Efficacy and Safety of a Biosimilar Liraglutide (Melitide®) Versus the Reference Liraglutide (Victoza®) in People with Type 2 Diabetes Mellitus: A Randomized, Double-Blind, Noninferiority Clinical Trial

Esteghamati, Alireza; Zamanzadeh, Mehran; Malek, Mojtaba; Khaledi, Mohammad; Monavari, Arezoo; Najafi, Laily; Banazadeh, Zahra; Malboosbaf, Ramin; Aghili, Rokhsareh; Mahdikhah, Sedigheh; Ganjizadeh-Zavereh, Hasan; Kafi, Hamidreza; Hosseinpanah, Farhad; Khamseh, Mohammad Ebrahim

doi:10.1007/s13300-023-01462-w

Cited by 2 publications

(2 citation statements)

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“…10 Glucagon-like peptide-1 (GLP-1) is a potent physiological glucose regulator that stimulates insulin secretion and can be used as the basis for the treatment of obesity and type 2 diabetes. [11][12][13] DPP4 degrades GLP-1 as well as several other peptides and cytokines 14 and is well known for its regulatory role in glucose metabolism. 15 DPP4 is upregulated in proinflammatory states such as obesity, diabetes, and atherosclerotic coronary artery diseases.…”

Section: Introductionmentioning

confidence: 99%

“…DPP4 cell surface expression marks an abundant adipose stem/progenitor cell population with high stemness in human white adipose tissue 10 . Glucagon‐like peptide‐1 (GLP‐1) is a potent physiological glucose regulator that stimulates insulin secretion and can be used as the basis for the treatment of obesity and type 2 diabetes 11–13 . DPP4 degrades GLP‐1 as well as several other peptides and cytokines 14 and is well known for its regulatory role in glucose metabolism 15 .…”

Section: Introductionmentioning

confidence: 99%

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Dipeptidyl peptidase‐4 disturbs adipocyte differentiation via the negative regulation of the glucagon‐like peptide‐1/adiponectin‐cathepsin K axis in mice under chronic stress conditions

Zhang,

Yue,

et al. 2024

The FASEB Journal

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Exposure to chronic psychosocial stress is a risk factor for metabolic disorders. Because dipeptidyl peptidase‐4 (DPP4) and cysteinyl cathepsin K (CTSK) play important roles in human pathobiology, we investigated the role(s) of DPP4 in stress‐related adipocyte differentiation, with a focus on the glucagon‐like peptide‐1 (GLP‐1)/adiponectin‐CTSK axis in vivo and in vitro. Plasma and inguinal adipose tissue from non‐stress wild‐type (DPP4+/+), DPP4‐knockout (DPP4−/−) and CTSK‐knockout (CTSK−/−) mice, and stressed DPP4+/+, DPP4−/−, CTSK−/−, and DPP4+/+ mice underwent stress exposure plus GLP‐1 receptor agonist exenatide loading for 2 weeks and then were analyzed for stress‐related biological and/or morphological alterations. On day 14 under chronic stress, stress decreased the weights of adipose tissue and resulted in harmful changes in the plasma levels of DPP4, GLP‐1, CTSK, adiponectin, and tumor necrosis factor‐α proteins and the adipose tissue levels of CTSK, preadipocyte factor‐1, fatty acid binding protein‐4, CCAAT/enhancer binding protein‐α, GLP‐1 receptor, peroxisome proliferator‐activated receptor‐γ, perilipin2, secreted frizzled‐related protein‐4, Wnt5α, Wnt11 and β‐catenin proteins and/or mRNAs as well as macrophage infiltration in adipose tissue; these changes were rectified by DPP4 deletion. GLP‐1 receptor activation and CTSK deletion mimic the adipose benefits of DPP4 deficiency. In vitro, CTSK silencing and overexpression respectively prevented and facilitated stress serum and oxidative stress‐induced adipocyte differentiation accompanied with changes in the levels of pref‐1, C/EBP‐α, and PPAR‐γ in 3T3‐L1 cells. Thus, these findings indicated that increased DPP4 plays an essential role in stress‐related adipocyte differentiation, possibly through a negative regulation of GLP‐1/adiponectin‐CTSK axis activation in mice under chronic stress conditions.

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