title: Green tea attenuates cardiovascular remodelling and metabolic symptoms in high carbohydrate-fed rats.
abstract: Excess carbohydrate in the diet may initiate a chronic state of oxidative stress exacerbating the clinical and biochemical symptoms of diet-induced type 2 diabetes, especially glucose intolerance, lipid abnormalities and cardiovascular complications. This study has tested whether green tea, rich in antioxidants, improves both cardiovascular symptoms and glucose intolerance and also reduces oxidative stress in rats fed a high carbohydrate diet. Male 8 week old Wistar rats were fed a diet including fructose and condensed milk (each 40%) for 16 weeks (112 days); control rats were fed corn starch. Green tea-containing food was started from day 1 for the prevention protocol and from day 56 for the reversal protocol. High carbohydrate diet-fed rats showed glucose intolerance, hypertension, mild left ventricular hypertrophy, approximate doubling of cardiac interstitial and perivascular collagen deposition, increased passive diastolic stiffness and increased plasma malondialdehyde concentrations. Administration of green tea to high carbohydrate diet-fed rats prevented and reversed glucose intolerance and the increased systolic blood pressure, left ventricular wet weight, interstitial collagen and passive diastolic stiffness. Plasma malondialdehyde concentrations were also normalized. In summary, treatment with green tea both prevented and reversed the cardiovascular remodelling and metabolic changes seen in high carbohydrate-fed rats suggesting a chronic state of oxidative stress plays a key role in the symptom initiation and progression. Further, green tea may be a useful complementary therapy in diet-induced type 2 diabetes.
authors.affiliation: School of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
authors.forename: Celestine
authors.initials: C
authors.lastname: Rickman
authors.forename: Abishek
authors.initials: A
authors.lastname: Iyer
authors.forename: Vincent
authors.initials: V
authors.lastname: Chan
authors.forename: Lindsay
authors.initials: L
authors.lastname: Brown
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001786:Blood Glucose; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D002319:Cardiovascular System / Q000187:drug effects / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism; D004452:Echocardiography; D005632:Fructose / Q000008:administration & dosage; D018149:Glucose Intolerance / Q000188:drug therapy / Q000378:metabolism; D006973:Hypertension; D008297:Male; D008659:Metabolic Diseases / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D013213:Starch / Q000008:administration & dosage; D013662:Tea; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D004040:Dietary Carbohydrates; D013662:Tea; D005632:Fructose; D013213:Starch