Abstract
Background: More than 40 of US adults are obese, and the prevalence of obesity and its comorbidities continue to be a major concern worldwide. Zyflamend, a mix of select herbal extracts, has been shown to activate the intracellular energy sensor Adenosine Monophosphate-Activated Protein Kinase (AMPK). Increased AMPK activity in white adipose tissue has been reported to promote the expression of brown adipose tissue specific genes and the subsequent improvement in metabolic homeostasis and glycemic control. Methods: In the current study, we investigated the effects of Zyflamend supplementation on high fat diet-induced metabolic dysregulation in male C57Bl6/J mice. Results: We report that Zyflamend supplementation for 24 weeks significantly reduced high fat diet- i nduced body weight gain, improved insulin sensitivity, and reduced plasma levels of non-essential fatty acids. These changes were concomitant with increased AMPK phosphorylation, reduced ER stress and inflammation in skeletal muscle. Additionally, Zyflamend inhibited acetyl CoA-carboxylase (ACC) and promoted mitochondria biogenesis and the expression of brown fat markers in white adipose tissue suggesting that it may exhibit anti-obesity and/or pro-lipolytic properties. Conclusions: Together, these findings suggest that Zyflamend supplementation might help in developing novel anti-obesity therapeutic strategies and warrant additional investigation on the beneficial effects of Zyflamend on metabolic homeostasis and glycemic control.