Abstract Title:

Anthocyanin-Rich Aronia Berry Extract Mitigates High-Fat and High-Sucrose Diet-Induced Adipose Tissue Inflammation by Inhibiting Nuclear Factor-B Activation.

Abstract Source:

J Med Food. 2021 Mar 22. Epub 2021 Mar 22. PMID: 33751905

Abstract Author(s):

Seok-Yeong Yu, Mi-Bo Kim, Young-Ki Park, Minkyung Bae, Hyunju Kang, Siqi Hu, Tho X Pham, Ryan Carpenter, Jungwoo Lee, Ok-Hwan Lee, Ji-Young Lee, Young-Cheul Kim

Article Affiliation:

Seok-Yeong Yu


Obesity-induced inflammation in adipose tissue (AT) promotes the development of metabolic dysregulations by increasing macrophage recruitment in the stromal vascular fraction (SVF). The activation of nuclear factor-B (NF-B) signaling in macrophages serves as a pivotal mediator of AT inflammatory responses by increasing the expression of proinflammatory genes in obesity. Given the purported anti-inflammatory effects of berry consumption in humans, we evaluated if anthocyanin-rich aronia berry extract (ARN) can prevent obesity-induced AT inflammation. We also examined whether ARN suppresses lipopolysaccharide (LPS)-induced NF-κB activation in RAW 264.7 macrophages and mouse bone marrow-derived macrophages (BMDMs). Male C57BL/6J mice were fed a low-fat diet, a high-fat (HF), and high-sucrose (HS) diet or HF/HS diet supplemented with 0.2% ARN (HF/HS + ARN) for 14 weeks. Compared to HF-/HS-fed mice, ARN supplementation tended to decrease fasting serum glucose ( = .07). Furthermore, ARN supplementation significantly inhibited the phosphorylation of NF-B p65 in epididymal AT with a concomitant decrease in the expression ofandmRNAs in epididymal SVF isolated, compared with those from HF-/HS-fed mice. Consistent with thesefindings, ARN treatment significantly decreased the phosphorylation of p65 in LPS-stimulated RAW 264.7 macrophages and BMDMs. Moreover, ARN suppressed LPS-induced mRNA expression of inflammation mediators (,,,, and) and glycolysis markers (,, and) in both cell types. Taken together, ourandresults suggest that ARN supplementation may attenuate obesity-induced AT inflammation by inhibiting NF-B signaling and glycolytic pathway in macrophages.

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