Prostaglandin (PG) F2 alpha synthesis in human subcutaneous and omental adipose tissue: modulation by inflammatory cytokines and role of the human aldose reductase AKR1B1.

Introduction: PGF2α may be involved in the regulation of adipose tissue function.

Objectives: 1) To examine PGF2α release by primary preadipocytes, mature adipocytes and whole tissue explants from the subcutaneous and omental fat compartments; 2) To assess which PGF synthase is the most relevant in human adipose tissue.

Methods: Fat samples were obtained by surgery in women.

Abdominal subcutaneous and omental adipocyte morphology and its relation to gene expression, lipolysis and adipocytokine levels in women.

Objective: We tested the hypothesis that women with adipocyte hypertrophy in either omental (OM) or subcutaneous (SC) adipose tissue are characterized by alterations in adipocyte lipolysis and adipose tissue expression of genes coding for proteins involved in adipocyte metabolism or inflammation, independent of overall adiposity and fat distribution.

Methods: OM and SC fat samples were obtained surgically in 44 women (age: 47.1±5.

Markers of macrophage infiltration and measures of lipolysis in human abdominal adipose tissues.

Objective: We tested the hypothesis that high lipolytic responsiveness is related to increased expression of ATM genes in human adipose tissues.

Design And Methods: Omental (OM) and subcutaneous (SC) fat samples were obtained surgically in 46 women (age: 47.2 ± 4.

Visceral fat accumulation is an indicator of adipose tissue macrophage infiltration in women.

We tested the hypothesis that visceral obesity is the best correlate of abdominal adipose tissue macrophage infiltration in women. Omental and subcutaneous fat samples were surgically obtained from 40 women (age, 47.0 ± 4.

Visceral adipocyte hypertrophy is associated with dyslipidemia independent of body composition and fat distribution in women.

Objective: We assessed whether subcutaneous and omental adipocyte hypertrophy are related to metabolic alterations independent of body composition and fat distribution in women.

Research Design And Methods: Mean adipocyte diameter of paired subcutaneous and omental adipose tissue samples was obtained in lean to obese women. Linear regression models predicting adipocyte size in both adipose tissue depots were computed using body composition and fat distribution measures (n = 150).

Expression of genes related to glucocorticoid action in human subcutaneous and omental adipose tissue.

Adipose tissue glucocorticoid action relies on local enzymatic interconversion and glucocorticoid receptor (GR) availability. 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1), 2 (11β-HSD2) and hexose-6-phosphate dehydrogenase (H6PDH) are likely involved in glucocorticoid activation/inactivation within adipose tissue. We examined adipose tissue mRNA expression of genes related to glucocorticoid action and their association with total and visceral adiposity.

Adipose tissue lamin A/C messenger RNA expression in women.

Mutations in the lamin A/C gene (LMNA) cause lipodystrophy. However, little data are available on lamin A/C expression in various fat depots in women. We recruited 34 women scheduled for gynecologic surgery.

Differential estrogenic 17beta-hydroxysteroid dehydrogenase activity and type 12 17beta-hydroxysteroid dehydrogenase expression levels in preadipocytes and differentiated adipocytes.

Estradiol (E2) is produced locally in adipose tissue and could play an important role in fat distribution and accumulation, especially in women. It is well recognized that aromatase is expressed in adipose tissue; however the identity of its estrogenic 17beta-hydroxysteroid dehydrogenase (17beta-HSD) partner is not identified. To gain a better knowledge about the enzyme responsible for the conversion of estrone into estradiol, we determined the activity and expression levels of known estrogenic 17beta-HSDs, namely types 1, 7 and 12 17beta-HSD in preadipocytes before and after differentiation into mature adipocytes using an adipogenic media.