Overweight Clinical Trial
Official title:
Dipeptidyl Peptidase 4 (DPP4) Activity and Its Associations With Endothelial Dysfunction, Inflammatory and Metabolic Markers, Heart Rate and Blood Pressure Variability, and Measures of Adiposity in Subjects With Different Grades of Glucose Tolerance
Dipeptidyl peptidase 4 (DPP4) is a serine exopeptidase able to inactivate various oligopeptides involved in inflammation, immunity and vascular function. Our aim was to investigate the associations between constitutive levels of DPP4 activity and inflammatory biomarkers, skin microvascular reactivity, gut peptides, insulin resistance indexes, heart rate and blood pressure variability, and measures of adiposity in subjects with different grades of glucose tolerance.
Dipeptidyl peptidase 4 (DPP4), also known as adenosine deaminase binding protein or cluster
of differentiation 26 (CD26), is a serine exopeptidase able to inactivate various
oligopeptides composed of proline, hydroxyproline, or alanine as the penultimate residue. In
recent years, DPP4 has received attention due to its ability to rapidly inactivate the main
incretins secreted by the gastrointestinal tract: glucagon-like peptide 1 (GLP-1) and
glucose-dependent insulinotropic polypeptide (GIP). As its own name already says, incretins
enhance insulin secretion in a glucose-dependent fashion, but also suppress or modulate
glucagon secretion. Since it was demonstrated that type 2 diabetes mellitus (T2D) have
incretin deficiency and hyperglucagonemia on its physiopathology, gliptins emerged as a new
class of drugs for the treatment of this disease, acting through the inhibition of DPP4 and
consequently ameliorating these defects.
DPP4 not only inactivate incretins but also a number of cytokines, chemokines, and
neuropeptides involved in inflammation, immunity and vascular function. Furthermore,
evidence from in vitro and in vivo studies, including clinical ones in T2D, suggested that
gliptins' inhibition of DPP4 was associated with reduction of inflammatory biomarkers and
also attenuation of endothelial dysfunction and atherogenesis, possibly through regulation
of the DPP4 substrates.
There is a paucity of studies that associate the constitutive levels of DPP4 activity (i.e.,
outside the context of pharmacological inhibition of the enzyme) with markers of
inflammation and endothelial function, specially tested on skin microcirculation. We
hypothesized that constitutive levels of DPP4 activity might be directly associated to
inflammation and inversely correlated with skin blood flux and one or more components of
vasomotion (suggesting an association with endothelial disfunction) even in the absence of
diabetes. Our aim was to investigate the associations between constitutive levels of DPP4
activity and inflammatory biomarkers, skin microvascular reactivity, gut peptides, insulin
resistance indexes, heart rate and blood pressure variability, and measures of adiposity in
subjects with different grades of glucose tolerance.
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