Metabolic Parameters and Energy Expenditure Before and After Weight Loss

Author(s):  
John M. Amatruda
2011 ◽  
Vol 35 (2) ◽  
pp. 214
Author(s):  
Alexander Schwartz ◽  
Rémi Rabasa-Lhoret ◽  
Jean-Marc Lavoie ◽  
Martin Brochu ◽  
Éric Doucet

2000 ◽  
Vol 71 (5) ◽  
pp. 1138-1146 ◽  
Author(s):  
Roland L Weinsier ◽  
Gary R Hunter ◽  
Paul A Zuckerman ◽  
David T Redden ◽  
Betty E Darnell ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2759
Author(s):  
Corinna Geisler ◽  
Manfred J. Müller

Brain gray (GM) and white matter (WM) are associated with resting energy expenditure (REE). The impact of weight loss on GM and WM masses, as well as on their associations with REE and the ratio between body and brain metabolism, i.e., encephalic measure (EM)), are unknown. Longitudinal data of 69 female Caucasian subjects (age range 19–69 years) with detailed information on fat mass (FM), fat free mas (FFM), GM, WM and REE. Mean weight loss was 14.5 ± 11.9 kg with changes in FM (−12.9 ± 9.8 kg), FFM (−1.7 ± 4.8 kg) and REE (−159 ± 191 kcal/24 h) (all p < 0.05). With weight loss, there were no changes in GM and WM. Before and after weight loss, FFM was the main determinant of REE (r2 = 0.483 and 0.413; p < 0.05). After weight loss, GM added to the variances in REE (3.6%), REEadjFFM (6.1%) and the REE on FFM residuals (6.6%). In addition, before and after weight loss GM explained 25.0% and 10.0% of the variances in EM (p < 0.05). Weight loss had no effect on volumes of GM and WM. After weight loss, both, GM added to the variances of REE, REE on FFM residuals and EM.


Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 839-840
Author(s):  
Jose E. Galgani ◽  
Frank L. Greenway ◽  
Ma-Li Wong ◽  
Julio Licinio ◽  
Eric Ravussin

ABSTRACT Context: Leptin regulates energy homeostasis by suppressing food intake; however, its role in energy expenditure and fat oxidation remains uncertain in humans. Objective: The aim of the study was to assess 24-h energy metabolism before and after weight loss induced by leptin treatment in congenital leptin-deficient subjects or low-calorie diet in controls. Design and Patients: We measured 24-h energy expenditure, 24-h fat oxidation, and body fat in three null homozygous leptin-deficient obese adults before and after weight loss induced by a 19-wk leptin replacement period (0.02-0.04 mg/kg/d). The same measures were performed in three obese controls pair-matched for sex, age, and weight loss induced by a 10- to 21-wk low-calorie diet. Measurements were preceded for 1 wk of weight stabilization. Energy expenditure was adjusted for fat-free mass, fat mass, sex, and age based on a reference population (n = 842; R2 = 0.85; P &lt; 0.0001). Similarly, fat oxidation was adjusted for fat-free mass, percentage body fat, energy balance, and diet composition during the 24-h respiratory chamber stay (R2 = 0.38; P &lt; 0.0001). Results: Before weight loss, congenital leptin-deficient and control subjects had similar energy expenditure. However, after weight loss (∼15 kg), controls had energy expenditures lower than expected for their new weight and body composition (−265 ± 76 kcal/d; P = 0.04), whereas leptin-treated subjects had values not different from the reference population (−128 ± 119 kcal/d; P = 0.67). Before weight loss, fat oxidation was similar between groups. However, after weight loss, leptin-treated subjects had higher fat oxidation than controls (P = 0.005) and higher than the reference population (P = 0.0001). Conclusion: In congenital leptin-deficient subjects, leptin replacement prevented the decrease in energy expenditure and fat oxidation often observed after weight loss.


2020 ◽  
Vol 92 (6) ◽  
pp. 53-59
Author(s):  
Sonya S. Gussaova ◽  
Irina N. Bobkova ◽  
Yury I. Yashkov ◽  
Natalya S. Bordan ◽  
Ekaterina V. Stavrovskaya ◽  
...  

Aim. To study the effect of weight loss in the short term after bariatric surgery (BO) on metabolic parameters and glomerular filtration rate (GFR) in patients with morbid obesity. Materials and methods. We studied 40 adult (over 18 years) patients with morbid obesity who underwent bariatric surgery. Metabolic indices and calculated GFR according to the CKD-EPI formula in patients before and after bariatric surgery were compared. Results. In the whole group of operated patients, the average body mass index (BMI) after surgery decreased from 45.8 to 30.5 kg/m2. In 11 (92%) patients with impaired carbohydrate metabolism, remission of diabetes mellitus was achieved and sugar-lowering drugs were canceled. In patients with baseline GFR90 ml/min/1.73 m2 after surgery, there is a tendency towards a decrease in GFR, probably due to a decrease in hyperfiltration. In patients with baseline GFR90 ml/min/1.73 m2 after surgery, a statistically significant increase in the level of GFR was noted. The greater metabolic efficacy of combined operations (mini-gastric bypass, biliopancreatic diversion) in relation to the correction of carbohydrate and fat metabolism was revealed. Conclusion. Obesity is a modifiable risk factor for decreased kidney function and the progression of chronic kidney disease. Bariatric surgery is an effective treatment for morbid obesity. The study proved the positive effect of weight loss after BO on renal function, including by improving the course of diseases associated with obesity.


2010 ◽  
Vol 95 (2) ◽  
pp. 851-855 ◽  
Author(s):  
Jose E. Galgani ◽  
Frank L. Greenway ◽  
Sinan Caglayan ◽  
Ma-Li Wong ◽  
Julio Licinio ◽  
...  

Abstract Context: Leptin regulates energy homeostasis by suppressing food intake; however, its role in energy expenditure and fat oxidation remains uncertain in humans. Objective: The aim of the study was to assess 24-h energy metabolism before and after weight loss induced by leptin treatment in congenital leptin-deficient subjects or low-calorie diet in controls. Design and Patients: We measured 24-h energy expenditure, 24-h fat oxidation, and body fat in three null homozygous leptin-deficient obese adults before and after weight loss induced by a 19-wk leptin replacement period (0.02–0.04 mg/kg/d). The same measures were performed in three obese controls pair-matched for sex, age, and weight loss induced by a 10- to 21-wk low-calorie diet. Measurements were preceded for 1 wk of weight stabilization. Energy expenditure was adjusted for fat-free mass, fat mass, sex, and age based on a reference population (n = 842; R2 = 0.85; P &lt; 0.0001). Similarly, fat oxidation was adjusted for fat-free mass, percentage body fat, energy balance, and diet composition during the 24-h respiratory chamber stay (R2 = 0.38; P &lt; 0.0001). Results: Before weight loss, congenital leptin-deficient and control subjects had similar energy expenditure. However, after weight loss (∼15 kg), controls had energy expenditures lower than expected for their new weight and body composition (−265 ± 76 kcal/d; P = 0.04), whereas leptin-treated subjects had values not different from the reference population (−128 ± 119 kcal/d; P = 0.67). Before weight loss, fat oxidation was similar between groups. However, after weight loss, leptin-treated subjects had higher fat oxidation than controls (P = 0.005) and higher than the reference population (P = 0.0001). Conclusion: In congenital leptin-deficient subjects, leptin replacement prevented the decrease in energy expenditure and fat oxidation often observed after weight loss.


2006 ◽  
Vol 155 (1) ◽  
pp. 161-165 ◽  
Author(s):  
M J Kim ◽  
M Maachi ◽  
C Debard ◽  
E Loizon ◽  
K Clément ◽  
...  

Objective: To investigate the mRNA expression of adiponectin, AdipoR1 and AdipoR2, the two recently cloned adiponectin receptors and peroxisome proliferator activated receptor (PPAR)γ2 in adipose tissue of obese individuals before and during a very low calorie diet (VLCD) inducing weight loss. Methods: Twenty-three non-diabetic obese subjects with normal (NGT, n=11) or impaired glucose tolerance (IGT, n=12) (age, 47±3 years; body mass index, 39.3±1.3 kg/m2) were studied before and after a 3-week 3.9 MJ diet daily without exercise. mRNA levels of nine IGT and six NGT subjects were measured by real-time PCR in s.c. abdominal adipose tissue. Results: Metabolic parameters and insulin sensitivity were improved by VLCD in the IGT group, but minimally affected in the NGT group. VLCD increased expression of AdipoR1 in the IGT (P=0.02), but not in the NGT group. Adiponectin, AdipoR2 and PPARγ2 mRNA levels did not change during VLCD in any group. In the IGT, but not in the NGT group, AdipoR1 and AdipoR2 expressions were positively related to that of PPARγ2 and, after VLCD, AdipoR1 and AdipoR2 expressions were positively related to each other and to that of adiponectin. Conclusion: In the NGT group, the 3-week VLCD inducing weight loss did not modify metabolic parameters, insulin sensitivity and the expression of the adiponectin system in adipose tissue. By contrast, in the IGT group, AdipoR1 expression increased and we found a coordinate regulation of the expression of adiponectin and its receptors. These modifications could participate, through adiponectin action on adipocytes, to the improved metabolic parameters observed in IGT subjects.


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