Mechanisms of weight regain after weight loss — the role of adipose tissue

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


Endocrinology ◽  
2013 ◽  
Vol 154 (9) ◽  
pp. 3118-3129 ◽  
Author(s):  
Jose M. Garcia ◽  
Thomas Scherer ◽  
Ji-an Chen ◽  
Bobby Guillory ◽  
Anriada Nassif ◽  
...  

Cachexia, defined as an involuntary weight loss ≥5%, is a serious and dose-limiting side effect of chemotherapy that decreases survival in cancer patients. Alterations in lipid metabolism are thought to cause the lipodystrophy commonly associated with cachexia. Ghrelin has been proposed to ameliorate the alterations in lipid metabolism due to its orexigenic and anabolic properties. However, the mechanisms of action through which ghrelin could potentially ameliorate chemotherapy-associated cachexia have not been elucidated. The objectives of this study were to identify mechanisms by which the chemotherapeutic agent cisplatin alters lipid metabolism and to establish the role of ghrelin in reversing cachexia. Cisplatin-induced weight and fat loss were prevented by ghrelin. Cisplatin increased markers of lipolysis in white adipose tissue (WAT) and of β-oxidation in liver and WAT and suppressed lipogenesis in liver, WAT, and muscle. Ghrelin prevented the imbalance between lipolysis, β-oxidation, and lipogenesis in WAT and muscle. Pair-feeding experiments demonstrated that the effects of cisplatin and ghrelin on lipogenesis, but not on lipolysis and β-oxidation, were due to a reduction in food intake. Thus, ghrelin prevents cisplatin-induced weight and fat loss by restoring adipose tissue functionality. An increase in caloric intake further enhances the anabolic effects of ghrelin.


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.


2016 ◽  
Vol 12 (01) ◽  
pp. 14
Author(s):  
Marion J Franz ◽  

Weight loss is important for the prevention of prediabetes, for halting the progression of prediabetes to diabetes, and for improving metabolic outcomes early after the diagnosis of type 2 diabetes. However, as type 2 diabetes progresses from being primarily related to insulin resistance to insulin deficiency, weight loss that can be achieved by many individuals may or may not improve outcomes. A reduced energy intake continues to be essential. For some it may lead to weight loss, for some it may prevent weight regain after weight loss, and for some it may prevent weight gain, but even without weight loss, it can have beneficial effects on metabolic outcomes.


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.


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