Circulating adipokines and mRNA expression in adipose tissue and the placenta in women with gestational diabetes mellitus.

Maternal adipose tissue and the placenta secrete various molecules commonly called adipokines such as chemerin, omentin-1, visfatin, adiponectin, and leptin that are important players in the pathogenesis of insulin resistance. Gestational diabetes mellitus (GDM) is defined as a state of glucose intolerance characterized by β-cell dysfunction and insulin resistance. To examine whether circulating adipokines and their mRNA expression in the adipose tissue and the placenta are altered in GDM pregnancy, we compared 15 GDM women [obese (BMI > 30) and non-obese (BMI < 30)] to 23 NGT (normal glucose tolerance) women [obese and non-obese], at the time of the Cesarean section.

High insulin and leptin increase resistin and inflammatory cytokine production from human mononuclear cells.

Resistin and the proinflammatory cytokines, such as TNF- α , IL-6, and IL-1 β , produced by adipocytes, and macrophages, are considered to be important modulators of chronic inflammation contributing to the development of obesity and atherosclerosis. Human monocyte-enriched mononuclear cells, from ten healthy individuals, were exposed to high concentrations of insulin, leptin, and glucose (alone or in combination) for 24 hours in vitro. Resistin, TNF- α , IL-6, and IL-1 β production was examined and compared to that in untreated cells.

Arterial stiffness is associated with increased monocyte expression of adiponectin receptor mRNA and protein in patients with coronary artery disease.

Background: Arterial stiffness and carotid intima-media thickness (IMT) constitute validated cardiovascular prognostic markers. Adiponectin and its receptors 1 (AdipoR1) and 2 (AdipoR2) are involved in coronary artery disease (CAD). We investigated whether AdipoR1 and R2 mRNA and protein expression are associated with arterial stiffness, IMT and extent of coronary atherosclerosis.

Adiponectin levels and expression of adiponectin receptors in isolated monocytes from overweight patients with coronary artery disease.

Background: Adiponectin has insulin-sensitizing and anti-atherosclerotic effects, partly mediated through its action on monocytes. We aimed to determine adiponectin levels and expression of its receptors (AdipoR1 and AdipoR2) in peripheral monocytes from overweight and obese patients with coronary artery disease (CAD).

Methods: Fifty-five overweight/obese patients, suspected for CAD, underwent coronary angiography: 31 were classified as CAD patients (stenosis ≥ 50% in at least one main vessel) and 24 as nonCAD.

Genetic variation in the adiponectin receptor 2 (ADIPOR2) gene is associated with coronary artery disease and increased ADIPOR2 expression in peripheral monocytes.

Background: Adiponectin is an adipose tissue secreted protein known for its insulin sensitising and anti-atherogenic actions. To this date two adiponectin receptors have been discovered, adiponectin receptor 1 (ADIPOR1) and adiponectin receptor 2 (ADIPOR2). The aim of this study was to investigate the association of ADIPOR2 gene variations with coronary artery disease (CAD).

Peripheral mononuclear cell resistin mRNA expression is increased in type 2 diabetic women.

Resistin has been shown to cause insulin resistance and to impair glucose tolerance in rodents, but in humans its physiological role still remains elusive. The aim of this study was to examine whether resistin mRNA expression in human peripheral mononuclear cells (PBMCs) and its corresponding plasma levels are altered in type 2 diabetes. Resistin mRNA levels were easily detectable in human PBMC, and found to be higher in DM2 compared to healthy women (P = .

Stress, the endoplasmic reticulum, and insulin resistance.

Stress, such as nutrient deprivation, viral infections, inflammation, heat shock, or lipid accumulation, imposes a serious threat to the body. These stimuli, acting both on the central control stations of the stress system and its final effectors, catecholamines and glucocorticoids, and on the peripheral target tissues, can modulate insulin action in the body. Metabolic complications, such as diabetes, visceral obesity, and atherosclerosis have emerged as major health threats in the modern societies.

Compound heterozygosity of a frameshift mutation in the coding region and a single base substitution in the promoter of the ACTH receptor gene in a family with isolated glucocorticoid deficiency.

Isolated glucocorticoid deficiency (IGD) is an autosomal recessive syndrome characterized by glucocorticoid insufficiency without mineralocorticoid deficiency. Mutations in the coding region of the ACTH receptor (MC2R) have been reported in several families with IGD. We amplified and sequenced the entire MC2R coding region in a new family with IGD.

Expression of leptin receptors in mononuclear cells from myelodysplastic syndromes and acute myeloid leukemias.

Leptin, the adipocyte hormone, and its receptor have been implicated in the differentiation/proliferation of hematopoietic cells. Given that the deregulated expression of a variety of growth factors and/or their receptors has been implicated in the pathogenesis of certain leukemias, we aimed to characterize the potential differences in the expression pattern of the two major leptin receptor transcript variants in peripheral blood mononuclear cells (PBMC) between different hematologic malignancies. Using RT-PCR and Southern blotting, we compared the expression levels of the two major leptin receptors, the longest (OB-R(L)) and the shortest (OB-R(S)) splice variants, in PBMC from patients with myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), healthy individuals and two human hematopoietic cell lines (HL-60 and K562).