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The prevalence of obesity and its comorbidities has sparked a worldwide concern to address rates of adipose tissue accrual. Recent studies have demonstrated a novel role of Zyflamend, a blend of natural herbal extracts, in regulating lipid metabolism in several cancer cell lines through the activation of the AMPK signalling pathway. Yet, the role of Zyflamend in adipogenic differentiation and lipid metabolism remains largely unexplored. The objective of this study is to investigate the effects of Zyflamend on white 3T3-MBX pre-adipocyte differentiation and elucidate the molecular mechanisms. We demonstrate that Zyflamend treatment altered cell cycle progression, attenuated proliferation, and increased cell death of 3T3-MBX pre-adipocytes. In addition, treatment with Zyflamend inhibited lipid accumulation during the differentiation of 3T3-MBX cells, consistent with decreased expression of lipogenic genes and increased lipolysis. Mechanistically, Zyflamend-induced alterations in adipogenesis were mediated, at least in part, through the activation of AMPK, PKA, and JNK. Inhibition of AMPK partially reversed Zyflamend-induced inhibition of differentiation, whereas the inhibition of either JNK or PKA fully restored adipocyte differentiation and decreased lipolysis. Taken together, the present study demonstrates that Zyflamend, as a novel anti-adipogenic bioactive mix, inhibits adipocyte differentiation through the activation of the PKA and JNK pathways.

BackgroundPancreatic cancer is the fourth leading cause of death in the United States with over 53,670 new cases and 80% mortality in 2017. The 5‐year relative survival rate for patients with pancreatic cancer is 8.2%. Currently available therapies have only moderate efficacy, but notable limitations. Hence, there is an urgent need for alternative therapeutic approaches. Zyflamend, touted as a natural herbal extract to treat inflammation, is credited as being able to benefit many other conditions such as cancer including oral, mammary, bone, skin, colorectal, and prostate cancer. However, its effects on pancreatic cancer in particular, remain largely unexplored.ObjectiveThe objective of this study is to investigate the effects of Zyflamend on pancreatic cancer survival and decipher the underlying molecular mechanismsMethodsPancreatic cancer cells were treated with Zyflamend and key signaling pathways involved in the survival and proliferation of cells were investigated.ResultsZyflamend treatment caused a dose‐dependent decrease in cell proliferation, consistent with an increase in apoptotic cell death. The effects of Zyflamend were mediated, at least partially, through alterations in autophagy and endoplasmic reticulum stress.ConclusionThese studies identify Zyflamend as a potential novel approach to treat pancreatic cancer.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.