Seabuckthorn Improves Diet-Induced Obesity and Associated Metabolic Disturbances

by | Mar 27, 2019 | 2017, Metabolic Syndrome, Obesity

Written by Angeline A. De Leon, Staff Writer. Both seabuckthorn leaves extract and the flavonoid glycosides extract from seabuckthorn leaves mitigated the effects of diet-induced obesity and metabolic syndrome in a mouse model.

weight controlObesity is associated with a variety of metabolic disturbances, including insulin resistance, dyslipidemia (abnormal elevation of blood lipids), and non-alcoholic fatty liver disease (NAFLD). Underlying these metabolic complications is the dysregulation of lipid metabolism in liver and adipose tissue 1, a research area garnering much investigation in both the pharmaceutical and nutraceutical markets. Seabuckthorn (Hippophae rhamnoides L.), a plant native to Europe and Asia, is a staple in herbal medicine, popular for its abundance in flavonoids and isoflavones (plant-derived phytoestrogens) 2. The leaves of the seabuckthorn plant, particularly, are associated with anti-inflammatory, anti-bacterial, and anti-tumor activity 3,4 and are known to contain a high content of flavonoid glycosides (sugar derivative) which demonstrate protective effects against adiposity and dyslipidemia 5,6. Based on these properties, seabuckthorn leaves are hypothesized to possess anti-obesity effects; however, research has not yet verified whether the seabuckthorn plant can actually help prevent metabolic disease by influencing lipid metabolism of adipose and liver tissue. In a 2017 study 7 published in Nutrients, Korean researchers looked at both seabuckthorn leaves (SL) and flavonoid glycosides extract from seabuckthorn leaves (SLG) and compared their effects on adiposity, hepatic steatosis (fatty liver), insulin response, and inflammation in a mouse model of diet-induced obesity.

A group of 40 four-week-old male mice were randomly divided into four groups and assigned to follow one of four diet regimens for 12 weeks: a normal diet (ND); a high-fat diet (60% of calories coming from fat) (HFD); a high-fat diet with 1.8% (w/w) of SL (SL); or a high-fat diet with 0.04 (w/w) of SLG (SLG). At the end of the trial, mice were anesthetized following a 12-hour fast, and blood samples were collected to determine plasma lipid, adipokine, and hormone concentrations. Liver and adipose tissue samples were removed and their morphology examined using a staining technique, and hepatic and fecal triglyceride, cholesterol, and fatty acid contents were analyzed using an enzymatic kit. Activities of glucose- and lipid-regulating enzymes (glucose-6-phosphate dehydrogenase, G6PD; fatty acid synthase, FAS; malic enzyme, ME, and phosphatidate phosphohydrolase, PAP; and phosphoenolpyruvate carboxykinase, PEPCK) were also measured, and gene expression in liver tissue quantified.

Results of the study indicated that both SL and SLG supplementation significantly lowered body weight gain (p < 0.001 for both) and decreased levels of plasma total-cholesterol, non-high-density-lipoprotein cholesterol, triglycerides, free fatty acid, and apolipoprotein B, relative to the HFD group (p < 0.05 for both groups on all parameters). Analysis also revealed that SL and SLG, relative to HFD, suppressed the activities of G6PD, ME, PAP, and ACAT, enzymes (p < 0.05 for both on all parameters) involved in lipogenesis (formation of fat), with SL supplementation also significantly diminishing FAS activity, compared to the HFD group (p < 0.05). SL and SLG appeared to improve hepatic steatosis based on reduced hepatic lipids accumulation (lower hepatic cholesterol, triglyceride, and fatty acid) and suppressed gene expression of SREBP1c (associated with fatty liver and increased visceral fat mass), while increasing CPT1α gene expression (involved in fatty acid oxidation-conversion of fat into energy), compared to the HFD group (p < 0.05 for both on all parameters). SLG significantly elevated fecal cholesterol, triglyceride, and fatty acid levels (p < 0.05 for all), and SL significantly increased fecal cholesterol (p < 0.05). Finally, researchers found that SL and SLG appeared to suppress gluconeogenesis (synthesis of glucose), based on decreased PEPCK activity and increased expression of IRS2 mRNA (involved in coordination of glucose homeostasis) (p < 0.05 for both on both parameters), and reduce inflammation, based on decreased levels of plasma pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and PAI-1 (p < 0.05 for both on all parameters).

Evidence from the study highlights the favorable effects of the seabuckthorn plant, in the form of seabuckthorn leaf extract and as a flavonoid glycosides extract, on diet-induced obesity and the metabolic disturbances associated with it. Both SL and SLG were found to prevent adiposity and dyslipidemia by suppressing the activities of enzymes involved in lipogenesis. Both formulations also showed the ability to improve adiposity, hepatic steatosis, and insulin resistance, while attenuating inflammation. Researchers conclude that the anti-obesity effects of seabuckthorn are associated with a mechanism which alters hepatic lipid and glucose metabolizing factors, reduces lipid absorption, and suppresses adipocyte lipogenesis.

Source: Kwon EY, Lee J, Kim YG, et al. Seabuckthorn leaves extract and flavonoid glycosides extract from Seabuckthorn leaves ameliorates adiposity, hepatic steatosis, insulin resistance, and inflammation in diet-induced obesity. Nutrients. 2017; 9: 569. DOI: 10.3390/nu9060569.

© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)

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Posted March 27, 2019.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

References:

  1. Kabir M, Catalano KJ, Ananthnarayan S, et al. Molecular evidence supporting the portal theory: a causative link between visceral adiposity and hepatic insulin resistance. American journal of physiology Endocrinology and metabolism. 2005;288(2):E454-461.
  2. Suomela JP, Ahotupa M, Yang B, Vasankari T, Kallio H. Absorption of flavonols derived from sea buckthorn (Hippophae rhamnoides L.) and their effect on emerging risk factors for cardiovascular disease in humans. J Agric Food Chem. 2006;54(19):7364-7369.
  3. Geetha S, Sai Ram M, Singh V, Ilavazhagan G, Sawhney RC. Anti-oxidant and immunomodulatory properties of seabuckthorn (Hippophae rhamnoides)–an in vitro study. J Ethnopharmacol. 2002;79(3):373-378.
  4. Ganju L, Padwad Y, Singh R, et al. Anti-inflammatory activity of Seabuckthorn (Hippophae rhamnoides) leaves. Int Immunopharmacol. 2005;5(12):1675-1684.
  5. Lee J, Jung E, Lee J, et al. Isorhamnetin represses adipogenesis in 3T3-L1 cells. Obesity (Silver Spring, Md). 2009;17(2):226-232.
  6. Yan SX, Li X, Sun CD, Chen KS. [Hypoglycemic and hypolipidemic effects of quercetin and its glycosides]. Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica. 2015;40(23):4560-4567.
  7. Kwon E-Y, Lee J, Kim Y, et al. Seabuckthorn leaves extract and flavonoid glycosides extract from seabuckthorn leaves ameliorates adiposity, hepatic steatosis, insulin resistance, and inflammation in diet-induced obesity. Nutrients. 2017;9(6):569.