Recombinant Human ADIPOQ /Adiponectin Protein
- Known as:
- Recombinant Human ADIPOQ /Adiponectin Protein
- Catalog number:
- ad-861
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human ADIPOQ /Adiponectin Protein
Related genes to: Recombinant Human ADIPOQ /Adiponectin Protein
- Gene:
- ADIPOQ NIH gene
- Name:
- adiponectin, C1Q and collagen domain containing
- Previous symbol:
- ACDC
- Synonyms:
- ACRP30, AdipoQ, apM1, GBP28, adiponectin
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human ADIPOQ /Adiponectin Protein
Related articles to: Recombinant Human ADIPOQ /Adiponectin Protein
- Diabetes is a major risk factor for osteoporosis, which negatively impacts bone health, but the mechanisms underlying the effects of hyperglycemia on bone marrow mesenchymal/stromal cells (BMSC) are not fully understood. This study investigated how high glucose levels influence BMSC differentiation, proliferation, viability, and metabolism. The results demonstrated that high glucose inhibits osteogenesis in human BMSC, as evidenced by reduced alkaline phosphatase activity, impaired calcium deposition, and downregulation of key osteogenic genes (RUNX2, ALP). Conversely, high glucose conditions promoted adipogenesis, characterized by increased percentage of cells with lipid droplets, and upregulation of adipogenic genes (PPARγ2, CEBPα, AdipoQ), suggesting a shift towards fat cell differentiation. Furthermore, BMSC cultured in high glucose showed decreased proliferation, elevated DNA damage, increased oxidative stress, enhanced apoptosis and senescence, particularly in later passages, highlighting the negative impact of hyperglycemia on BMSC viability. Metabolomic profiling of osteogenic and adipogenic differentiation in normal and high glucose conditions revealed key metabolic shifts, with nicotinamide adenine dinucleotide (NAD+) and l-glutamate/α-ketoglutarate (α-KG) identified as critical metabolites driving these processes. Supplementation with NAD+ and α-KG in high glucose conditions significantly enhanced ALP activity. These findings suggest that high glucose promotes adipogenesis at the expense of osteogenesis, exacerbating cellular damage and accelerating aging in BMSC. The identification of NAD+ and α-KG as key regulators in this process provides new insights into the metabolic mechanisms behind impaired bone health in diabetes and highlights potential therapeutic avenues to counteract these detrimental effects to better manage diabetes-related bone diseases. - Source: PubMed
Shirazi SuzannaEsawi EzaldeenNassar Zeyad DGronthos StanCakouros Dimitrios - Previous meta-analyses have reported lower serum adiponectin levels in patients with schizophrenia treated with second-generation antipsychotics. However, the relationships among serum adipokines, psychiatric symptoms, and antipsychotic use remain unclear. This study aimed to clarify associations between serum adipokines, psychiatric symptoms, and antipsychotic treatment in patients with chronic schizophrenia compared with healthy controls. - Source: PubMed
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