Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Jun 1:178:9-16.
doi: 10.1016/j.lfs.2017.04.010. Epub 2017 Apr 14.

Vitamin B2 deficiency enhances the pro-inflammatory activity of adipocyte, consequences for insulin resistance and metabolic syndrome development

Affiliations

Vitamin B2 deficiency enhances the pro-inflammatory activity of adipocyte, consequences for insulin resistance and metabolic syndrome development

Agnieszka Irena Mazur-Bialy et al. Life Sci. .

Abstract

Aims: Adipose tissue is an endocrine organ important for regulation of such physiological processes as energy metabolism or lipids homeostasis. In an obesity state, it participates in the induction of chronic systemic inflammation accompanied by pro-inflammatory cytokines and fatty acid elevation. For this reasons, adipose tissue is involved in, e.g., insulin resistance, type 2 diabetes or hyperlipidemia development. In our previous study, we have shown that riboflavin deficiency induces a pathological pro-inflammatory response of macrophages, the main component of adipose tissue. Therefore, in the current study, we investigated the alteration of the pro-inflammatory activity of adipocytes.

Main methods: The study was conducted on mouse 3T3 L1 preadipocytes differentiated to adipocyte and culture in the state of riboflavin deficiency (3.1nM) or control condition (10.4nM). The cell viability, adiposity and glucose uptake was assessed. Moreover, mRNA expression, as well as crucial pro-inflammatory cytokines (TNFα, IL-6) and adipokines (adiponectin, leptin, resistin) release and NFκB activation, were evaluated.

Key findings: Results showed that riboflavin deprivation induced a significant elevation in adipocyte lipolysis and enhance obesity-related apoptosis of adipocytes. The generation of reactive oxygen species was enhanced in riboflavin-deficient adipocytes by 43%. Moreover, NFκB phosphorylation and the expression and release of both TNFα, IL-6 as well as leptin were elevated in a deficient group what was accompanied by a reduction of adiponectin level.

Conclusion: Our study shows that riboflavin deficiency can promote the intensification of pro-inflammatory activity of adipocyte cells, leading consequently to the severity of chronic inflammation that accompanies obesity state.

Keywords: Adipocyte tissue; Ariboflavinosis; Inflammation; Insulin resistance; Obesity.

PubMed Disclaimer

Similar articles

Cited by

LinkOut - more resources