Kyle J. Norton
Green tea may have a therapeutic and positive effect in improved glucose metabolism, some scientists suggested.
The beverage is a precious drink processed with a number of health benefits, known to almost everyone in Asia and the Western world.
Glucose metabolism is an action of the body to convert glucose intake to energy for the needs of body tissue and organs through oxidized glucose to carbon dioxide and water.
Stages of abnormal glucose metabolism stretch from mild forms of glucose intolerance (pre-diabetes), to diabetes and finally to pregravid forms of diabetes associated with the end-organ disease.
Long-term abnormal glucose metabolism is considered a leading cause of diabetes and diabetic complications.
Some researchers even suggested that abnormalities of glucose metabolism can induce excess body weight and increase potentially modifiable risk factors for cardiac morbidity and mortality.
And, long-term impaired glucose tolerance (IGT) is considered as a marker for the state of insulin resistance and prediction of vessel vascular complications, independent of a patient’s progression to diabetes.
Normal blood glucose levels (tested while fasting) of healthy individuals are in the range of 3.9 and 5.5 mmol/L (70 to 100 mg/dL). ...and no more than 7.8 mmol/L (140 mg/dL) 2 hours after eating.
Green tea extract, in the evaluation of the carbohydrate metabolic key enzymes in control and streptozotocin high fat diet-induced diabetic rats in 30 days, demonstrated significant activity in ameliorated overexpression of plasma glucose, glycosylated hemoglobin (HbA1c) and increase in the levels of insulin and hemoglobin.
Expression of hemoglobin A1c is the average level of blood sugar over the past 2 to 3 months.
The typical hemoglobin molecule measured in a volume of blood is 13.8 to 17.2 grams per deciliter (g/dL) for men and 12.1 to 15.1 g/dL for women.
Further analysis also found that the application exerted a profound effect to restore, to some extends, the function of altered activities of the key enzymes of carbohydrate metabolism, such as hexokinase, pyruvate kinase, and lactate dehydrogenase in both diabetic and control groups.
Abnormal (over 10−5M or 0.9 mg%) function of hexokinase in converted glucose into glucose-6-phosphate was associated with moderate to severe hypoglycemia.
Pyruvate Kinase is an enzyme with function in catalyzed the last step of glycolysis.
Deficiency of pyruvate kinase is associated with the risk of metabolic disorders.
Lactate dehydrogenase (LDH or LD) is an enzyme with the function to catalyze the conversion of lactate to pyruvic acid and back.
In the diabetic rats' group, green tea extract strongly averted the abnormal expression of glycogen phosphorylase in the liver to near-normal levels.
Additionally, the diabetic group after administration of green tea extract exhibited antihyperglycemic potential, observed through improved muscle and hepatic glycogen content.
Glycogen phosphorylase is an enzyme with the function to release sugar from cells.
The findings showed that green tea extract has a direct implication in attenuating abnormal glucose metabolism in comparison to the effectiveness of conventional medicine metformin, a standard oral hypoglycemic drug.
Moreover, in the study to confirm the epidemiological studies' suggestion of green tea in the improvement of glucose metabolism in diabetic mice, researchers found that injection of green tea in diabetic mice and streptozotocin-induced diabetic mice after 2-6 h expresses lower levels of glucose with no alternation of serum insulin level, at a dose of 300 mg/kg in compared to normal and control mice.
In protein differentiation, green tea extract administration decreased the serum protein level with function in stimulated glucose production and minimized the increase in blood glucose levels by stimulating additional small amounts of insulin in diabetes.
These results addressed another impact of green tea function in exerting direct influence in the modulation of glucose metabolism in the tested subjects.
Interestingly, in the investigation of green tea's effect on glucose uptake inhibitory activity in Caco-2 cells, scientists also indicated that green tea at a temperature of 60 degrees Celsius significantly improves the capacity of antioxidants in the inhibition of glucose uptake through regulation of cell glucose metabolism.
Incredibly, in temperatures over 60 degrees Celsius, green tea application did not increase or show an upward trend in the inhibitory potential, the Huazhong Agricultural University suggested.
Taken together, green tea with abundant bioactive phytochemicals may be considered as a functional food in improved glucose metabolism in reduced risk of diabetes onset.
People with high-risk diabetes such as prediabetics may want to add 1 or 2 cups of green tea into their daily diet for preventive measures.
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Author Biography
Kyle J. Norton, Master of Nutrients
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blog, self-growth, best before it's news, the Karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been referenced in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Modulatory effect of green tea extract on hepatic key enzymes of glucose metabolism in streptozotocin and high fat diet-induced diabetic rats by Sundaram R1, Naresh R, Shanthi P, Sachdanandam P.(PubMed)
(2) Effect of green tea on blood glucose levels and serum proteomic patterns in diabetic (db/db) mice and on glucose metabolism in healthy humans by Tsuneki H1, Ishizuka M, Terasawa M, Wu JB, Sasaoka T, Kimura I.(PubMed)
(3) Effect of steeping temperature on antioxidant and inhibitory activities of green tea extracts against α-amylase, α-glucosidase, and intestinal glucose uptake by Liu S1, Ai Z2, Qu F3, Chen Y4, Ni D5. (PubMed)
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