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Topical Area: Obesity

Obesity (Poster Session)

(P31-055-23) Immature Ginger Reduces Lipogenesis by Down Regulating Acyl CoA Carboxylase and Phosphoenolpyruvatecarboxykinase-1 Genes in 3T3-L1 Adipocytes

Monday, July 24, 2023
12:45 PM – 1:45 PM ET
Location: Poster Board 277
Disclosure(s):
Rafat A. Siddiqui, PhD: No relevant financial relationship(s) with ineligible companies to disclose.


Objectives:

The objective of this study was to examine the underlying mechanisms of immature ginger on adipocyte differentiation and lipogenesis in a 3T3-L1 cellular model.

Methods:

Ginger samples, extracted in 80% methanol, were dried and resuspended in DMSO at 50 mg/ml as stock solution. For analysis, the extracted samples were further diluted in media. Effects on adipogenesis was evaluated by determining lipid droplet and triglyceride accumulation, whereas lipogenesis was determined by measuring triglyceride contents and fatty acid profile. The expression of key regulatory genes involved in adipogenesis, and lipogenesis was also determined.

Results:

Our data indicate that the intracellular lipid accumulation decreased significantly by 15% or 25% on treatment with 25 or 50 μg/ml of ginger extract. Consistent with this data, significantly reduced triglyceride levels by 30% or 50% were observed on 25 or 50 mg/ml treatment with ginger extracts. In addition, ginger treatment significantly inhibited the differentiation-induced de novo lipogenesis and D9 desaturase activity. Furthermore, ginger treatment reduced adipogenesis genes, C/ebpβ and C/ebpd , expression by 47% or 64%, respectively, but significantly increased Pparγ expression by 60% and adiponectin by 75%. Ginger extracts had no effect on Fas genes but reduced lipogenesis genes, acyl CoA Carboxylase (Acc) expression by 2-fold and phosphoenolpyruvate carboxy kinase 1( Pepck1) expression by 50%.

Conclusions: Our findings suggest immature ginger can potentially inhibit lipogenesis pathways by limiting the channeling of glucose carbon in fatty acid synthesis by inhibiting the expression of ACC and glycerol production via inhibiting the expression of PEPCK, which consequently inhibits triglyceride formation.

Funding Sources: This work was supported by an Evens-Allen grant and a Capacity Building grant to RAS from NIFA-USDA (2021-38821-34601).