“…Moreover, experiments using a single or limited number of cell types provide knowledge about detailed molecular events directly evoked by propolis or propolis-derived compounds. Indeed, by employing adipocyte cell lines, one can identify kinases and transcription factors whose activity is directly modified by propolis supplementation [49,50,51].…”
Section: Advantages and Disadvantages Of Animal And Cellular Modelsmentioning
confidence: 99%
“…Hence, one or more other distinct components seem to be involved in leptin induction. Additionally, compound 1 (8-[1-(4′-hydroxy-3′-methoxyphenyl)prop-2-en-1-yl]-chrysin), which was originally isolated from Mexican propolis [119], also functions as a ligand for PPARα, γ and δ, and promotes differentiation of human bone marrow mesenchymal stem cell (hBM-MSC)-derived adipocytes at a 10 μM dosage [51]. In contrast to APC and compound 1 , CAPE was found to suppress differentiation of adipocytes.…”
Section: Obesity and Adipocitymentioning
confidence: 99%
“…For example, APC (10 or 25 μM) potentiated adiponectin expression by 1.5–2.0-fold in 3T3-L1 cells [49,118]. Similarly, compound 1 (10 μM) also potentiated adiponectin secretion in hBM-MCS-derived adipocytes [51]. Although CAPE (10 μM) decreased leptin expression, it evoked a more than two-fold increase in adiponectin expression in human ASC-derived adipocytes [116].…”
Propolis is a natural product resulting from the mixing of bee secretions with botanical exudates. Since propolis is rich in flavonoids and cinnamic acid derivatives, the application of propolis extracts has been tried in therapies against cancer, inflammation, and metabolic diseases. As metabolic diseases develop relatively slowly in patients, the therapeutic effects of propolis in humans should be evaluated over long periods of time. Moreover, several factors such as medical history, genetic inheritance, and living environment should be taken into consideration in human studies. Animal models, especially mice and rats, have some advantages, as genetic and microbiological variables can be controlled. On the other hand, cellular models allow the investigation of detailed molecular events evoked by propolis and derivative compounds. Taking advantage of animal and cellular models, accumulating evidence suggests that propolis extracts have therapeutic effects on obesity by controlling adipogenesis, adipokine secretion, food intake, and energy expenditure. Studies in animal and cellular models have also indicated that propolis modulates oxidative stress, the accumulation of advanced glycation end products (AGEs), and adipose tissue inflammation, all of which contribute to insulin resistance or defects in insulin secretion. Consequently, propolis treatment may mitigate diabetic complications such as nephropathy, retinopathy, foot ulcers, and non-alcoholic fatty liver disease. This review describes the beneficial effects of propolis on metabolic disorders.
“…Moreover, experiments using a single or limited number of cell types provide knowledge about detailed molecular events directly evoked by propolis or propolis-derived compounds. Indeed, by employing adipocyte cell lines, one can identify kinases and transcription factors whose activity is directly modified by propolis supplementation [49,50,51].…”
Section: Advantages and Disadvantages Of Animal And Cellular Modelsmentioning
confidence: 99%
“…Hence, one or more other distinct components seem to be involved in leptin induction. Additionally, compound 1 (8-[1-(4′-hydroxy-3′-methoxyphenyl)prop-2-en-1-yl]-chrysin), which was originally isolated from Mexican propolis [119], also functions as a ligand for PPARα, γ and δ, and promotes differentiation of human bone marrow mesenchymal stem cell (hBM-MSC)-derived adipocytes at a 10 μM dosage [51]. In contrast to APC and compound 1 , CAPE was found to suppress differentiation of adipocytes.…”
Section: Obesity and Adipocitymentioning
confidence: 99%
“…For example, APC (10 or 25 μM) potentiated adiponectin expression by 1.5–2.0-fold in 3T3-L1 cells [49,118]. Similarly, compound 1 (10 μM) also potentiated adiponectin secretion in hBM-MCS-derived adipocytes [51]. Although CAPE (10 μM) decreased leptin expression, it evoked a more than two-fold increase in adiponectin expression in human ASC-derived adipocytes [116].…”
Propolis is a natural product resulting from the mixing of bee secretions with botanical exudates. Since propolis is rich in flavonoids and cinnamic acid derivatives, the application of propolis extracts has been tried in therapies against cancer, inflammation, and metabolic diseases. As metabolic diseases develop relatively slowly in patients, the therapeutic effects of propolis in humans should be evaluated over long periods of time. Moreover, several factors such as medical history, genetic inheritance, and living environment should be taken into consideration in human studies. Animal models, especially mice and rats, have some advantages, as genetic and microbiological variables can be controlled. On the other hand, cellular models allow the investigation of detailed molecular events evoked by propolis and derivative compounds. Taking advantage of animal and cellular models, accumulating evidence suggests that propolis extracts have therapeutic effects on obesity by controlling adipogenesis, adipokine secretion, food intake, and energy expenditure. Studies in animal and cellular models have also indicated that propolis modulates oxidative stress, the accumulation of advanced glycation end products (AGEs), and adipose tissue inflammation, all of which contribute to insulin resistance or defects in insulin secretion. Consequently, propolis treatment may mitigate diabetic complications such as nephropathy, retinopathy, foot ulcers, and non-alcoholic fatty liver disease. This review describes the beneficial effects of propolis on metabolic disorders.
“…For cryptoyunnanone I ( 2 ), this is the first time to report the complex flavanone bearing a phenylpropanoid unit from the genus Cryptocarya . Actually, this is the first case of complex flavanone coupled with a phenyl‐propanol unit although there have been a few compounds reported with similar structures but complex flavanone or flavone with a phenylpropionic acid unit [31,32] and complex flavone or flavonol with a phenylallyl moiety [33,34] …”
Two new flavonoids, cryunchalcone (1) and cryptoyunnanone I (2), were isolated from the leaves and twigs of Cryptocarya yunnanensis. Their structures were elucidated by the detailed spectroscopic data analysis and electronic circular dichroism (ECD) calculations. Cryunchalcone (1) is a biflavonoid constructed by a dihydrochalcone coupled with a chalcone through an unprecedented C‐2′′−C‐6 linkage. Cryptoyunnanone I (2) is a unique complex flavanone bearing a phenylpropanoid moiety.
“…Anti-diabetic peroxisome proliferator-activated receptor γ (PPARγ) agonists, such as troglitazone and pioglitazone, as well as sulfonylureas, such as glibenclamide, significantly enhance adiponectin production during adipogenesis in hBM-MSCs [17,18]. Although a direct molecular target has not been identified yet, aspirin upregulates adiponectin production in the differentiated adipocytes in a concentration-dependent manner [19,20]. Diverse nuclear receptors, such as PPARα, PPARγ, PPARδ, glucocorticoid receptor (GR), estrogen receptor (ER), and liver X receptor (LXR) are also directly or indirectly associated with adiponectin production during adipogenesis in hBM-MSCs [21,22].…”
Adiponectin is an adipocyte-derived cytokine having an insulin-sensitizing activity. During the phenotypic screening of secondary metabolites derived from the marine fungus Aspergillus terreus, a poly cyclin-dependent kinase (CDK) inhibitor butyrolactone I affecting CDK1 and CDK5 was discovered as a potent adiponectin production-enhancing compound in the adipogenesis model of human bone marrow-derived mesenchymal stem cells (hBM-MSCs). CDK5 inhibitors exhibit insulin-sensitizing activities by suppressing the phosphorylation of peroxisome proliferator-activated receptor γ (PPARγ). However, the adiponectin production-enhancing activities of butyrolactone I have not been correlated with the potency of CDK5 inhibitor activities. In a target identification study, butyrolactone I was found to directly bind to PPARγ. In the crystal structure of the human PPARγ, the ligand-binding domain (LBD) in complex with butyrolactone I interacted with the amino acid residues located in the hydrophobic binding pockets of the PPARγ LBD, which is a typical binding mode of the PPARγ partial agonists. Therefore, the adiponectin production-enhancing effect of butyrolactone I was mediated by its polypharmacological dual modulator activities as both a CDK5 inhibitor and a PPARγ partial agonist.
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