Purpose: Myeloperoxidase (MPO) is a major neutrophil-derived protein known to play an important role in inflammation, oxidative stress, and atherosclerosis. Like other angiopoietin-like protein (ANGPTL), ANGPTL6 is reported to regulate metabolic processes but is thought to counteract obesity through increased energy expenditure. This study evaluated the plasma level of both MPO and ANGPTL6 in obese and diabetic people to investigate their clinical association.

Methods: A total of 204 people were enrolled in this study (109 nondiabetic and 95 T2D). ANGPTL6, MPO, and other biomarkers plasma levels were measured by ELISA.

Results: MPO plasma level was unchanged between diabetics and nondiabetics, whereas ANGPTL 6 plasma level increased in diabetics (33.73±1.31 pg/mL) compared to nondiabetics (28.74±1.01 pg/mL) (P <0.003). However, MPO plasma level increased in obese diabetics (75.28±3.19 ng/mL) compared to non-obese diabetics (65.71±2.54 ng/mL) (P <0.02). Similarly, ANGPTL6 plasma level was increased in obese diabetics (35.74±1.68 pg/mL) compared to non-obese diabetics (29.05 ± 1.61 pg/mL) (P <0.01). Obese nondiabetics had a higher level of MPO compared to non-obese nondiabetics although it did not reach statistical significance (P = 0.05). In contrast, no changes in the plasma levels of ANGPTL6 were seen in nondiabetics irrespective of weight. Both MPO and ANGPTL plasma levels were higher in obese than non-obese people (P < 0.05). MPO was positively associated with ANGPTL6, TG, BMI, TNF alpha, HsCRP, IL6, and PAI1.

Conclusion: Both MPO and ANGPTL6 seem to regulate obesity, although MPO might do it independently of diabetes status and they might be also involved in wound healing as previously reported. The positive association of MPO with several biomarkers of inflammation and atherosclerosis may underlie its pathogenic mechanism in obesity and diabetes related wound healing and other diabetes related pathways.


M.G. Qaddoumi: None. M. Abu-farha: None. P.T. Cherian: None. I. Al khairi: None. A.M. Channanath: None. M. Alanbaei: None. J. Abubaker: None. F. Al-Mulla: None.

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