Wheat germ supplementation alleviates insulin resistance and cardiac mitochondrial dysfunction in an animal model of diet-induced obesity

Br J Nutr. 2017 Aug;118(4):241-249. doi: 10.1017/S0007114517002082.

Abstract

Obesity is strongly associated with insulin resistance (IR), along with mitochondrial dysfunction to metabolically active tissues and increased production of reactive O2 species (ROS). Foods rich in antioxidants such as wheat germ (WG), protect tissues from damage due to ROS and modulate some negative effects of obesity. This study examined the effects of WG supplementation on markers of IR, 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-high-sucrose (HFS) diet. Male C57BL/6 mice, 6-week-old, were randomised into four dietary treatment groups (n 12 mice/group): control (C, 10 % fat kcal), C+10 % WG, HFS (60 % fat kcal) or HFS+10 % WG (HFS+WG). After 12 weeks of treatment, HFS+WG mice had significantly less visceral fat (-16 %, P=0·006) compared with the HFS group. WG significantly reduced serum insulin (P=0·009), the insulinotropic hormone, gastric inhibitory peptide (P=0·0003), and the surrogate measure of IR, homoeostatic model assessment of IR (P=0·006). HFS diet significantly elevated (45 %, P=0·02) cardiac complex 2 mitochondrial VO2, suggesting increased metabolic stress, whereas WG stabilised this effect to the level of control. Consequently, genes which mediate antioxidant defense and mitochondrial biogenesis (superoxide dismutase 2 (Sod2) and PPARγ coactivator 1-α (Pgc1a), respectively) were significantly reduced (P<0·05) in the heart of the HFS group, whereas WG supplementation tended to up-regulate both genes. WG significantly increased hepatic gene expression of Sod2 (P=0·048) but not Pgc1a. Together, these results showed that WG supplementation in HFS diet, reduced IR and improved cardiac mitochondrial metabolic functions.

Keywords: C control; GIP gastric inhibitory peptide; HFS high fat–high sucrose; HFS+WG HFS+10 % WG; IR insulin resistance; OCR VO2 rates; Pgc1α PPARγ coactivator 1-α; ROS reactive O2 species; Sod2 superoxide dismutase 2; WG wheat germ; Heart; High-fat diet; Insulin resistance; Mitochondria; Obesity; Wheat; Wheat germ.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use
  • Diet, High-Fat
  • Dietary Supplements*
  • Disease Models, Animal
  • Gastric Inhibitory Polypeptide / blood
  • Gene Expression / drug effects
  • Heart / drug effects*
  • Insulin / blood
  • Insulin Resistance*
  • Intra-Abdominal Fat / metabolism
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Mice, Inbred C57BL
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Myocardium / metabolism
  • Obesity / complications*
  • Obesity / drug therapy
  • Obesity / etiology
  • Obesity / metabolism
  • Oxidative Stress / drug effects
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / genetics
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / metabolism
  • Plant Preparations / pharmacology
  • Plant Preparations / therapeutic use
  • Reactive Oxygen Species
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Triticum*

Substances

  • Antioxidants
  • Insulin
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Plant Preparations
  • Ppargc1a protein, mouse
  • Reactive Oxygen Species
  • Gastric Inhibitory Polypeptide
  • Superoxide Dismutase
  • superoxide dismutase 2