The extract of the leaves of Ginkgo biloba, a popular dietary supplement, may offer some therapeutic benefits in fighting Type 2 diabetes, according to a study co-authored by a researcher at the University of Cincinnati (UC) College of Medicine.
“In diabetic rats Ginkgo biloba had a very good effect on the beta cells of Langerhans – cells in the pancreas responsible for insulin secretion – by creating a restorative effect similar to what we see in healthy non-diabetic rats,” says Helal Fouad Hetta, Ph.D., a postdoctoral fellow and scientist in the UC Division of Digestive Diseases. Hetta is also on faculty at Egypt’s Assiut University College of Medicine in the Department of Medical Microbiology and Immunology.
The study in animal models by an international team of 13 researchers was published in the journal Diabetes, Metabolic Syndrome and Obesity:
Targets and Therapy and is available online. The first author on the research is Ahmed Saleh, Ph.D., Jazan University in Saudi Arabia.
“The extracts derived from Ginkgo biloba have been frequently used in traditional medicine and have been shown to exhibit antioxidant potency,” says Hetta.
“Magnetized water, which has been passed through a magnetic field, has also been reported to reduce blood glucose, improve antioxidant status and lipid profiles in diabetic rat models.”
In this study, Type 2 Diabetes was induced by feeding rats a high-fat-diet for eight weeks followed by intra-peritoneal injection of a single low dose of streptozotocin, explains Hetta.
Forty rats were randomly assigned to four groups: a non-diabetic control group and three diabetic groups.
One diabetic group served as a positive control (diabetic), while the other two groups were orally administered with water extract of Ginkgo biloba leaves and magnetized water for four weeks, respectively.
The beta cells of diabetic rats are reduced and insulin secretion is curtailed.
After having Ginkgo biloba and magnetized water added to their diets, the mass of the pancreatic beta cells and the amount of insulin in these cells was shown to increase markedly, almost back to normal levels, particularly in the Ginkgo biloba-treated group, says Hetta.
In addition, both Ginkgo biloba and magnetized water improved the anti-oxidant status and reduced the oxidative stress associated with type 2 diabetes by down regulation of the two antioxidant enzymes, glutathione and superoxide dismutase 2, in the pancreatic tissue, says Hetta.
These findings for Ginkgo biloba’s impact on Type 2 diabetes are preliminary, says Hetta.
“We still need more evidence about possible benefits for Type 2 diabetes so there is ongoing research,” says Hetta. “Our findings need to be tested in human clinical trials of large sample size.
“Gingko biloba is one of the oldest living tree species,” says Hetta.
“Most Ginkgo products are made with extract prepared from leaves. Most research on Gingko focuses on its effects on dementia and age-related memory impairment such as Alzheimer’s disease and pain caused by too little blood flow or claudication. It is commonly available as an oral tablet, extract, capsule or tea. It is not toxic when used in low dosages, but can interact with other medicines.”
“I would not recommend eating raw or roasted Ginkgo seeds because they can be poisonous,” says Hussein. “It should be taken as a capsule or in tablets if used. Also, if you are currently taking medications please consult with your physicians before considering Ginkgo biloba.”
Collaborators on the study include Mamdouh Anwar, Ahmed E. Zayed, Gamal Afifi, Emad Shaheen, and Hassien Alnashiri, all from Jazan University in Saudi Arabia. Additional co-collaborators, all from Assiut University in Egypt include Manal El Sayed Ezz Eldeen, Asmaa MS Gomaa, Mahmoud Abd-Elkareem, Alaa Sayed Abou-Elhamd, Ghada Mohamed and Ahmed M. Kotb.
The work was funded by the Deanship of Scientific Research, Jazan University, Saudi Arabia, Grant # 37/7/00110. The authors of the study report no conflicts of interest in this work.
The definition of white adipose tissue (WAT) as an inert mass for energy storage is long gone; over the last two decades the adipose tissue has been recognized as a dynamic tissue and key player in the modulation of energy metabolism (1, 2). Adipokines such as leptin, adiponectin, and tumour necrosis factor-α (TNF-α) have a direct effect on energy homeostasis and modulation of low-grade inflammation (3). The intake of high fat diets has the potential to not only disturb normal adipokine secretion but also to remodel adipose tissue by increasing adipocyte size and/or number, contributing to the development of a pro-inflammatory microenvironment (4, 5). These perturbations have been positively associated with metabolic disorders such as obesity, type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), insulin resistance, and cardiovascular diseases (6, 7).
In obesity, particularly visceral obesity, enlarged WAT visceral adipocytes show dysregulated lipolysis, inducing high levels of circulating non-esterified fatty acids (NEFAs) (8, 9). NEFAs in normal circumstances are utilized as energy by tissues such as liver and muscle; however, when in excess they contribute to the development of insulin resistance (4, 9–11). Furthermore, in response to overnutrition, hypertrophic adipocytes contribute to increased circulating triacylglycerol (TAG) levels mainly from de novo lipogenesis, in which fatty acids (FA) are synthetized from non-lipid substrates, particularly carbohydrates, or from FA obtained from ex-situ lipid sources such as chylomicrons and very-low-density lipoproteins (VLDL) (12, 13). Visceral obesity seems to play a central role in the development of metabolic disorders, being associated with low-grade chronic inflammation and the production of pro-inflammatory cytokines which have the potential to trigger insulin resistance and endothelial dysfunction (14–16).
In this context, several pharmacological approaches have been tried for the treatment of obesity. However, more often than not such approaches were followed by undesired side effects, including psychiatric manifestations, increased risk of cardiovascular events, and others (17). Considering the dramatic increase in the prevalence of obesity over the last decades globally, a range of anti-obesogenic alternative supplementation therapies based on plant extracts (18) have been investigated.
More recently, Ginkgo biloba Extract (GbE) has been investigated as an alternative therapy for metabolic disorders associated with obesity. GbE, a herbal extract containing flavonoids, terpenoids, and terpene lactones (19), is a well-known phytotherapic compound often employed as coadjuvant supplement in neurodegenerative diseases (20, 21), NAFLD (22, 23), type 1 and 2 diabetes (24, 25). Previous findings from our research group showed that diet-induced obese (DIO) rats supplemented with GbE showed reduced food and energy intake, reduced body adiposity, improved insulin signalling and sensitivity, enhanced insulin receptor and AKT phosphorylation, and reduced NFκB-p65 phosphorylation in retroperitoneal adipose tissue (26, 27).
GbE may have a potentially therapeutic use for menopause-associated obesity; supplementation with 500 mg/kg of GbE stimulated hypothalamic serotonergic activity in ovariectomized rats (28). GbE isolated bioactive compounds have been demonstrated to stimulate lipolysis in 3T3-L1 adipocytes (29), and to inhibit adipogenesis through activation of the AMPK pathway (30). However, the effects of GbE supplementation on metabolic processes of visceral adipose tissue in DIO rats remain largely unknown. In view of the considerations highlighted above, the aim of the present study was to investigate the effects of GbE supplementation as a potentially anti-obesogenic effector for improvement in lipid metabolism of epididymal adipose tissue of DIO rats.
More information: Ahmed Saleh et al. Impact of Ginkgo biloba extract and magnetized water on the survival rate and functional capabilities of pancreatic β-cells in type 2 diabetic rat model, Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy (2019). DOI: 10.2147/DMSO.S209856
Provided by University of Cincinnati