Table 1.

The multiple metabolic toxicities of the A-flight-u Acronym

Multiple injurious stimuli responsible for the production of ROS.
A	Angiotensin II (also induces protein kinase C – β isoform) Amylin (hyperamylinemia) islet amyloid polypeptide toxicity AGEs/AFEs (advanced glycosylation/fructosylation endproducts) Apolipoprotein B Antioxidant reserve compromised Absence of antioxidant network Aging ADMA (Asymmetrical DiMethyl Arginine) Adipose toxicity: Obesity toxicity – Lipid Triad (decreased HDL-C, increased triglycerides and small dense LDL-C) Adipocytokine toxicity: Increased TNF alpha, Il-6, TGF beta, PAI-I and the increased hormones resistin, leptin and decreased adiponectin.
F	Free fatty acid toxicity: Obesity toxicity – Lipid Triad
L	Lipotoxicity – Hyperlipidemia – Obesity toxicity – Lipid Triad Leptin toxicity
I	Insulin toxicity (endogenous hyperinsulinemia-hyperproinsulinemia) IGF-1 – (GH-IGF-I axis) toxicity: This may serve to increase bone metabolism within the media of the AVW Inflammation toxicity
G	Glucotoxicity (compounds peripheral insulin resistance) and induces reductive stress through the sorbitol/polyol pathway Pseudohypoxia (increased NADH/NAD ratio)
H	Hypertension toxicity Homocysteine toxicity hs-CRP
T	Triglyceride toxicity: Obesity toxicity – Lipid Triad
U	Uric Acid – Xanthine Oxidase toxicity: Uric acid is an antioxidant early in physiological range of atherogenesis and a conditional prooxidant late when elevated through xanthine oxidase enzyme and generation of ROS: thus generating the paradoxical (antioxidant → prooxidant): URATE REDOX SHUTTLE Endothelial cell dysfunction with eNOS uncoupling, decreased eNO and increased ROS