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Wheat Germ Supplementation Alleviates Insulin Resistance and Cardiac Mitochondrial Dysfunction in an Animal Model of Diet‐Induced Obesity
Author(s) -
Ojo Babajide,
Simenson Ashley J,
O'Hara Crystal,
Wu Lei,
Guo Xin,
Peterson Sandra K,
Lin Daniel,
Smith Brenda J,
Lucas Edralin A
Publication year - 2017
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.31.1_supplement.793.8
Subject(s) - insulin resistance , medicine , sod2 , endocrinology , mitochondrial biogenesis , oxidative stress , reactive oxygen species , mitochondrial ros , antioxidant , mitochondrion , biology , insulin , chemistry , superoxide dismutase , biochemistry
Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction in metabolically active tissues and increased production of reactive oxygen species (ROS). Foods rich in antioxidants such as wheat germ (WG), are thought to protect tissues from damage due to ROS and modulate some negative effects of obesity‐induced IR. This study examined the effects of WG supplementation on insulin resistance, mitochondrial substrate metabolism and innate antioxidant markers in two metabolically active tissues (i.e. liver and heart) of C57BL/6 mice fed a high fat (HF) diet. Six‐week‐old male C57BL/6 mice were randomized into four dietary treatment groups (n=12 mice/group): control (C, 10% fat kcal), control + 10% WG (C+WG), high fat (HF, 60% fat kcal), or HF+WG. After 90 days of treatment, one‐way ANOVA results indicate that HF+WG mice had significantly less visceral fat (−11%, P=0.0012), were less hyperinsulinemic (P=0.0091), and less insulin resistant (−57%, P=0.011) compared to the HF group. Addition of WG to the control diet showed no considerable effect. HF feeding compared to the control diet, significantly elevated (45%, P=0.008) cardiac mitochondrial oxygen consumption in complex 2, suggesting increased metabolic stress, while WG supplementation in the HF diet stabilized this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis ( Sod2 and Pgc1a, respectively) were significantly reduced (P<0.05) in the heart of the HF group compared to control while WG supplementation tended to upregulate both genes. These effects of WG were not observed in the liver. Put together, these results showed that WG supplementation in HF diet reduced insulin resistance and improved metabolic functions of the cardiac mitochondria. Support or Funding Information Oklahoma Agriculture Experiment Station and College of Human Sciences, Oklahoma State University

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