Visceral fat and cardiometabolic future in children and adolescents: a critical update.

Cardiovascular disease (CVD) is a process whose pathogenetic mechanisms start very early in life. Recently, the importance of visceral adipose tissue (VAT) has been highlighted in the development of CVD. VAT does not always depend on body mass index (BMI) and has been implicated in unfavorable metabolic activity and cardiovascular adverse events.

Pro-inflammatory chemokines CCL2, chemerin, IP-10 and RANTES in human serum during an oral lipid tolerance test.

Background: There is a strong coincidence of obesity and a chronic state of modest inflammation. Secretion of pro-inflammatory cytokines from adipocytes and immune cells represents a key mechanism in this process and is affected by fatty acids.

Material And Methods: A study cohort of 100 overnight fasted healthy volunteers underwent an oral lipid tolerance test (OLTT) by ingestion of 160ml of a protein- and sugar-free lipid emulsion of defined composition.

CTRP family: linking immunity to metabolism.

It is well known that infectious and inflammatory diseases such as sepsis and severe inflammatory response syndrome are accompanied by metabolic alterations such as insulin resistance. Conversely, metabolic diseases such as visceral obesity and type 2 diabetes are characterized by high levels of proinflammatory cytokines. Metabolism and immunity are linked by proteins of dual function.

Admission visfatin levels predict pancreatic and peripancreatic necrosis in acute pancreatitis and correlate with clinical severity.

Objectives: Adipocytes of peripancreatic and intrapancreatic adipose tissue secret adipocytokines such as leptin, adiponectin, and resistin. For resistin, a role as an early predictor of peripancreatic necrosis and clinical severity in acute pancreatitis has been reported. It was the aim of this study to investigate whether the adipocytokine visfatin is able to serve as an early marker predicting peripancreatic necrosis and clinical severity.

Fatty acid-induced induction of Toll-like receptor-4/nuclear factor-kappaB pathway in adipocytes links nutritional signalling with innate immunity.

To study the effects of fatty acids and the involvement of the Toll-like receptor-4/nuclear factor-kappaB (TLR-4/NF-kappaB) pathway with respect to the secretion of adipokines from adipocytes 3T3-L1 adipocytes were stimulated with increasing doses of fatty acids. The secretion of adiponectin, resistin and monocyte chemoattractant protein-1 (MCP-1) was measured by enzyme-linked immunosorbent assay. The NF-kappaB p65 nuclear translocation and TLR-4 expression were investigated by Western blot.

Mechanisms of disease: adipokines and breast cancer - endocrine and paracrine mechanisms that connect adiposity and breast cancer.

A vast number of epidemiological studies suggest an important, but still controversial, role for obesity and adipose tissue mass in breast cancer risk and an association with tumor phenotype. The main conclusions from these studies raise the possibility that the adipose tissue can act as an effector organ that influences both cancer risk and tumor behavior. Here we also review heterotypic mechanisms in breast-cancer tumorigenesis; these mechanisms involve soluble secreted factors from peritumoral cells, extracellular-matrix components and interactions between stromal cells and tumor cells that create a specific and local peritumoral microenvironment.

Regulation and function of collagenous repeat containing sequence of 26-kDa protein gene product "cartonectin".

Objective: Collagenous repeat containing sequence of 26-kDa protein (CORS-26) was identified as a new gene transcript expressed in cartilage with unknown function. It was the aim of this study to investigate expression, regulation, and function of CORS-26 in adipocytes.

Research Methods And Procedures: CORS-26 mRNA and protein expression was studied by reverse transcriptase-polymerase chain reaction, Western blot analysis, and quantitative real-time polymerase chain reaction.

Frequency and significance of the novel single nucleotide missense polymorphism Val109Asp in the human gene encoding omentin in Caucasian patients with type 2 diabetes mellitus or chronic inflammatory bowel diseases.

Background: The omental adipose tissue is pathogenetically involved in both type 2 diabetes mellitus (T2D) and chronic inflammatory bowel diseases (IBD) such as Ulcerative colitis (UC) and Crohn's Disease (CD). Thus, adipokines secreted from omental adipose tissue might play an important role in these diseases. Omentin represents a new adipokine expressed in and secreted by omental adipose tissue.

The role of 'adipotropins' and the clinical importance of a potential hypothalamic-pituitary-adipose axis.

Since adipocytes express specific receptors for pituitary hormones and hypothalamic releasing factors, adipose tissue has to be regarded as a fast-acting endocrine gland under the control of the brain. Expanding on this suggestion, the existence and clinical impact of a hypothalamic-pituitary-adipose axis is reviewed. The term 'adipotropins' is introduced in order to describe pituitary and hypothalamic hormones or releasing factors that directly target adipocytes by their specific receptors.

Role of specificity protein-1, PPARgamma, and pituitary protein transcription factor-1 in transcriptional regulation of the murine CORS-26 promoter.

The collagenous repeat-containing sequence of 26-kDa protein (CORS-26) was recently described as a new gene that is induced during adipocyte differentiation. Since the transcription factors specificity protein-1 (SP-1) and PPARgamma have been demonstrated to modulate transcriptional activation of adipocytic genes, we investigated the putative role of SP-1 and PPARgamma in the regulation of the murine CORS-26 promoter. Computer-based sequence analysis revealed two putative SP-1 binding sites and binding sites for PPARgamma and Pit-1 within the TATA-box containing promoter.