GIP Peptides for Treatment of Diabetes, Obesity and Related Metabolic Disease
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Gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP) plays a key role in glucose-stimulated insulin secretion and the regulation of post-prandial nutrient homeostasis.
GIP, like GLP-1, is rapidly degraded in the blood by dipeptidyl peptidase 4 (DPPIV) to the inactive N-terminally truncated GIP (3-42).
Like GLP-1, N-terminal modification of GIP prevents degradation by DPPIV and prolongs biological activity, facilitating the use of such stable analogues for treatment of diabetes, obesity and related metabolic disorders.
Therapeutic exploitation of the incretin system represents a new approach to diabetes treatment as evident from the introduction of GLP-1 mimetics and gliptins.
Exploitation of GIP is hindered by DPPIV degradation and beta cell insensitivity, however these barriers are removed by enzyme resistant forms of GIP and restoration of insulin-releasing effects by temporarily lowering hyperglycaemia with other therapeutics.
Although GIP agonists promote glucose lowering by acute actions on beta cells, there is now increasing awareness of a beneficial effect of GIP antagonism in diet-induced obesity, leading to amelioration of insulin resistance, body weight loss and preferential burning of fat.
Ulster’s peptide analogues have been evaluated in a variety of animal models for obesity and diabetes with the following results:
- Enhanced bioactivity and resistance to DPPIV.
- Once daily injection leads to significant decreases in non-fasting glucose and glycated haemoglobin, as well as improved glucose tolerance, insulin secretion and/or insulin sensitivity.
- Synergistic benefits of using GIP analogues in combination with GLP-1 agonists.
Jennifer Cook: firstname.lastname@example.org / +44 (0) 2890 366 705