Premium
Dietary blueberry attenuates obesity‐associated insulin resistance by reducing adipocyte death and macrophage pro‐inflammatory activation in adipose tissue of high fat‐fed mice
Author(s) -
DeFuria Jason,
Bennett Grace,
Strissel Katherine J,
Perfield James W,
Greenberg Andrew S,
Obin Martin S
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.910.1
Subject(s) - adipocyte , insulin resistance , endocrinology , medicine , adipose tissue , oxidative stress , inflammation , biology , insulin , chemistry
Adipose tissue (AT) inflammation promotes insulin resistance (IR) and other obesity complications. AT inflammation and IR are associated with AT oxidative stress, adipocyte death, and the scavenging of dead adipocytes by M1‐polarized CD11c+ AT macrophages (ATMs). We test the hypothesis that blueberry (BB) supplementation of an obesigenic diet protects against these AT events. Male C57B/6j mice were fed one of three diets for 8 weeks: 10% fat (LF), 60% fat (HF) or HF containing 4% (w:w) BB powder (1:1 V. ashei and V. corymbosum ). We assessed energy intake, metabolic rate, insulin resistance (insulin tolerance tests), body and AT weights, adipocyte size, adipocyte death, as well as AT gene expression by Q‐PCR of CD11c, inflammatory mediators and markers of oxidative stress (GPx3). Relative to the HF cohort, mice fed the HFB diet were significantly protected from insulin resistance. This protection was associated with enhanced antioxidant (GPx3) gene expression, reduced adipocyte death, attenuated expression of CD11c, and abrogation of ATM expression of TNF‐α and iNOS. BB supplementation had no effect on HF diet‐associated alterations in energy intake, metabolic rate, body / AT weight, adipocyte size or markers of alternative (M2) ATM activation. BB's salutary effect on IR may reflect beneficial actions of BB anthocyanins on antioxidant and inflammatory gene expression in adipocytes and ATM. Grant Funding Source NIH (1RO1DKO74979) and the Highbush Blueberry Council