D-Arabitol

D-Arabitol is an orally active D-enantiomer of arabitol. D-Arabitol modulates the composition of gut microbiota, increases short-chain fatty acids, and promotes AMPK-PGC-1α-related browning of white adipose tissue. D-Arabitol improves weight gain, fat accumulation, insulin resistance, lipid deposition and inflammatory responses. D-Arabitol serves as the sole carbon/energy source for Bacillus methanolicus MGA3, a strain that can co-utilize it with mannitol. D-Arabitol is applicable to obesity-related research^[1][2]. In Vitro:D-arabitol (10-60 mM; duration of growth phase) supports growth of Bacillus methanolicus MGA3 as a sole carbon source with a growth rate of 0.20 h⁻¹ at 15 mM, and is co-consumed with mannitol in equimolar mixtures^[2].
D-arabitol (15 mM; growth to mid-exponential phase, OD₆₀₀ = 1.0) induces significant upregulation of the atlABCD gene cluster in Bacillus methanolicus MGA3, with atlD transcript levels also elevated in co-consumption conditions with mannitol^[2].
D-arabitol (30 mM; duration of growth phase) allows heterologous expression of B. methanolicus MGA3 atlD alone, or the full atlABCD gene cluster, to restore growth of arabitol-negative Corynebacterium glutamicum ΔmtlD^[2].
D-arabitol (15 mM; growth to mid-exponential phase, OD₆₀₀ = 1.0) induces elevated arabitol phosphate dehydrogenase activity (0.05 U/mg) in crude cell extracts of Bacillus methanolicus MGA3, with high affinity for xylulose 5-phosphate (K_m = 0.03 mM)^[2]. In Vivo:D-Arabitol (4-8%; dietary supplement; daily administration; 10 weeks) dose-dependently improves high-fat diet (HFD)-induced obesity, insulin resistance, lipid deposition and inflammation in male SD rats. Its mechanism of action involves regulating the gut microbiota, increasing SCFA production, and promoting white adipose tissue (WAT) browning via the AMPK-PGC-1α pathway^[1].