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Abdominal subcutaneous adipose tissue cellularity in men and women.

https://arctichealth.org/en/permalink/ahliterature294588
Source
Int J Obes (Lond). 2017 10; 41(10):1564-1569
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
10-2017
Author
D P Andersson
E Arner
D E Hogling
M Rydén
P Arner
Author Affiliation
Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
Source
Int J Obes (Lond). 2017 10; 41(10):1564-1569
Date
10-2017
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Absorptiometry, Photon
Adipocytes - cytology
Adolescent
Adult
Aged
Body Composition
Body Fat Distribution
Body mass index
Female
Humans
Insulin Resistance
Male
Middle Aged
Sex Characteristics
Subcutaneous Fat, Abdominal - cytology
Sweden
Young Adult
Abstract
Differences in subcutaneous abdominal adipose tissue (SAT) fat cell size and number (cellularity) are linked to insulin resistance. Men are generally more insulin resistant than women but it is unknown whether there is a gender dimorphism in SAT cellularity. The objective was to determine SAT cellularity and its relationship to insulin sensitivity in men and women.
In a cohort study performed at an outpatient academic clinic in Sweden, 798 women and 306 men were included. Estimated SAT mass (ESAT) was derived from measures of dual-energy X-ray absorptiometry and a formula. SAT biopsies were obtained to measure mean fat cell size; SAT adipocyte number was obtained by dividing ESAT with mean fat cell weight. Fat cell size was also compared with level of insulin sensitivity in vivo.
Over the entire range of body mass index (BMI) both fat cell size and number correlated positively with ESAT in either sex. On average, fat cell size was larger in men than in women, which was driven by significantly larger fat cells in non-obese men compared with non-obese women; no gender effect on fat cell size was seen in obese subjects. For all subjects fat cell number was larger in women than men, which was driven by a gender effect among non-obese individuals (P
Notes
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PubMed ID
28630459 View in PubMed
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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
Less detail

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
Less detail

Visceral fat cell lipolysis and cardiovascular risk factors in obesity.

https://arctichealth.org/en/permalink/ahliterature130361
Source
Horm Metab Res. 2011 Oct;43(11):809-15
Publication Type
Article
Date
Oct-2011
Author
D P Andersson
P. Löfgren
A. Thorell
P. Arner
J. Hoffstedt
Author Affiliation
Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Source
Horm Metab Res. 2011 Oct;43(11):809-15
Date
Oct-2011
Language
English
Publication Type
Article
Keywords
Adult
Bariatric Surgery
Biopsy, Needle
Body mass index
Cardiovascular Diseases - epidemiology
Cells, Cultured
Female
Glycerol - metabolism
Humans
Intra-Abdominal Fat - metabolism - pathology
Lipolysis
Metabolic Syndrome X - complications
Middle Aged
Norepinephrine - metabolism
Obesity, Morbid - complications - metabolism - pathology - surgery
Organ Specificity
Risk factors
Subcutaneous Fat, Abdominal - metabolism - pathology
Sweden - epidemiology
Young Adult
Abstract
Visceral fat accumulation relates to cardiovascular risk factors, but the underlying mechanisms are not well understood. We investigated the role of visceral adipocyte triglyceride breakdown (lipolysis) for several risk factors of cardiovascular disease. In 73 obese women, fat mass and distribution, blood pressure, blood samples for cardiometabolic risk factors, and whole-body insulin sensitivity were determined. A subcutaneous and a visceral fat biopsy were taken. Fat cell glycerol release after stimulation with a major lipolytic hormone, noradrenaline, was measured. In simple regression analysis, visceral fat cell lipolysis, but not subcutaneous adipocyte lipolysis was related to components of the metabolic syndrome. Moreover, subjects in the highest quartile of catecholamine-induced visceral lipolysis had higher levels of systolic blood pressure, estimated liver fat, plasma levels of glucose, insulin, cholesterol, LDL-cholesterol, triglycerides and apolipoprotein B and lower whole-body insulin sensitivity than those in the lowest quartile (p=0.0004-0.048). Among subjects with the metabolic syndrome, visceral fat cell lipolysis was 40% higher than in the remaining subjects (p=0.0052). Catecholamine-activated lipolysis in visceral but not subcutaneous fat cells is associated with cardiovascular risk factors in obesity.
PubMed ID
22009377 View in PubMed
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