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Postnatal diet-induced obesity in rats upregulates systemic and adipose tissue glucocorticoid metabolism during development and in adulthood: its relationship with the metabolic syndrome.
TLDR
The experimental paradigm of postnatal overfeeding is a powerful tool to understand the pathophysiology of glucocorticoid-induced programming of metabolic axes and leads to permanent upregulation of the HPA axis and increased adipose tissue glucoc Corticoid sensitivity.
Maternal Undernutrition during Late Gestation Induces Fetal Overexposure to Glucocorticoids and Intrauterine Growth Retardation, and Disturbs the Hypothalamo-Pituitary Adrenal Axis in the Newborn Rat.
TLDR
The effects of maternal 50% food restriction in rats during the last week of gestation on the hypothalamo-pituitary adrenal (HPA) axis activity in both mothers and their fetuses were investigated.
[Corticotropin releasing factor].
TLDR
The search for a neurohormone specifically controlling ACTH secretion resulted in the discovery of the corticotropin-releasing factor, which is the predominant component of a complex control system of adrenal cortex secretion, which also includes catecholamines and the antidiuretic hormone.
Human somatostatin receptor subtypes in acromegaly: distinct patterns of messenger ribonucleic acid expression and hormone suppression identify different tumoral phenotypes.
TLDR
The quantitative expression of messenger ribonucleic acid for the 5 SSTR subtypes and the inhibitory effects of SRIF14; SRIF28; octreotide; the SSTR2-preferential analog, BIM-23197; and the S STR5-preferring analogs on GH and PRL secretion were analyzed, showing a highly variable ratio of the Sstr2 and SSTR5 transcripts, according to tumors.
Maternal undernutrition during late gestation induces fetal overexposure to glucocorticoids and intrauterine growth retardation, and disturbs the hypothalamo-pituitary adrenal axis in the newborn rat.
TLDR
It is suggested that maternal undernutrition during late gestation induces both IUGR and an overexposure of fetuses to maternal B, which disturb the development of the HPA axis.
Expression of the mRNA coding for 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue from obese patients: an in situ hybridization study.
TLDR
Observations suggest that an overexpression of 11beta-HSD-1 may explain part of the glucocorticoid-induced metabolic disorders linked to obesity and may promote visceral fat deposition.
Stromal Cells Are the Main Plasminogen Activator Inhibitor‐1‐Producing Cells in Human Fat: Evidence of Differences Between Visceral and Subcutaneous Deposits
TLDR
It is demonstrated that PAI‐1 production is mainly due to stromal cells, which were more numerous in the visceral than in the subcutaneous depot, which could explain the strong relationship observed between circulating PAI-1 levels and the accumulation of visceral fat.
The inflammatory receptor CD40 is expressed on human adipocytes: contribution to crosstalk between lymphocytes and adipocytes
TLDR
Adipocyte CD40 may contribute to obesity-related inflammation and insulin resistance through both the release of soluble factor(s) and heterotypic contact with adipocytes involving CD40, and through the involvement of a cell–cell contact with lymphocyte/adipocyte co-culture.
11β‐Hydroxysteroid Dehydrogenase Type 1 mRNA is Increased in Both Visceral and Subcutaneous Adipose Tissue of Obese Patients
TLDR
Data from rodents provide evidence for a causal role of 11β‐hydroxysteroid dehydrogenase type 1 (11β‐HSD‐1) in the development of obesity and its complications, although VAT is the major predictor for insulin resistance and the metabolic syndrome.
Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and
TLDR
The data show for the first time that postnatal manipulation programs high-fat diet–induced upregulation of MAT glucocorticoid exposure, sensitivity, and inflammatory status and therefore reveal the pivotal role of the environment during the perinatal period on the development of diet-induced adipose tissue dysregulation in adulthood.
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