Last updated on November 19, 2018 at 17:16
It’s assumed that you know the insulin pathway by now. If you don’t you should read the insulin topic of biochem 1. You’ll definitely need it for the exam anyway
Insulin resistance is characterized as an impaired biological response to insulin, meaning that the effect of insulin on the cells isn’t as strong as it used to be. It causes changes in the metabolism and growth and differentiation (as insulin stimulates many transcription factors).
When insulin resistance is combined with the dysfunction of the insulin-producing β-cells, the result is type 2 diabetes, when the β-cells no longer can produce enough insulin to compensate for the insulin resistance. This causes hyperglycemia.
Intestinal cells produce proteins called incretins after a meal. Incretins stimulate β-cells to produce insulin.
The PPARs have already been introduced in biochemistry 1, and were mostly talked about here.
PPARγ increase the expression many enzymes and proteins involved in fatty acid metabolism. One of them is lipoprotein lipase, which releases free fatty acids from lipoproteins. It also increases expression of fatty acid transporters. Lastly, it increases transcription of PEPCK in the adipocyte. The combination of these three mechanisms increase the flow of FFAs into adipocytes. By giving PPARγ agonists like thiazolidinedione as drugs to patients with diabetes, we can decrease the insulin resistance and treat the diabetes.
Incretins are hormones that decrease blood glucose levels by increasing the secretion of insulin and decreasing the secretion of glucagon. The two important incretins are GLP-1 and GIP.
An enzyme called dipeptidyl peptidase 4 or DPP-4 breaks down GLP-1 and GIP so that they no longer have effects. By using a DPP-4 inhibitor as medication, we can increase the effect of the incretins and therefore lower blood glucose levels.
19. pH regulation
21. Molecular mechanisms of glucose uptake