Disease relevance of Adipogenesis

• Dwarfism, impaired skin development, skeletal muscle atrophy, delayed bone development, and impeded adipogenesis in mice lacking Akt1 and Akt2 [1].
• Our data show that a decrease in expression of genes normally involved in adipogenesis is associated with obesity, and we further identify genes important for subsequent development of type 2 diabetes mellitus [2].
• CONCLUSION: These data demonstrate that PIs may play a role in the insulin resistance observed in lipodystrophy by affecting glucose uptake, adipogenesis and lipolysis [3].
• Gene expression profiling of orbital adipose tissue from patients with Graves' ophthalmopathy: a potential role for secreted frizzled-related protein-1 in orbital adipogenesis [4].
• CLINICAL RELEVANCE: Steroid-induced adipogenesis by bone progenitor cells in marrow may influence the development of osteonecrosis [5].

Psychiatry related information on Adipogenesis

• Thus, deficiency of both leptin and HSL has unmasked novel roles of HSL in adipogenesis as well as in feeding behavior [6].

High impact information on Adipogenesis

• By contrast, within the context of the 3-dimensional (3-D) ECM, normal adipocyte maturation requires a burst in MT1-MMP-mediated proteolysis that modulates pericellular collagen rigidity in a fashion that controls adipogenesis [7].
• The Rho GTPase appears to play a crucial role in this decision of cellular fate, promoting myogenesis and inhibiting adipogenesis [8].
• In vitro, activation of Rho-kinase by Rho inhibits adipogenesis and is required for myogenesis [9].
• E2F repression by C/EBPalpha is required for adipogenesis and granulopoiesis in vivo [10].
• This suggests that an endogenous PPAR gamma ligand may be an important regulator of adipogenesis [11].

Chemical compound and disease context of Adipogenesis

• To further assess whether the increase in body weight by troglitazone or pioglitazone was due to adipogenesis, the weight of intraabdominal fat tissue (epididymal, retroperitoneal, and perirenal) was determined [12].
• Evidence of osteonecrosis was observed in steroid treated chickens, whereas sections from animals treated with steroids and lovastatin showed less adipogenesis and no bone death [13].

Biological context of Adipogenesis

• The specificity of the association of lipid globules with vimentin IFs during adipose conversion is discussed as a special form of compartmentalization supporting adipogenesis and is taken as an example of a possible IF function in relation to a cell differentiation process [14].
• Studies from the past several years have revealed that adipogenesis is controlled by an interplay of transcription factors, including members of the CCAAT/enhancer binding protein family and peroxisome proliferator activated receptor gamma [15].
• These results define multiple roles for C/EBP alpha in adipogenesis and show that cross-regulation between PPAR gamma and C/EBP alpha is a key component of the transcriptional control of this cell lineage [16].
• Ecotin, an inhibitor of serine proteases, inhibits cell-shape change, adipocyte-specific gene expression, and lipid accumulation during adipogenesis in culture [17].
• To examine the long-term function of ADSF in adipogenesis and glucose homeostasis, we constructed an expression vector for a dominant inhibitory form of ADSF by fusing it to the human IgGgamma constant region (hFc) [18].

Anatomical context of Adipogenesis

• Stimulation of adipogenesis in fibroblasts by PPAR gamma 2, a lipid-activated transcription factor [19].
• TRAP220 has been reported to show ligand-enhanced interaction with peroxisome proliferator-activated receptor gamma(2) (PPAR gamma(2)), a nuclear receptor essential for adipogenesis [20].
• Here we show that PPAR-gamma agonists suppress monocyte elaboration of inflammatory cytokines at agonist concentrations similar to those found to be effective for the promotion of adipogenesis [21].
• In 3T3-L1 cells, expression of ZFP55 resulted in >50% reduction in gamma2 expression but had no effect on gamma1, whereas adipogenesis was similarly reduced by 50% [22].
• Conditional ectopic expression of C/EBP beta in NIH-3T3 cells induces PPAR gamma and stimulates adipogenesis [23].

Associations of Adipogenesis with chemical compounds

• Activation of adipogenesis in 3T3 preadipocytes by exposure to the adipogenic inducers dexamethasone, methylisobutylxanthine, insulin, and fetal bovine serum is accompanied by a transient burst of C/EBP beta protein expression that precedes the induction of the fat gene program [23].
• Peroxisome proliferator-activated receptor gamma (PPARgamma) is the master regulator of adipogenesis as well as the target of thiazolidinedione (TZD) antidiabetic drugs [24].
• Inhibition of adipogenesis and development of glucose intolerance by soluble preadipocyte factor-1 (Pref-1) [25].
• 15-deoxy-Delta12,14-PGJ2 (15d-PGJ2) has been identified as an endogenous ligand for PPARgamma, inducing adipogenesis in vitro [26].
• Expression of BMP-RII together with BMP-RIA or BMP-RIB suppressed adipogenesis of 3T3-F442A cells and promoted full osteoblastic differentiation in response to retinoic acid [27].

Gene context of Adipogenesis

• Transcription coactivator TRAP220 is required for PPAR gamma 2-stimulated adipogenesis [20].
• In addition, Akt1/Akt2 DKO mice display impeded adipogenesis [1].
• Retinoic acid inhibited adipose conversion and cooperated with BMP-2 to enhance proliferation, inhibit adipogenesis, and promote early osteoblastic differentiation [27].
• Our results indicate that endogenous TGF-beta signaling regulates the rate of adipogenesis, and that Smad2 and Smad3 have distinct functions in this endogenous control of differentiation [28].
• Stromelysin-1 regulates adipogenesis during mammary gland involution [29].

Analytical, diagnostic and therapeutic context of Adipogenesis

• Our results show that the 3T3-F442A/C4 cells represent a new 3T3 preadipose clone that could be useful as a bioassay to evaluate growth hormone activity, as well as to purify and characterize hormones, adipogenic factors, and those compounds that affect mammalian adipogenesis [30].
• To better delineate how mitochondrial dysfunction induces triglyceride accumulation in preadipocytes, we developed a low-density DNA microarray containing 89 probes, which allows gene expression analysis for major effectors and/or markers of adipogenesis [31].
• In this study, we demonstrate on the cellular and molecular level that supplementation of bFGF in different phases of cell culture leads to a strong enhancement of adipogenesis of MSCs, as induced by an adipogenic hormonal cocktail [32].
• Microarray analysis of early adipogenesis in C3H10T1/2 cells: cooperative inhibitory effects of growth factors and 2,3,7,8-tetrachlorodibenzo-p-dioxin [33].
• Time course of de novo adipogenesis in matrigel by gelatin microspheres incorporating basic fibroblast growth factor [34].

References