Chlorella unsaturated fatty acids suppress high‐fat diet‐induced obesity in C57/BL6J mice

Abstract

Chlorella has been identified as a rich source of unsaturated fatty acids. Since the antiobesity effects of unsaturated fatty acids have been well documented; therefore, we explored the antiobesity actions of chlorella unsaturated fatty acids (C.UFAs) in the current study. The obtained results demonstrated C.UFAs, which contain abundant linoleic acid, could retard body weight gain (reducing body weigh by 13.93% after 16 weeks of treatment), improve blood glucose (19.29% lower) and lipid profile (23.45% lower in TG, 8.76% lower in TC) compared to high-fat diet-fed C57BL/6J mice. The possible underlying mechanisms might involve reducing hepatic lipid accumulation via down-regulation of lipogenic genes (PPARγ, C/EBPα, LPL, aP2, FAS, and SREBP-1c) and upregulation of lipolytic gene (adiponectin). We also demonstrate C.UFAs could reduce HFD-induced adipocyte hypertrophy via activation of AMPK signaling pathway in adipose tissue and liver. In summary, our study highlights the potential of C.UFAs as a functional food for obesity management. K E Y W O R D Santiobesity, bioactive compound, chlorella, polyunsaturated fatty acid Practical Application: Chlorella has already been commercialized as a functional food antiobesity function. In the current study, the unsaturated fatty acids isolated from chlorella were found to exert beneficial effects on hyperglycemia, hyperlipidemia, hepatic steatosis, and adipocyte hypertrophy in high-fat diet-fed mice. This may provide theoretical foundation for developing novel chlorella-based functional foods.

Differences and Similarities in Lipid Composition, Nutritional Value, and Bioactive Potential of Four Edible Chlorella vulgaris Strains

“…Indeed, the health potential of FAs from C. vulgaris were already addressed in the literature. For instance, in mice fed with a high-fat diet, the administration of FAs from C. vulgaris promoted a beneficial effect on hyperglycemia, hyperlipidemia, hepatic steatosis, and adipocyte hypertrophy [ 38 ]. Another study evaluated the effect of auto- and heterotrophic C. vulgaris in zebrafish and showed that both strains have anti-obesity, anti-steatosis, and anti-inflammatory activity [ 39 ].…”

Nanoliposome-Mediated Encapsulation of Chlorella Oil for the Development of a Controlled-Release Lipid-Lowering Formulation

“…In an illuminating study, Regueiras et al [ 37 ] demonstrated the capacity of Chlorella vulgaris and Chlorococcum amblystomatis to modulate lipid metabolism in zebrafish larvae, concurrently mitigating steatosis in HepG2 liver cells burdened with excessive fatty acids. Furthermore, research by Yang and collaborators [ 38 ] revealed that Chlorella unsaturated fatty acids (C. UFAs), rich in linoleic acid, positively influenced body weight (resulting in a 13.93% reduction after 16 weeks of treatment), improved blood glucose levels (a 19.29% decrease), and enhanced lipid profiles (with a 23.45% reduction in triglycerides and an 8.76% decrease in total cholesterol) compared to C57BL/6J mice on a high-fat diet. This notable effect may be attributed to the reduction of hepatic lipid accumulation, achieved through the down-regulation of lipogenic genes (PPARγ, C/EBPα, LPL, aP2, FAS, and SREBP-1c) and the up-regulation of the lipolytic gene (adiponectin), representing a plausible underlying mechanism.…”

Dietary supplementation with short‐ and long‐chain structured lipids alleviates obesity via regulating hepatic lipid metabolism, inflammation and gut microbiota in high‐fat‐diet‐induced obese mice

“…Studies have shown that unsaturated fatty acids rich in Chlorella can improve the hyperglycemia and hyperlipidemia caused by HFD diet and the hypertrophy of fat cells, and slow the accumulation of fat in liver cells by downregulating lipopogenic genes and upregulating adiponectin. 40 The improvement of fat vacuole in mice was achieved by activating the AMPK signaling pathway. These data indicated that SLCTs supplementation could effectively ameliorate HFD-induced hepatic steatosis and liver injury.…”