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USING INCRETIN IN TREATMENT OF DIABETES MELLITUS DISEASE
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Incretin hormones are gut peptides secreted in response to nutrient ingestion, which play a key role in the regulation of islet function and blood glucose levels. In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose- dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect which is defined as the phenomenon whereby orally ingested glucose elicits a much greater insulin response than that obtained when glucose isinfused intravenously to give identical blood glucose levels. there is evidence to suggest that impairments in secretion and/or action of incretin hormones arise secondarily to the development of insulin resistance, glucose intolerance, and/or increases in body weight rather than being causative factors. In separate studies, insulin sensitivity, glucose tolerance, and body mass index (BMI) have all been identified as independent factors associated with reductions in GLP-1 secretion and an impaired incretin effect. In patients with type 2 diabetes, the incretin effect is clearly reduced, which results in an inappropriately low insulin response to the ingestion of nutrients. Several early studies indicated that the reduced incretin effect could, at least in part, be related to impaired secretion of GLP- 1 (whereas secretion of GIP is generally found to be unaltered). Impaired meal-stimulated GLP-1 levels have been reported in some studies of patients with type 2 diabetes. incretins exert antidiabetic actions in a glucose-dependent manner Glucagon-like peptide 1 receptor (GLP-1r) agonists, but not dipeptidyl peptidase-4 (DPP-4) inhibitors, inhibit gastricemptying and might cause weight loss DPP-4 inhibitors can be administered orally and are well tolerated GLP-1r agonists must be administered by subcutaneous injection and commonly cause nausea
Title: USING INCRETIN IN TREATMENT OF DIABETES MELLITUS DISEASE
Description:
Incretin hormones are gut peptides secreted in response to nutrient ingestion, which play a key role in the regulation of islet function and blood glucose levels.
In humans, the major incretin hormones are glucagon-like peptide (GLP)-1 and glucose- dependent insulinotropic polypeptide (GIP), and together they fully account for the incretin effect which is defined as the phenomenon whereby orally ingested glucose elicits a much greater insulin response than that obtained when glucose isinfused intravenously to give identical blood glucose levels.
there is evidence to suggest that impairments in secretion and/or action of incretin hormones arise secondarily to the development of insulin resistance, glucose intolerance, and/or increases in body weight rather than being causative factors.
In separate studies, insulin sensitivity, glucose tolerance, and body mass index (BMI) have all been identified as independent factors associated with reductions in GLP-1 secretion and an impaired incretin effect.
In patients with type 2 diabetes, the incretin effect is clearly reduced, which results in an inappropriately low insulin response to the ingestion of nutrients.
Several early studies indicated that the reduced incretin effect could, at least in part, be related to impaired secretion of GLP- 1 (whereas secretion of GIP is generally found to be unaltered).
Impaired meal-stimulated GLP-1 levels have been reported in some studies of patients with type 2 diabetes.
incretins exert antidiabetic actions in a glucose-dependent manner Glucagon-like peptide 1 receptor (GLP-1r) agonists, but not dipeptidyl peptidase-4 (DPP-4) inhibitors, inhibit gastricemptying and might cause weight loss DPP-4 inhibitors can be administered orally and are well tolerated GLP-1r agonists must be administered by subcutaneous injection and commonly cause nausea.
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