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Download Background Insulin resistance, eg. reduced possibility for body cells
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Background Insulin resistance, eg. reduced possibility for body cells to react on insulin-‐signaling by enhancing glucose uptake from blood, is a key event in Diabetes type II, leading to high blood-‐glucose-‐levels. Hypothesis A novel co-‐factor A is suspected to change the transcription of the insulin-‐receptor gene (B) leading to altered conformity of the insulin-‐receptor (C), promoting binding of substance D instead of insulin. In this way substance D will obstruct insulin and thereby block glucose up-‐take. Methods We aim to compare glucose tolerance, meaning how well a mouse can handle sugar-‐uptake, in diabetic knock-‐out mice lacking co-‐factor A, diabetic mice with intact co-‐factor A and normal mice. Results When analyzing our diabetic mice lacking co-‐factor A we found a much higher glucose-‐tolerance compared to diabetic mice with intact co-‐factor A, however not as high as in normal mice. This indicates a decrease in insulin resistance thereby supporting our hypothesis. Conclusions We conclude that co-‐factor A has an important, although not sole, function in type II diabetes regulating blood-‐glucose levels by increasing insulin resistance. Importance With the findings in this study we can now take the next step to investigate food-‐content of co-‐factor A, which might lead to better dietary recommendations. We also find it possible to develop a synthetic anti-‐co-‐factor A drug to be tested in a diabetic animal setting.
