy-containing beverages for 6 months. Outcome measures included total energy expenditure by doubly labeled water, RMR by indirect calorimetry, and body composition by BOD POD. Predictions for RMR and EEPA were derived from baseline linear regression models including age, sex, fat mass, and fat free mass. Baseline regression coefficients were used to calculate the predicted RMR and EEPA at 6 months. Residuals were calculated as the difference between measured and predicted values and were adjusted for body weight. The presence of metabolic adaptation was evaluated by a paired t-test comparing measured and predicted RMR at 6 months. Differences between 6-month RMR and EEPA residuals were evaluated by the same method. Linear regression was used to assess the association between 6-month residuals and weight loss maintenance (% weight change, 6 to 12 months). Results Mean weight loss was 6.9% at 6 months with 2.1% regain from 6 to 12 months. No adaptation in RMR was observed at 6 months (mean residual: 19 kcal; 95% confidence interval: −9, 48; P = 0.18). However, significant adaptation was observed in EEPA (mean residual: −199 kcal; −126, −272; P < 0.0001). In addition, the mean 6-month RMR residual was significantly greater than the mean 6-month EEPA residual (218 kcal; 133, 304; P < 0.0001). There was no significant association between 6-month RMR or EEPA residuals and weight regain at 12 months (P = 0.56, 0.34). Conclusions There was no measurable decrease in RMR with weight loss after adjusting for changes in fat free mass and fat mass, but there was a decrease in EEPA. Changes in RMR and EEPA with weight loss over 6 months did not predict weight regain at 12 months. Funding Sources Jean Mayer USDA Human Nutrition Research Center on Aging Doctoral Scholarship; USDA agreement #8050–51000-105–01S

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