Associate professor Per M lgaard and postdoc Joan Campbell-Tofte from the Department of Medicinal Chemistry have previously tested the tea on genetically diabetic mice. The results of the tests showed that after six weeks of daily treatment with the African tea, combined with a low-fat diet, resulted in changes in the combination and amount of fat in the animals' eyes and protection of the fragile pancreas of the mice.
The researchers have recently completed a four month long clinical test on 23 patients with type-2 diabetes and are more than satisfied with the result.
'The research subjects drank 750ml of tea each day. The cure appears to differentiate itself from other current type-2 diabetes treatments because the tea does not initially affect the sugar content of the blood. But after four months of treatment with tea we can, however, see a significant increase in glucose tolerance,' said postdoc Joan Campbell-Tofte from the University of Copenhagen.
The clinical tests show another pattern in the changes in fatty acid composition with the patients treated in comparison with the placebo group.
'In the patient group who drank the tea, the number of polyunsaturated fatty acids increased. That is good for the body's cells because the polyunsaturated fat causes the cell membranes to be more permeable, which results in the cells absorbing glucose better from the blood,' said Joan Campbell-Tofte.
The researchers hope that new clinical tests and scientific experiments in the future will result in a new treatment for type-2 diabetics.
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His group studied two separate strains of mice, each carrying a specific genetic alteration that makes them especially prone to develop atherosclerosis. The mice also lacked CHOP, disabling the prodeath branch of the ER stress pathway.
When fed a diet high in fat and cholesterol for 10 weeks, one strain of those CHOP deficient mice with atherosclerosis developed smaller lesions than mice with CHOP, they report. Most importantly, cell death and plaque necrosis dropped by about 50 percent. The second strain of atherosclerotic mice showed essentially the same result.
Despite the fact that evidence had pointed to ER stress and the UPR before, Tabas said the result - and particularly the magnitude of the effect - still came as a considerable surprise.
"The fact that we were able to isolate one gene encoding one protein with such a profound effect on plaque necrosis was a big surprise," he said. That's because there could be many other processes at work, including some that might compensate for CHOP loss.
The findings in mice could have some real implications in the clinic, Tabas added.
"The results of this study, together with recent findings showing expression of CHOP in vulnerable human atherosclerotic plaques, suggest that the CHOP pathway may be a potential therapeutic target related to the formation of dangerous atheromata," the researchers concluded. "In particular, it will be interesting to determine whether so-called chemical chaperones, which have been successfully used in other animal models of UPR-associated diseases, have a beneficial effect on advanced atherosclerotic lesion progression."
cell