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Grapefruit Oil

GRAPEFRUIT OIL

• Stimulates lipolysis
• Stimulates fatty acid oxidation
• Stimulates thermogenesis / heat production (energy consumption)
• Grapefruit oil inhibits triglyceride storage in fat cells and blocks generation of new fat cells
• Appetite suppressant

Grapefruit oil excites the sympathetic nerve innervating the white adipose tissue. Grapefruit oil excites the sympathetic nerves innervating the brown adipose tissue and adrenal gland and inhibited the parasympathetic gastric nerve. Grapefruit oil excites the sympathetic innervation of adipose tissue, and excitation of the sympathetic nerves in adipose tissue causes triglyceride hydrolysis / lipolysis to release stored fats as free fatty acids.

Grapefruit oil enhances heat production through the activation of uncoupling protein 1 (UCP1), which increases body temperature and energy consumption by uncoupling oxidation from ATP production in mitochondria. It has been reported that grapefruit oil increases energy consumption and induces thermogenesis and elevates skin temperature, reflecting heat production in the brown fat and beige / brite fat.

Instantly and temporarily reduces appetite and reduces food intake by inhibition of the parasympathetic gastric nerve that regulates digestion and nutrient absorption.

Grapefruit essential oil modulates PPAR and specifically activates PPAR-alpha to improve fatty acid release, improve insulin sensitivity and prevent against spikes in insulin and blood glucose that switch off fat burning. Furthermore, D-limonene increased the mRNA expression levels of PPARα target genes in the WAT of HFD-fed mice in the prevention study, such as UCP-2, ACC and PGC-1α, which are closely related to fatty acid synthesis and oxidation. The results further demonstrated that D-limonene activates PPARα trans activity, indicating that D-limonene may protect against the development of dyslipidaemia through the regulation of PPARα signalling.

Limonene stimulated both glucose uptake (17.4%) and lipolysis (17.7%); the mRNA expression of glucose transporter 1 (GLUT1) was upregulated but glucose transporter 4 (GLUT4) was unaffected, and adipose triglyceride lipase (ATGL) was suppressed.

Lipolytic effect was found to be high when the oils included a higher content of gamma-terpinene and p-cymene. Limonene showed potential lipolytic effect, and its effect is likely to be enhanced by the presence of gamma-terpinene (as found in grapefruit) and p-cymene (grapefruit).

Limonene has been reported to alleviate fatty liver induced by a high-fat diet. Here we determined the preventive and therapeutic effects of d-limonene on metabolic disorders in mice with high-fat diet-induced obesity. In the preventive treatment, limonene decreased the size of white and brown adipocytes, lowered serum triglyceride and fasting blood glucose levels, and prevented liver lipid accumulations in high-fat diet-fed C57BL/6 mice. In the therapeutic treatment, d-limonene reduced serum TG, low-density lipoprotein cholesterol (LDL-c) and fasting blood glucose levels and glucose tolerance, and increased serum high-density lipoprotein cholesterol (HDL-c) in obese mice. Using a reporter assay and gene expression analysis, we found that d-limonene activated peroxisome proliferator-activated receptor (PPAR)-α signalling, and inhibited liver X receptor (LXR)-β signalling. Our data suggest that the intake of d-limonene may benefit patients with dyslipidaemia and hyperglycaemia and is a potential dietary supplement for preventing and ameliorating metabolic disorders.

 

References


 

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