Meglumine

Meglumine was identified as a bioactive compound capable of inducing the AMPK‑related enzyme SNARK (NUAK2) in murine C2C12 myoblasts in a dose‑dependent manner. This stimulation was more potent and longer‑lasting than that produced by sorbitol. The increase in SNARK expression was associated with enhanced phosphorylation of MYPT1 at Ser507, a known SNARK substrate that regulates myosin light chain kinase and reinforces actin stress fiber formation and muscle contraction. In normal SV129 mice, oral administration of meglumine for six weeks significantly increased muscle stamina as measured by inverted grid grasping test and limited weight gain over longer treatment periods, without causing gastrointestinal distress or diarrhea. In the KK.Cg-Ay/J mouse model of type II diabetes, chronic oral meglumine treatment significantly improved glycemic control, lowered fasting blood glucose levels, reduced plasma and liver triglycerides, and ameliorated diabetic nephropathy.

Fig. 1 Meglumine increases SNARK levels in myoblasts. (Bravo-Nuevo A.; et al. 2014)

Meglumine was investigated to modulate the internal microstructure of soybean oil‑based oil-in-water microemulsions for enhancing the solubility and release rate of BCS Class II hydrophobic drugs (sulfamerazine and indomethacin). Pseudoternary phase diagrams revealed that the presence of meglumine favored higher proportions of oil phase and improved drug incorporation. Conductivity studies, particle size analysis, and zeta potential measurements confirmed that the microemulsion structure remained intact with reduced droplet sizes after meglumine incorporation. The highest drug incorporations reached 35.6 mg/mL for sulfamerazine and 73.1 mg/mL for indomethacin.

Fig. 2 Pseudoternary phase diagram of ME containing (a) water; (b) 1.8% ßCD; (c) 12% MßCD; (d) 2.5% HPßCD; and (e) 5% MEG, in the aqueous phase. (Aloisio C.; et al. 2016)