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Adipose tissue morphology predicts improved insulin sensitivity following moderate or pronounced weight loss.

https://arctichealth.org/en/permalink/ahliterature272781
Source
Int J Obes (Lond). 2015 Jun;39(6):893-8
Publication Type
Article
Date
Jun-2015
Author
D. Eriksson-Hogling
D P Andersson
J. Bäckdahl
J. Hoffstedt
S. Rössner
A. Thorell
E. Arner
P. Arner
M. Rydén
Source
Int J Obes (Lond). 2015 Jun;39(6):893-8
Date
Jun-2015
Language
English
Publication Type
Article
Keywords
Adipocytes - metabolism - pathology
Adipose Tissue, White - metabolism - pathology
Adult
Bariatric Surgery
Blood Glucose - metabolism
Body mass index
Cell Enlargement
Cohort Studies
Diabetes Mellitus, Type 2 - etiology - metabolism - prevention & control
Diet, Reducing
Female
Humans
Inflammation - etiology - metabolism
Male
Obesity - complications - metabolism - pathology - surgery
Randomized Controlled Trials as Topic
Sweden
Weight Loss
Abstract
Cross-sectional studies show that white adipose tissue hypertrophy (few, large adipocytes), in contrast to hyperplasia (many, small adipocytes), associates with insulin resistance and increased risk of developing type 2 diabetes. We investigated if baseline adipose cellularity could predict improvements in insulin sensitivity following weight loss.
Plasma samples and subcutaneous abdominal adipose biopsies were examined in 100 overweight or obese individuals before and 10 weeks after a hypocaloric diet (7±3% weight loss) and in 61 obese subjects before and 2 years after gastric by-pass surgery (33±9% weight loss). The degree of adipose tissue hypertrophy or hyperplasia (termed the morphology value) in each individual was calculated on the basis of the relationship between fat cell volume and total fat mass. Insulin sensitivity was determined by homeostasis model assessment-estimated insulin resistance (HOMAIR).
In both cohorts at baseline, subjects with hypertrophy displayed significantly higher fasting plasma insulin and HOMAIR values than subjects with hyperplasia (P
PubMed ID
25666530 View in PubMed
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The fat cell epigenetic signature in post-obese women is characterized by global hypomethylation and differential DNA methylation of adipogenesis genes.

https://arctichealth.org/en/permalink/ahliterature272775
Source
Int J Obes (Lond). 2015 Jun;39(6):910-9
Publication Type
Article
Date
Jun-2015
Author
I. Dahlman
I. Sinha
H. Gao
D. Brodin
A. Thorell
M. Rydén
D P Andersson
J. Henriksson
A. Perfilyev
C. Ling
K. Dahlman-Wright
P. Arner
Source
Int J Obes (Lond). 2015 Jun;39(6):910-9
Date
Jun-2015
Language
English
Publication Type
Article
Keywords
Adipocytes - metabolism
Adipogenesis - genetics
Adult
Biomarkers - metabolism
Body mass index
CpG Islands
DNA Methylation - genetics
Female
Follow-Up Studies
Gastric Bypass
Gene Expression Regulation
Genome-Wide Association Study
Humans
Middle Aged
Obesity - genetics - metabolism - surgery
Promoter Regions, Genetic
Reproducibility of Results
Subcutaneous Fat - metabolism
Sweden - epidemiology
Weight Gain - genetics
Weight Loss
Abstract
Obese subjects have increased number of enlarged fat cells that are reduced in size but not in number in post-obesity. We performed DNA methylation profiling in fat cells with the aim of identifying differentially methylated DNA sites (DMS) linked to adipose hyperplasia (many small fat cells) in post-obesity.
Genome-wide DNA methylation was analyzed in abdominal subcutaneous fat cells from 16 women examined 2 years after gastric bypass surgery at a post-obese state (body mass index (BMI) 26±2?kg?m(-2), mean±s.d.) and from 14 never-obese women (BMI 25±2?kg?m(-2)). Gene expression was analyzed in subcutaneous adipose tissue from nine women in each group. In a secondary analysis, we examined DNA methylation and expression of adipogenesis genes in 15 and 11 obese women, respectively.
The average degree of DNA methylation of all analyzed CpG sites was lower in fat cells from post-obese as compared with never-obese women (P=0.014). A total of 8504 CpG sites were differentially methylated in fat cells from post-obese versus never-obese women (false discovery rate 1%). DMS were under-represented in CpG islands and surrounding shores. The 8504 DMS mapped to 3717 unique genes; these genes were over-represented in cell differentiation pathways. Notably, 27% of the genes linked to adipogenesis (that is, 35 of 130) displayed DMS (adjusted P=10(-8)) in post-obese versus never-obese women. Next, we explored DNA methylation and expression of genes linked to adipogenesis in more detail in adipose tissue samples. DMS annotated to adipogenesis genes were not accompanied by differential gene expression in post-obese compared with never-obese women. In contrast, adipogenesis genes displayed differential DNA methylation accompanied by altered expression in obese women.
Global CpG hypomethylation and over-representation of DMS in adipogenesis genes in fat cells may contribute to adipose hyperplasia in post-obese women.
PubMed ID
25783037 View in PubMed
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