PMID- 27916987
OWN - NLM
STAT- MEDLINE
DCOM- 20180430
LR  - 20181113
IS  - 1476-5497 (Electronic)
IS  - 0307-0565 (Linking)
VI  - 41
IP  - 6
DP  - 2017 Jun
TI  - Weight loss-induced cellular stress in subcutaneous adipose tissue and the risk 
      for weight regain in overweight and obese adults.
PG  - 894-901
LID - 10.1038/ijo.2016.221 [doi]
AB  - BACKGROUND/OBJECTIVE: Weight loss is often followed by weight regain after the 
      dietary intervention (DI). Cellular stress is increased in adipose tissue of 
      obese individuals. However, the relation between cellular stress and weight 
      regain is unclear. Previously, we observed increased adipose tissue cellular 
      stress of participants regaining weight compared with participants maintaining 
      weight loss. In the current study, we further investigated the relation between 
      weight regain and changes in the expression of stress-related genes and stress 
      protein levels to determine possible predictors of weight regain. 
      PARTICIPANTS/METHODS: In this randomized controlled trial, sixty-one healthy 
      overweight/obese participants followed a DI of either a 5-week very-low-calorie 
      diet (500 kcal per day) or a 12-week low-calorie diet (1250 kcal per day; WL 
      period) with a subsequent 4-week weight stable diet (WS period), and a 9-month 
      follow-up. The WL and WS period taken together was named the DI. Abdominal 
      subcutaneous adipose tissue biopsies were collected in 53 participants for 
      microarray and liquid chromatography-mass spectrometry analysis. RNA and protein 
      levels for a broad set of stress-related genes were correlated to the weight 
      regain percentage. RESULTS: Different gene sets correlated to weight regain 
      percentage during WS and DI. Bioinformatics clustering suggests that during the 
      WS phase-defined genes for actin filament dynamics, glucose handling and nutrient 
      sensing are related to weight regain. HIF-1 (hypoxia-inducible factor-1) is 
      indicated as an important regulator. With regard to DI, clustering of correlated 
      genes indicate that LGALS1, ENO1 and ATF2 are important nodes for conferring risk 
      for weight regain. CONCLUSIONS: Our present findings indicate that the risk for 
      weight regain is related to expression changes of distinct sets of stress-related 
      genes during the first 4 weeks after returning to energy balance, and during the 
      DI. Further research is required to investigate the mechanistic significance of 
      these findings and find targets for preventing weight regain.
FAU - Roumans, N J T
AU  - Roumans NJT
AD  - Department of Human Biology, NUTRIM, School of Nutrition and Translational 
      Research in Metabolism, Maastricht University Medical Centre, Maastricht, The 
      Netherlands.
FAU - Vink, R G
AU  - Vink RG
AD  - Department of Human Biology, NUTRIM, School of Nutrition and Translational 
      Research in Metabolism, Maastricht University Medical Centre, Maastricht, The 
      Netherlands.
FAU - Bouwman, F G
AU  - Bouwman FG
AD  - Department of Human Biology, NUTRIM, School of Nutrition and Translational 
      Research in Metabolism, Maastricht University Medical Centre, Maastricht, The 
      Netherlands.
FAU - Fazelzadeh, P
AU  - Fazelzadeh P
AD  - Nutrition, Metabolism and Genomics Group, Division of Human Nutrition, Wageningen 
      University, Wageningen, The Netherlands.
FAU - van Baak, M A
AU  - van Baak MA
AD  - Department of Human Biology, NUTRIM, School of Nutrition and Translational 
      Research in Metabolism, Maastricht University Medical Centre, Maastricht, The 
      Netherlands.
FAU - Mariman, E C M
AU  - Mariman ECM
AD  - Department of Human Biology, NUTRIM, School of Nutrition and Translational 
      Research in Metabolism, Maastricht University Medical Centre, Maastricht, The 
      Netherlands.
LA  - eng
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20161205
PL  - England
TA  - Int J Obes (Lond)
JT  - International journal of obesity (2005)
JID - 101256108
RN  - 0 (ATF2 protein, human)
RN  - 0 (Activating Transcription Factor 2)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Galectin 1)
RN  - 0 (LGALS1 protein, human)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 4.2.1.11 (ENO1 protein, human)
RN  - EC 4.2.1.11 (Phosphopyruvate Hydratase)
SB  - IM
MH  - Activating Transcription Factor 2
MH  - Adipocytes/*metabolism
MH  - Adult
MH  - Biomarkers, Tumor
MH  - Body Weight Maintenance/*physiology
MH  - Caloric Restriction
MH  - Computational Biology
MH  - DNA-Binding Proteins
MH  - Energy Metabolism
MH  - Female
MH  - Galectin 1
MH  - Gene Expression Regulation/physiology
MH  - Humans
MH  - Male
MH  - Obesity/*diet therapy/genetics/metabolism
MH  - Overweight/metabolism/*physiopathology
MH  - Oxidative Stress/*physiology
MH  - Phosphopyruvate Hydratase
MH  - Subcutaneous Fat, Abdominal/*metabolism
MH  - Tumor Suppressor Proteins
MH  - Weight Gain/physiology
MH  - Weight Loss/*physiology
EDAT- 2016/12/06 06:00
MHDA- 2018/05/01 06:00
CRDT- 2016/12/06 06:00
PHST- 2016/08/01 00:00 [received]
PHST- 2016/10/28 00:00 [revised]
PHST- 2016/11/22 00:00 [accepted]
PHST- 2016/12/06 06:00 [pubmed]
PHST- 2018/05/01 06:00 [medline]
PHST- 2016/12/06 06:00 [entrez]
AID - ijo2016221 [pii]
AID - 10.1038/ijo.2016.221 [doi]
PST - ppublish
SO  - Int J Obes (Lond). 2017 Jun;41(6):894-901. doi: 10.1038/ijo.2016.221. Epub 2016 
      Dec 5.