Modifications of Activity of Autonomic Nervous System, and Resting Energy Expenditure in Women Using Hormone-Replacement Therapy

2016 ◽  
Vol 8 (5) ◽  
Author(s):  
Monda V ◽  
Valenzano A
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Hormone Replacement Therapy ◽  
Energy Expenditure ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Resting Energy Expenditure ◽  
Autonomic Nervous ◽  
Resting Energy

Enhanced Rate of Resting Energy Expenditure in Women Using Hormone-Replacement Therapy: Preliminary Results

2008 ◽  
Vol 16 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Mylène Aubertin-Leheudre ◽  
Eric D.B. Goulet ◽  
Isabelle J. Dionne
Keyword(s):  
Body Composition ◽  
Hormone Replacement Therapy ◽  
Energy Expenditure ◽  
Replacement Therapy ◽  
Postmenopausal Women ◽  
Hormone Replacement ◽  
Resting Energy Expenditure ◽  
Long Term Treatment ◽  
Resting Energy

Hormone-replacement therapy (HRT) attenuates the menopause-associated alterations in body composition. It is not known, however, whether this effect is a result of a concomitant increase in energy expenditure. The authors examined whether women submitted to a long-term HRT treatment presented greater energy expenditure than women who had never used HRT. We compared 13 postmenopausal women using HRT (>1 yr) with 13 age- (±2 yr) and body-mass-index-matched (BMI; ±1.5kg/m2) postmenopausal women not using HRT. Resting energy expenditure (REE; indirect calorimetry), body composition, and daily (DEE) and physical activity (PAEE) energy expenditure (accelerometry) were obtained. Although BMI, fat mass, fat-free mass, DEE, and PAEE were similar between groups, the HRT group displayed a significantly greater REE than the no-HRT group (Δ +222 kcal/day). In conclusion, the authors observed that a long-term treatment with HRT is associated with a greater REE in postmenopausal women. These results need to be confirmed.

Resting Energy Expenditure in Obese Women with Primary Hypothyroidism and Appropriate Levothyroxine Replacement Therapy

2020 ◽  
Vol 105 (4) ◽  
pp. e1741-e1748 ◽  
Author(s):  
Emanuele Muraca ◽  
Stefano Ciardullo ◽  
Alice Oltolini ◽  
Francesca Zerbini ◽  
Eleonora Bianconi ◽  
...  
Keyword(s):  
Body Composition ◽  
Energy Expenditure ◽  
Replacement Therapy ◽  
Resting Energy Expenditure ◽  
Primary Hypothyroidism ◽  
Normal Serum ◽  
Fat Free Mass ◽  
Model Assessment ◽  
Obese Women ◽  
Resting Energy

Abstract Context Growing evidence suggests that appropriate levothyroxine (LT4) replacement therapy may not correct the full set of metabolic defects afflicting individuals with hypothyroidism. Objective To assess whether obese subjects with primary hypothyroidism are characterized by alterations of the resting energy expenditure (REE). Design Retrospective analysis of a set of data about obese women attending the outpatients service of a single obesity center from January 2013 to July 2019. Patients A total of 649 nondiabetic women with body mass index (BMI) > 30 kg/m2 and thyrotropin (TSH) level 0.4–4.0 mU/L were segregated into 2 groups: patients with primary hypothyroidism taking LT4 therapy (n = 85) and patients with normal thyroid function (n = 564). Main outcomes REE and body composition assessed using indirect calorimetry and bioimpedance. Results REE was reduced in women with hypothyroidism in LT4 therapy when compared with controls (28.59 ± 3.26 vs 29.91 ± 3.59 kcal/kg fat-free mass (FFM)/day), including when adjusted for age, BMI, body composition, and level of physical activity (P = 0.008). This metabolic difference was attenuated only when adjustment for homeostatic model assessment of insulin resistance (HOMA-IR) was performed. Conclusions This study demonstrated that obese hypothyroid women in LT4 therapy, with normal serum TSH level compared with euthyroid controls, are characterized by reduced REE, in line with the hypothesis that standard LT4 replacement therapy may not fully correct metabolic alterations related to hypothyroidism. We are not able to exclude that this feature may be influenced by the modulation of insulin sensitivity at the liver site, induced by LT4 oral administration.

scholarly journals Novel Perspectives for Progesterone in Hormone Replacement Therapy, with Special Reference to the Nervous System

2007 ◽  
Vol 28 (4) ◽  
pp. 387-439 ◽  
Author(s):  
Michael Schumacher ◽  
Rachida Guennoun ◽  
Abdel Ghoumari ◽  
Charbel Massaad ◽  
Françoise Robert ◽  
...  
Keyword(s):  
Nervous System ◽  
Hormone Replacement Therapy ◽  
Special Reference ◽  
Replacement Therapy ◽  
Hormone Replacement

scholarly journals Autonomic Nervous System in the Control of Energy Balance and Body Weight: Personal Contributions

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
G. Messina ◽  
V. De Luca ◽  
An. Viggiano ◽  
A. Ascione ◽  
T. Iannaccone ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Autonomic Nervous System ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Sympathetic Activity ◽  
The Body ◽  
World Health ◽  
Autonomic Nervous

The prevalence of obesity is increasing in the industrialized world, so that the World Health Organization considers obesity as a “pandemia” in rich populations. The autonomic nervous system plays a crucial role in the control of energy balance and body weight. This review summarizes our own data and perspectives, emphasizing the influence exerted by autonomic nervous system on energy expenditure and food intake, which are able to determine the body weight. Activation of the sympathetic discharge causes an increase in energy expenditure and a decrease in food intake, while reduction of food intake and body weight loss determines a reduction of the sympathetic activity. On the other hand, pathophysiological mechanisms of the obesity involve alterations of the sympathetic nervous system in accordance with the “Mona Lisa Hypothesis,” an acronym for “most obesities known are low in sympathetic activity.” Furthermore, the parasympathetic influences on the energy expenditure are analyzed in this review, showing that an increase in parasympathetic activity can induce a paradoxical enhancement of energy consumption.

Mice lacking melanin-concentrating hormone receptor 1 demonstrate increased heart rate associated with altered autonomic activity

2004 ◽  
Vol 287 (4) ◽  
pp. R749-R758 ◽  
Author(s):  
Annika Åstrand ◽  
Mohammad Bohlooly-Y ◽  
Sara Larsdotter ◽  
Margit Mahlapuu ◽  
Harriet Andersén ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Body Temperature ◽  
Energy Expenditure ◽  
Dark Phase ◽  
Wild Type ◽  
Autonomic Nervous ◽  
Significant Difference ◽  
Melanin Concentrating Hormone

Melanin-concentrating hormone (MCH) plays an important role in energy balance. The current studies were carried out on a new line of mice lacking the rodent MCH receptor (MCHR1−/− mice). These mice confirmed the previously reported lean phenotype characterized by increased energy expenditure and modestly increased caloric intake. Because MCH is expressed in the lateral hypothalamic area, which also has an important role in the regulation of the autonomic nervous system, heart rate and blood pressure were measured by a telemetric method to investigate whether the increased energy expenditure in these mice might be due to altered autonomic nervous system activity. Male MCHR1−/− mice demonstrated a significantly increased heart rate [24-h period: wild type 495 ± 4 vs. MCHR1−/− 561 ± 8 beats/min ( P < 0.001); dark phase: wild type 506 ± 8 vs. MCHR1−/− 582 ± 9 beats/min ( P < 0.001); light phase: wild type 484 ± 13 vs. MCHR1−/− 539 ± 9 beats/min ( P < 0.005)] with no significant difference in mean arterial pressure [wild type 110 ± 0.3 vs. MCHR1−/− 113 ± 0.4 mmHg ( P > 0.05)]. Locomotor activity and core body temperature were higher in the MCHR1−/− mice during the dark phase only and thus temporally dissociated from heart rate differences. On fasting, wild-type animals rapidly downregulated body temperature and heart rate. MCHR1−/− mice displayed a distinct delay in the onset of this downregulation. To investigate the mechanism underlying these differences, autonomic blockade experiments were carried out. Administration of the adrenergic antagonist metoprolol completely reversed the tachycardia seen in MCHR1−/− mice, suggesting an increased sympathetic tone.

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