Faculty Opinions recommendation of The role for adipose tissue in weight regain after weight loss.

Author(s):  
David Wasserman
2019 ◽  
Vol 317 (2) ◽  
pp. E185-E193 ◽  
Author(s):  
Michal Kasher-Meron ◽  
Dou Y. Youn ◽  
Haihong Zong ◽  
Jeffery E. Pessin

Weight regain after weight loss is a well-described phenomenon in both humans and animal models of obesity. Reduced energy expenditure and increased caloric intake are considered the main drivers of weight regain. We hypothesized that adipose tissue with obesity memory (OM) has a tissue-autonomous lipolytic defect, allowing for increased efficiency of lipid storage. We utilized a mouse model of diet-induced obesity, which was subjected to 60% caloric restriction to achieve lean body weight, followed by a short period of high-fat diet (HFD) rechallenge. Age-matched lean mice fed HFD for the first time were used as the control group. Upon rechallenge with HFD, mice with OM had higher respiratory exchange ratios than lean mice with no OM despite comparable body weight, suggesting higher utilization of glucose over fatty acid oxidation. White adipose tissue explants with OM had comparable lipolytic response after caloric restriction; however, reduced functional lipolytic response to norepinephrine was noted as early as 5 days after rechallenge with HFD and was accompanied by reduction in hormone-sensitive lipase serine phosphorylation. The relative lipolytic defect was associated with increased expression of inflammatory genes and a decrease in adrenergic receptor genes, most notably Adrb3. Taken together, white adipose tissue of lean mice with OM shows increased sensitization to HFD compared with white adipose tissue with no OM, rendering it resistant to catecholamine-induced lipolysis. This relative lipolytic defect is tissue-autonomous and could play a role in the rapid weight regain observed after weight loss.


2016 ◽  
Vol 7 ◽  
Author(s):  
Erin D. Giles ◽  
Amy J. Steig ◽  
Matthew R. Jackman ◽  
Janine A. Higgins ◽  
Ginger C. Johnson ◽  
...  

2020 ◽  
Vol 129 (4) ◽  
pp. 909-919
Author(s):  
Alexander T. Sougiannis ◽  
Brandon N. VanderVeen ◽  
Taryn L. Cranford ◽  
Reilly T. Enos ◽  
Kandy T. Velazquez ◽  
...  

We examined the immune and inflammatory status of adipose tissue in mice after they underwent weight loss followed by partial weight regain. We show an increase in selected immune cells and inflammatory mediators, in high-fat diet-fed mice that had prior exposure to a high-fat diet. Although weight fluctuations appear to exacerbate immune cell abundance and inflammation in adipose tissue, severity is less than in mice that were exposed to sustained high-fat diet feedings.


2019 ◽  
Vol 15 (5) ◽  
pp. 274-287 ◽  
Author(s):  
Marleen A. van Baak ◽  
Edwin C. M. Mariman

2000 ◽  
Vol 279 (5) ◽  
pp. E1012-E1019 ◽  
Author(s):  
Barbara J. Nicklas ◽  
Ellen M. Rogus ◽  
Dora M. Berman ◽  
Karen E. Dennis ◽  
Andrew P. Goldberg

This study determines whether changes in abdominal (ABD) and gluteal (GLT) adipose tissue lipoprotein lipase (LPL) activity in response to a 6-mo weight loss intervention, comprised of a hypocaloric diet and low-intensity walking, affect changes in body composition, fat distribution, lipid metabolism, and the magnitude of weight regain in 36 obese postmenopausal women. Average adipose tissue LPL activity did not change with an average 5.6-kg weight loss, but changes in LPL activity were inversely related to baseline LPL activity (ABD: r= −0.60, GLT: r = −0.48; P < 0.01). The loss of abdominal body fat and decreases in total and low-density lipoprotein cholesterol were greater in women whose adipose tissue LPL activity decreased with weight loss despite a similar loss of total body weight and fat mass. Moreover, weight regain after a 6-mo follow-up was less in women whose adipose tissue LPL activity decreased than in women whose LPL increased (ABD: 0.9 ± 0.5 vs. 2.8 ± 0.6 kg, P < 0.05; GLT: 0.2 ± 0.5 vs. 2.8 ± 0.5 kg, P < 0.01). These results suggest that a reduction in adipose tissue LPL activity with weight loss is associated with improvements in lipid metabolic risk factors with weight loss and with diminished weight regain in postmenopausal women.


2015 ◽  
Vol 16 (S1) ◽  
pp. 45-54 ◽  
Author(s):  
P. S. MacLean ◽  
J. A. Higgins ◽  
E. D. Giles ◽  
V. D. Sherk ◽  
M. R. Jackman

2016 ◽  
Vol 115 (5) ◽  
pp. 913-920 ◽  
Author(s):  
Nadia J. T. Roumans ◽  
Stefan G. Camps ◽  
Johan Renes ◽  
Freek G. Bouwman ◽  
Klaas R. Westerterp ◽  
...  

AbstractInitial successful weight loss is often followed by weight regain after the dietary intervention. Compared with lean people, cellular stress in adipose tissue is increased in obese subjects. However, the relation between cellular stress and the risk for weight regain after weight loss is unclear. Therefore, we determined the expression levels of stress proteins during weight loss and weight maintenance in relation to weight regain. In vivo findings were compared with results from in vitro cultured human Simpson–Golabi–Behmel syndrome (SGBS) adipocytes. In total, eighteen healthy subjects underwent an 8-week diet programme with a 10-month follow-up. Participants were categorised as weight maintainers or weight regainers (WR) depending on their weight changes during the intervention. Abdominal subcutaneous adipose tissue biopsies were obtained before and after the diet and after the follow-up. In vitro differentiated SGBS adipocytes were starved for 96 h with low (0·55 mm) glucose. Levels of stress proteins were determined by Western blotting. WR showed increased expressions of β-actin, calnexin, heat shock protein (HSP) 27, HSP60 and HSP70. Changes of β-actin, HSP27 and HSP70 are linked to HSP60, a proposed key factor in weight regain after weight loss. SGBS adipocytes showed increased levels of β-actin and HSP60 after 96 h of glucose restriction. The increased level of cellular stress proteins in the adipose tissue of WR probably resides in the adipocytes as shown by in vitro experiments. Cellular stress accumulated in adipose tissue during weight loss may be a risk factor for weight regain.


Endocrinology ◽  
2015 ◽  
Vol 157 (2) ◽  
pp. 666-678 ◽  
Author(s):  
Jaclyn S. Lerea ◽  
Laurence E. Ring ◽  
Rim Hassouna ◽  
Angie C. N. Chong ◽  
Klara Szigeti-Buck ◽  
...  

Abstract Although most adults can lose weight by dieting, a well-characterized compensatory decrease in energy expenditure promotes weight regain more than 90% of the time. Using mice with impaired hypothalamic leptin signaling as a model of early-onset hyperphagia and obesity, we explored whether this unfavorable response to weight loss could be circumvented by early intervention. Early-onset obesity was associated with impairments in the structure and function of brown adipose tissue mitochondria, which were ameliorated by weight loss at any age. Although decreased sympathetic tone in weight-reduced adults resulted in net reductions in brown adipose tissue thermogenesis and energy expenditure that promoted rapid weight regain, this was not the case when dietary interventions were initiated at weaning. Enhanced energy expenditure persisted even after mice were allowed to resume overeating, leading to lasting reductions in adiposity. These findings reveal a time window when dietary interventions can produce metabolic improvements that are stably maintained.


2016 ◽  
Vol 41 (6) ◽  
pp. 894-901 ◽  
Author(s):  
N J T Roumans ◽  
R G Vink ◽  
F G Bouwman ◽  
P Fazelzadeh ◽  
M A van Baak ◽  
...  

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