Scope
Effective health‐promoting results of either anthocyanins or whole wheat against chronic diseases are well reported. The current study is designed to understand the effect and underlying mechanism of anthocyanins‐biofortified whole wheat on high‐fat diet (HF)‐induced obesity and its comorbidities.
Method and Results
Mice are fed a HFD supplemented with isoenergetic white, purple, or black whole wheat for 12 weeks and analyzed by physiological, biochemical, and nutrigenomics studies (qRT‐PCR and RNA‐Seq analysis). Black wheat significantly reduces body weight gain and fat pad. Both black and purple wheats reduce total cholesterol, triglyceride, and free fatty acid levels in serum, with the restoration of blood glucose and insulin resistance. Black wheat significantly elevates the expression of enzymes related to fatty acid balancing, β‐oxidation, and oxidative stress that supported the biochemical and physiological positive outcomes. Moreover, the transcriptome analysis of adipose and liver tissue reveals activation of multiple pathways and genes related to fatty acid‐β oxidation (crat, acca2, lonp2 etc.), antioxidative enzymes (gpx1, sod1, nxnl1 etc.), along with balancing of fatty acid metabolism specifically in black wheat supplemented mice.
Conclusion
Taken together, the results suggest that the incorporation of colored wheat (especially black wheat) in the diet can prevent obesity and related metabolic complications.
Glucagon mediated mechanisms have been shown to play clinically significant role in energy expenditure. The present study was designed to understand whether pharmacological mimicking of cold using menthol (TRPM8 modulator) can induce glucagon-mediated energy expenditure to prevent weight gain and related complications. Acute oral and topical administration of TRPM8 agonists (menthol and icilin) increased serum glucagon concentration which was prevented by pre-treatment with AMTB, a TRPM8 blocker. Chronic administration of menthol (50 and 100 mg/kg/day for 12 weeks) to HFD fed animals prevented weight gain, insulin resistance, adipose tissue hypertrophy and triacylglycerol deposition in liver. These effects were not restricted to oral administration, but also observed upon the topical application of menthol (10% w/v). The metabolic alterations caused by menthol in liver and adipose tissue mirrored the known effects of glucagon, such as increased glycogenolysis and gluconeogenesis in the liver, and enhanced thermogenic activity of white and brown adipose tissue. Correlation analysis suggests a strong correlation between glucagon dependent changes and energy expenditure markers. Interestingly, in-vitro treatment of the serum of menthol treated mice increased energy expenditure markers in mature 3T3L1 adipocytes, which was prevented in the presence of non-competitive glucagon receptor antagonist, L-168,049, indicating that menthol-induced increase in serum glucagon is responsible for increase in energy expenditure phenotype. In conclusion, the present work provides evidence that glucagon plays an important role in the preventive effect of menthol against HFD-induced weight gain and related complications.
Taxifolin (98%) and catechin (86.6%) are the major polyphenols in KM-PRE and FM-PRE. FM-PRE and KM-PRE prevent obesity, hepatic steatosis, and gut bacterial dysbiosis however, the effects of KM-PRE are more profound compared to FM-PRE.
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