Abstract
Abstract
BACKGROUND: Fructose intake has been increased steadily during the past two decades. Fructose, like other reducing sugars can react with proteins, which may account for aging and myocardial infarction. Fructose participates in glycation (fructation) and AGE formation some 10 times faster than glucose. This study aims to determine the fructose concentration and correlate with antioxidant status in senile diabetic and non-diabetic patients with myocardial infarction.
METHODS: The study included one hundred twenty six subjects. Out of them 31 were normal senile subjects, 33 were senile diabetic patients without myocardial infarction, 32 were senile diabetic patients with myocardial infarction and 30 were senile non-diabetic patients with myocardial infarction. The patients were selected on clinical grounds from National Institute of Cardiovascular Diseases, Karachi and Jinnah Postgraduate Medical Centre, Karachi, Pakistan.
RESULTS: Serum fructose was significantly increased in senile diabetic patients with and without myocardial infarction and senile non-diabetic patients with myocardial infarction as compared with senile control subjects. Serum total antioxidant status was found to be significantly decreased in senile diabetic patients with and without myocardial infarction and senile non-diabetic patients with myocardial infarction as compared with senile control subjects. Fasting blood glucose, HbA
1C
and serum fructosamine were significantly increased in senile diabetic patients with or without myocardial infarction as compared with senile non-diabetic patients with myocardial infarction and senile control subjects. Negative significant correlation was observed between serum fructose and serum total antioxidant status in diabetic and non-diabetic patients with myocardial infarction. Positive significant correlation was observed between serum fructose and s-AGEs in diabetic and non-diabetic patients with myocardial infarction.
CONCLUSIONS: This study revealed that increased fructose concentration and decreased antioxidant status might have a role in the myocardial infarction.