Research article summary (published 8 Jun 2009):

Dietary blueberry attenuates whole-body insulin resistance in high fat-fed mice by reducing adipocyte death and its inflammatory sequelae.

Full Abstract

Adipose tissue (AT) inflammation promotes insulin resistance (IR) and other obesity complications. AT inflammation and IR are associated with oxidative stress, adipocyte death, and the scavenging of dead adipocytes by proinflammatory CD11c+ AT macrophages (ATMPhi). We tested the hypothesis that supplementation of an obesitogenic (high-fat) diet with whole blueberry (BB) powder protects against AT inflammation and IR. Male C57Bl/6j mice were maintained for 8 wk on 1 of 3 diets: low-fat (10% of energy) diet (LFD), high-fat (60% of energy) diet (HFD) or the HFD containing 4% (wt:wt) whole BB powder (1:1 Vaccinium ashei and V. corymbosum) (HFD+B). BB supplementation (2.7% of total energy) did not affect HFD-associated alterations in energy intake, metabolic rate, body weight, or adiposity. We observed an emerging pattern of gene expression in AT of HFD mice indicating a shift toward global upregulation of inflammatory genes (tumor necrosis factor-alpha, interleukin-6, monocyte chemoattractant protein 1, inducible nitric oxide synthase), increased M1-polarized ATMPhi (CD11c+), and increased oxidative stress (reduced glutathione peroxidase 3). This shift was attenuated or nonexistent in HFD+B-fed mice. Furthermore, mice fed the HFD+B were protected from IR and hyperglycemia coincident with reductions in adipocyte death. Salutary effects of BB on adipocyte physiology and ATMPhi gene expression may reflect the ability of BB anthocyanins to alter mitogen-activated protein kinase and nuclear factor-kappaB stress signaling pathways, which regulate cell fate and inflammatory genes. These results suggest that cytoprotective and antiinflammatory actions of dietary BB can provide metabolic benefits to combat obesity-associated pathology.

Author information

Author/s: DeFuria, Jason (J); Bennett, Grace (G); Strissel, Katherine J (KJ); Perfield, James W (JW); Milbury, Paul E (PE); Greenberg, Andrew S (AS); Obin, Martin S (MS);

Affiliation: Obesity and Metabolism Laboratory and 5Antioxidants Research Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.

Grants: T32DK062032 (Agency:NIDDK NIH HHS) ; TH32HL69772 (Agency:NHLBI NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.

Journal: The Journal of nutrition (J Nutr), published in United States. (Language: eng)

Reference: 2009-Aug; vol 139 (issue 8) : pp 1510-6

Dates: Created 2009/07/21; Completed 2009/08/13;

PMID: 19515743, status: MEDLINE (last retrieved date: 8/21/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Adipocytes - drug effects Adiposity - drug effects Animals Anthocyanins - pharmacology Anti-Inflammatory Agents - pharmacology Blueberry Plant - chemistry Cell Death - drug effects; genetics Chemokine CCL2 - metabolism Diet Dietary Fats - administration & dosage Fruit Gene Expression - drug effects

Glutathione Peroxidase - metabolism Hyperglycemia - prevention & control Insulin Resistance Interleukin-6 - metabolism Macrophages - metabolism Male Mice Mice, Inbred C57BL Nitric Oxide Synthase Type II - metabolism Plant Preparations - chemistry; pharmacology Signal Transduction Tumor Necrosis Factor-alpha - metabolism

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Anthocyanins (0) ; Anti-Inflammatory Agents (0) ; Chemokine CCL2 (0) ; Dietary Fats (0) ; Interleukin-6 (0) ; Plant Preparations (0) ; Tumor Necrosis Factor-alpha (0) ; Gpx3 protein, mouse (EC 1.11.1.-) ; Glutathione Peroxidase (EC 1.11.1.9) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)

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