The rationale for PHB enhancement by the presence of acetate or glucose was described as these compounds can be metabolized to PHB substrate as acetyl-CoA. Glucose will be degraded to acetyl-CoA, and acetate will be chemically transformed into acetyl-CoA under presence of free CoA; as a result, acetyl-CoA can be transformed into PHB or fatty acids (Poirier 2002; Abed et al. 2009). However, supplying excess carbon can cause accumulation of PHB or by-product (i.e. fatty acid, glycogen). Thus, further investigation on the metabolic flux of reserved carbons and enzymatic activities involved might address metabolic network regulation of PHB synthesis and other related carbon molecules.