3.9 Review

Lipoprotein effects of incretin analogs and dipeptidyl peptidase 4 inhibitors

Journal

CLINICAL LIPIDOLOGY
Volume 10, Issue 1, Pages 103-112

Publisher

FUTURE MEDICINE LTD
DOI: 10.2217/CLP.14.59

Keywords

apoB-48; DPP-4; GLP-1; incretins; lipoproteins

Funding

  1. NIH [R01ES017290, R01ES015146]
  2. EPA [RC063384OSU]
  3. American Heart Association [13POST17210033]
  4. National Natural Science Foundation of China [81101553/H1604]
  5. American Heart Association NCRP Scientist Development grant [13SDG14500015]

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Elevated post-prandial lipoprotein levels are common in patients with type 2 diabetes. Post-prandial lipoprotein alterations in type 2 diabetics are widely believed to drive inflammation and are considered a major risk factor for cardiovascular disease in diabetic patients. The incretins glucagon like peptide-1 (GLP-1) and glucose insulinotropic peptide (GIP) modulate post-prandial lipoproteins through a multitude of pathways that are independent of insulin and weight loss. Evidence from both animal models and humans seems to suggest an important effect on triglyceride rich lipoproteins (Apo48 containing) with little to no effects on other lipoproteins at least in humans. Dipeptidyl peptidase-4 (DPP4) inhibitors also appear to share these effects suggesting an important role for incretins in these effects. In this review, we will summarize lipid modulating effects of incretin analogs and DPP-4 inhibitors in both animal models and human studies and provide an overview of mechanisms responsible for these effects.

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