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Table 4 Lab – garbage acronym

From: Is type 2 diabetes mellitus a vascular disease (atheroscleropathy) with hyperglycemia a late manifestation? The role of NOS, NO, and redox stress.

Factors related to eNOS dysfunction with decreased NO. factors known to uncouple the eNOS enzyme.
L – Lipids LDL – Cholesterol elevated both native and oxidized. Elevated Triglycerides of metabolic syndrome. Decreases or impairs dimethylarginine dimethylaminohydrolase (DDAH). Decline in DDAH activity. Increase in ADMA activity.
A – Arginine (L-arginine) decreased or impaired: By competitive interaction with ADMA (asymmetric dimethylarginine) an endogenous nitric oxide synthase inhibitor. Elevated in proatherogenic conditions. ACE, Ang II, endothelin, hypertension, insulin resistance, prediabetes, T2DM, and hyperhomocysteinemia.
B – BH4 Decreased or impaired Folic acid regeneration of the cofactor BH4 i.e. BH2 → BH4 with 5 methyl tetrahydrofolate (5-MTHF) active form of folic acid.
G – Glucose elevation. T2DM. DDAH effect increasing ADMA similar to lipids and elevated homocysteine.
A – Arginine (L-arginine) decreased or impaired: By nitrosylation (nitroarginine). By ONOO' peroxynitrite similar to nitrosylation of tyrosine (nitrotyrosine).
R – ROS reactive oxygen species. Specifically O2' and ONOO' Decline in DDAH activity results in increased ADMA.
B – BH4 decreased or impaired. BH4 oxidized to BH2. Loss of a naturally occurring antioxidant with diminished ROS scavenging capability.
A – ADMA Homocysteine impairs DDAH enzyme and increases ADMA.
G – Glucose elevated – glycated eNOS.
E – Endothelial NOS enzyme decreased and or dysfunctional. Gene polymorphism Glu298 → Asp, additional unidentified gene polymorphisms, CRP causing marked down regulation of eNOS mRNA and protein expression, eNOS enzyme glycation. Last but most importantly . . . ......