Most recent data strongly implicate moderate metabolic endotoxemia, enhanced by fatty foods, in obesity often culminating in insulin resistance and diabetes. The effects of endotoxemia, mediated by lipopolysaccharide (LPS), involve Toll-like receptor 4 that is also activated by fatty acids. Receptor interaction is followed by stimulation of NF B signaling and expression of inflammatory cytokine genes such as TNF- and IL-6. Another consequence of LPS action is stimulation of adipose lipolysis resulting in increased levels of free fatty acids and insulin resistance. Moderate endotoxemia is considered to yield low-grade inflammation with different consequences compared to high-grade inflammation caused by massive infection leading to sepsis and weight loss. ZL's drug inactivates LPS and reduces low-grade inflammation which is one of the mechanisms accounting for the anti-obesity and some of the anti-diabetic effects of PLAP.
It is generally accepted that in addition to infection or over-activity of endogenous Gram negative bacteria, other types of stress can also lead to obesity and then insulin resistance. ZL's protein generally protects cells against stress-induced death (by up-regulating survival mechanisms) which is likely to contribute to its anti-inflammatory/anti-obesity effects.
It is generally accepted that in addition to infection or over-activity of endogenous Gram negative bacteria, other types of stress can also lead to obesity and then insulin resistance. ZL's protein generally protects cells against stress-induced death (by up-regulating survival mechanisms) which is likely to contribute to its anti-inflammatory/anti-obesity effects.