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Adipocyte Fatty Acid-binding Protein (adipocyte + fatty_acid-binding_protein)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Serum levels of adipocyte fatty acid-binding protein (AFABP) are increased in chronic haemodialysis (CD)

CLINICAL ENDOCRINOLOGY, Issue 6 2008
Grit Sommer
Summary Objective Adipocyte fatty acid-binding protein (AFABP) was recently introduced as an adipocyte-expressed factor, serum levels of which independently correlate with the development of the metabolic syndrome and cardiovascular disease in humans. In the current study, we investigated renal elimination of this protein by comparing circulating AFABP levels in patients on chronic haemodialysis (CD) with controls. We hypothesized that if renal filtration is a significant route of elimination of AFABP, it would accumulate in CD patients. Patients and measurements AFABP was determined by ELISA in control (n = 60) and CD (n = 60) patients and correlated to clinical and biochemical measures of renal function, glucose and lipid metabolism, as well as inflammation, in both groups. Results Median serum AFABP levels were more than 10-fold higher in CD patients (510·9 ± 294·7 µg/l) as compared to controls (44·3 ± 35·2 µg/l). Furthermore, CD independently predicted AFABP concentrations in multiple regression analysis. In addition, body mass index and free fatty acids were independently associated with circulating AFABP. Conclusions Renal filtration appears as an important route of elimination of AFABP. Future studies should elucidate whether this adipocyte-expressed factor contributes to the increased risk of cardiovascular disease found in end-stage renal disease. [source]

Regulation of Human Skeletal Stem Cells Differentiation by Dlk1/Pref-1

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2004
Basem M Abdallah
Abstract Dlk-1/Pref-1 was identified as a novel regulator of human skeletal stem cell differentiation. Dlk1/Pref-1 is expressed in bone and cultured osteoblasts, and its constitutive overexpression led to inhibition of osteoblast and adipocyte differentiation of human marrow stromal cells. Introduction: Molecular control of human mesenchymal stem cell (hMSC) differentiation into osteoblasts and adipocytes is not known. In this study, we examined the role of delta-like 1/preadipocyte factor-1 (Dlk1/Pref-1) in regulating the differentiation of hMSCs. Materials and Methods: As a model for hMSCs, we have stably transduced telomerase-immortalized hMSC (hMSC-TERT) with the full length of human Dlk1/Pref-1 cDNA and tested its effect on hMSC growth and differentiation into osteoblasts or adipocytes as assessed by cytochemical staining, FACS analysis, and real time PCR. Ex vivo calvaria organ cultures assay was used to confirm the in vitro effect of Dlk/Pref-1 on bone formation. Results: Dlk1/Pref-1 was found to be expressed in fetal and adult bone, hMSCs, and some osteoblastic cell lines. A retroviral vector containing the human Dlk1/Pref-1 cDNA was used to create a cell line (hMSC-dlk1) expressing high levels of Dlk1/Pref-1 protein. Overexpression of Dlk1/Pref-1 did not affect the proliferation rate of hMSC, but the ability to form mature adipocytes, mineralized matrix in vitro, and new bone formation in neonatal murine calvariae organ cultures was reduced. These effects were associated with inhibition of gene expression markers of late stages of adipocyte (adipocyte fatty acid-binding protein [aP2], peroxisome proliferator-activated receptor-gamma2 [PPAR,2], and adiponectin [APM1]) and osteoblast differentiation (alkaline phosphatase [ALP], collagen type I [Col1], and osteocalcin [OC]). Lineage commitment markers for adipocytes (adipocyte determination and differentiation factor ,1 [ADD1]) and osteoblasts (core binding factor/runt-related binding factor 2 [Cbfa1/Runx2]) were not affected. Conclusion: During hMSC differentiation, Dlk1/Pref-1 maintains the size of the bipotential progenitor cell pool by inhibiting the formation of mature osteoblasts and adipocytes. [source]

SIRT6 protects against pathological damage caused by diet-induced obesity

AGING CELL, Issue 2 2010
Yariv Kanfi
Summary The NAD+-dependent SIRT6 deacetylase is a therapeutic candidate against the emerging metabolic syndrome epidemic. SIRT6, whose deficiency in mice results in premature aging phenotypes and metabolic defects, was implicated in a calorie restriction response that showed an opposite set of phenotypes from the metabolic syndrome. To explore the role of SIRT6 in metabolic stress, wild type and transgenic (TG) mice overexpressing SIRT6 were fed a high fat diet. In comparison to their wild-type littermates, SIRT6 TG mice accumulated significantly less visceral fat, LDL-cholesterol, and triglycerides. TG mice displayed enhanced glucose tolerance along with increased glucose-stimulated insulin secretion. Gene expression analysis of adipose tissue revealed that the positive effect of SIRT6 overexpression is associated with down regulation of a selective set of peroxisome proliferator-activated receptor-responsive genes, and genes associated with lipid storage, such as angiopoietin-like protein 4, adipocyte fatty acid-binding protein, and diacylglycerol acyltransferase 1, which were suggested as potential targets for drugs to control metabolic syndrome. These results demonstrate a protective role for SIRT6 against the metabolic consequences of diet-induced obesity and suggest a potentially beneficial effect of SIRT6 activation on age-related metabolic diseases. [source]