Limits...
Carnosic Acid Inhibits Lipid Accumulation in 3T3-L1 Adipocytes Through Attenuation of Fatty Acid Desaturation.

Park MY, Sung MK - J Cancer Prev (2015)

Bottom Line: CA significantly decreased mRNA expression of peroxisome proliferator-activated receptor-γ, sterol regulatory element-binding protein 1, and CCAAT/enhancer binding protein-α in a dose-dependent manner.Moreover, it decreased the ratio of both C16:1/C16:0 and C18:1/C18:0, with reduced expression of stearoyl CoA desaturase 1 mRNA and protein.These results suggest that CA efficiently suppressed adipogenesis in 3T3-L1 adipocytes and its action, at least in part, is associated with the downregulation of adipogenesis-related genes and the fatty acid composition of TG accumulated in adipocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition Education, Graduate School of Education, Soonchunhyang University, Asan.

ABSTRACT

Background: Excess body fat accumulation contributes to the development of metabolic disorders that can cause adverse health effects. Carnosic acid (CA), a major bioactive component of rosemary (Rosemarinus officinalis), has been suggested to possess anti-adipogenic properties. The present study was conducted to elucidate the mechanism underlying the anti-adipogenic effects of CA.

Methods: 3T3-L1 pre-adipocytes were treated with CA (0.1, 1, and 10 μM) from day 0 to day 8 of differentiation. On day 8, biochemical markers of lipid accumulation and the degree of fatty acid desaturation were measured.

Results: Oil Red O staining results, triglyceride (TG) accumulation, and glycerol 3-phosphate dehydrogenase activity suggested that CA significantly inhibited lipid accumulation in 3T3-L1 adipocytes. CA significantly decreased mRNA expression of peroxisome proliferator-activated receptor-γ, sterol regulatory element-binding protein 1, and CCAAT/enhancer binding protein-α in a dose-dependent manner. Moreover, it decreased the ratio of both C16:1/C16:0 and C18:1/C18:0, with reduced expression of stearoyl CoA desaturase 1 mRNA and protein.

Conclusions: These results suggest that CA efficiently suppressed adipogenesis in 3T3-L1 adipocytes and its action, at least in part, is associated with the downregulation of adipogenesis-related genes and the fatty acid composition of TG accumulated in adipocytes.

No MeSH data available.


Related in: MedlinePlus

The hypothetical scheme of a mechanism in which carnosic acid (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. CA effectively inhibits lipid accumulation in differentiating 3T3-L1 adipocytes by blocking adipocyte-associated gene expression and glycerol 3-phosphate dehydrogenase (GPDH) activity, leading to changes in fatty acid composition. PPARγ, peroxisome proliferator-activated receptor-γ; C/EBPα, CCAAT/enhancer binding protein-α; SREBP1, sterol regulatory element-binding protein 1; TG, triglycerides; SCD1, stearoyl CoA desaturase 1; DHAP, dihydroxyacetone phosphate; C16:1, palmitoleate; C18:1, oleate.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4384713&req=5

f5-jcp-20-41: The hypothetical scheme of a mechanism in which carnosic acid (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. CA effectively inhibits lipid accumulation in differentiating 3T3-L1 adipocytes by blocking adipocyte-associated gene expression and glycerol 3-phosphate dehydrogenase (GPDH) activity, leading to changes in fatty acid composition. PPARγ, peroxisome proliferator-activated receptor-γ; C/EBPα, CCAAT/enhancer binding protein-α; SREBP1, sterol regulatory element-binding protein 1; TG, triglycerides; SCD1, stearoyl CoA desaturase 1; DHAP, dihydroxyacetone phosphate; C16:1, palmitoleate; C18:1, oleate.

Mentions: Taken together, the diverse effects of CA on adipocyte lipid accumulation are associated with adipocyte-related gene expression as well as fatty acid composition (Fig. 5). These changes could lead to improvements in insulin resistance and abnormal glucose control induced by obesity, although further in vivo studies are needed to confirm this relationship.


Carnosic Acid Inhibits Lipid Accumulation in 3T3-L1 Adipocytes Through Attenuation of Fatty Acid Desaturation.

Park MY, Sung MK - J Cancer Prev (2015)

The hypothetical scheme of a mechanism in which carnosic acid (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. CA effectively inhibits lipid accumulation in differentiating 3T3-L1 adipocytes by blocking adipocyte-associated gene expression and glycerol 3-phosphate dehydrogenase (GPDH) activity, leading to changes in fatty acid composition. PPARγ, peroxisome proliferator-activated receptor-γ; C/EBPα, CCAAT/enhancer binding protein-α; SREBP1, sterol regulatory element-binding protein 1; TG, triglycerides; SCD1, stearoyl CoA desaturase 1; DHAP, dihydroxyacetone phosphate; C16:1, palmitoleate; C18:1, oleate.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4384713&req=5

f5-jcp-20-41: The hypothetical scheme of a mechanism in which carnosic acid (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. CA effectively inhibits lipid accumulation in differentiating 3T3-L1 adipocytes by blocking adipocyte-associated gene expression and glycerol 3-phosphate dehydrogenase (GPDH) activity, leading to changes in fatty acid composition. PPARγ, peroxisome proliferator-activated receptor-γ; C/EBPα, CCAAT/enhancer binding protein-α; SREBP1, sterol regulatory element-binding protein 1; TG, triglycerides; SCD1, stearoyl CoA desaturase 1; DHAP, dihydroxyacetone phosphate; C16:1, palmitoleate; C18:1, oleate.
Mentions: Taken together, the diverse effects of CA on adipocyte lipid accumulation are associated with adipocyte-related gene expression as well as fatty acid composition (Fig. 5). These changes could lead to improvements in insulin resistance and abnormal glucose control induced by obesity, although further in vivo studies are needed to confirm this relationship.

Bottom Line: CA significantly decreased mRNA expression of peroxisome proliferator-activated receptor-γ, sterol regulatory element-binding protein 1, and CCAAT/enhancer binding protein-α in a dose-dependent manner.Moreover, it decreased the ratio of both C16:1/C16:0 and C18:1/C18:0, with reduced expression of stearoyl CoA desaturase 1 mRNA and protein.These results suggest that CA efficiently suppressed adipogenesis in 3T3-L1 adipocytes and its action, at least in part, is associated with the downregulation of adipogenesis-related genes and the fatty acid composition of TG accumulated in adipocytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Food and Nutrition Education, Graduate School of Education, Soonchunhyang University, Asan.

ABSTRACT

Background: Excess body fat accumulation contributes to the development of metabolic disorders that can cause adverse health effects. Carnosic acid (CA), a major bioactive component of rosemary (Rosemarinus officinalis), has been suggested to possess anti-adipogenic properties. The present study was conducted to elucidate the mechanism underlying the anti-adipogenic effects of CA.

Methods: 3T3-L1 pre-adipocytes were treated with CA (0.1, 1, and 10 μM) from day 0 to day 8 of differentiation. On day 8, biochemical markers of lipid accumulation and the degree of fatty acid desaturation were measured.

Results: Oil Red O staining results, triglyceride (TG) accumulation, and glycerol 3-phosphate dehydrogenase activity suggested that CA significantly inhibited lipid accumulation in 3T3-L1 adipocytes. CA significantly decreased mRNA expression of peroxisome proliferator-activated receptor-γ, sterol regulatory element-binding protein 1, and CCAAT/enhancer binding protein-α in a dose-dependent manner. Moreover, it decreased the ratio of both C16:1/C16:0 and C18:1/C18:0, with reduced expression of stearoyl CoA desaturase 1 mRNA and protein.

Conclusions: These results suggest that CA efficiently suppressed adipogenesis in 3T3-L1 adipocytes and its action, at least in part, is associated with the downregulation of adipogenesis-related genes and the fatty acid composition of TG accumulated in adipocytes.

No MeSH data available.


Related in: MedlinePlus