Investigating the role of Annexin A1 in Adipogenesis and its ability to dampen Obesity associated Inflammation

Sajid, Sehar; Renshaw, Derek; Burke, Bernard; Mee, Christopher

doi:10.1530/endoabs.50.p335

Cited by 1 publication

(3 citation statements)

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“…They concluded that the decrease in Annexin A1 (anti-inflammatory protein) that occurred concurrently with the increase in body fat is strongly associated with obesity-related inflammation and cardiometabolic complications ( 16 ). In addition, the findings of the present study agree with Sajid et al ( 30 ) who concluded that Annexin A1 could decrease the accumulation of fat in adipocytes and suppress the process of adipogenesis. They also suggested a therapeutic role for Annexin A1/FPR2 to eliminate obesity accompanying inflammation ( 30 ).…”

Section: Discussionsupporting

confidence: 93%

“…In addition, the findings of the present study agree with Sajid et al ( 30 ) who concluded that Annexin A1 could decrease the accumulation of fat in adipocytes and suppress the process of adipogenesis. They also suggested a therapeutic role for Annexin A1/FPR2 to eliminate obesity accompanying inflammation ( 30 ).…”

Section: Discussionsupporting

confidence: 93%

“…Annexin A1 is an anti-inflammatory protein that acts through formyl-peptide-receptor-2 (FPR-2) in many cellular functions. It diminishes the production of pro-inflammatory cytokines by neutrophils and enhances the apoptosis of neutrophils, inhibits phospholipase A2 and consequently dampens the eicosanoid biosynthesis, and suppresses the process of adipogenesis ( 13 , 14 , 30 ).…”

Section: Discussionmentioning

confidence: 99%

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Circulating miR‑15b, Annexin A1, procalcitonin and interleukin‑6 levels differentiate children with metabolically unhealthy obesity from those with metabolically healthy obesity: A case‑control study

et al. 2022

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The present study assessed serum miR-15b, Annexin A1, procalcitonin, and interleukin-6 (IL-6) levels in children with metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) and compared them to these levels in a non-obese healthy control group. It also tested the ability of each of these parameters to early differentiate children with MUO from those with MHO. The present study included 620 children [434 males (70%) and 186 females (30%); aged 9-15 years] divided into the following groups: G1, healthy non-obese controls (n=200); G2, MHO (n=246); G3, MUO (n=174). Serum miR-15b, Annexin A1 procalcitonin, IL-6, and other metabolic parameters levels were measured, and clinical examinations were conducted for all of the children. After testing the normality of the variable, Kruskal-Wallis one-way-ANOVA, and Spearman correlation coefficients were used. The area under the receiver operating characteristic curve (AUC) was determined to test the variable's ability to differentiate MUO from MHO. miR-15b, procalcitonin, and IL-6 levels were significantly higher while Annexin A1 levels were significantly lower in G2 and G3 when compared to G1, and in G3 when compared to G2. These levels were positively correlated (Annexin A1 was negatively correlated) with body mass index (BMI) and waist circumference percentiles, and with serum levels of LDL-cholesterol, glucose, HbA1c, insulin, and C-reactive protein (CRP) and with the homeostasis model of insulin resistance (HOMA-IR). The AUC was 0.92, 0.84, 0.82, and 0.67 for miR-15b, Annexin A1, procalcitonin, and IL-6, respectively. In conclusion, determination of serum miR-15b, Annexin A1, and procalcitonin levels could differentiate children with MUO from those with MHO. This may help the early management of these cases and their accompanying complications.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%