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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
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