Protozoan parasitic diseases such as leishmaniasis, toxoplasmosis, and sleeping sickness are one of the major causes of death worldwide. The emerging resistance of parasitic species and adaptive mechanisms of infection are a major concern in developing medical treatment. Understanding the genotype/phenotype of parasites during infection can help in developing effective anti-parasitic therapies. In recent years, systems biology approaches, in particular, genome-scale metabolic modelling has been proposed to attain such understanding. This methodology allows incorporating omics data (e.g. transcriptomics, proteomics and metabolomics) to understand stage-specific metabolism of many organisms including protozoan parasites such as Leishmania, Toxoplasma, and Plasmodium. Metabolic behaviour during infection can be characterized, including the metabolic involvement of small or complex carbohydrates that has been poorly studied, so far, at the systems level. This thesis aims to present a comprehensive understanding of protozoan parasites metabolism and specifically the influence of glycans and glycoconjugates during infection. First, a review on different data types and methodologies used to study glycans and glycoconjugates from their structures to functions in protozoan parasites is presented. Glycobiology databases, in particular, glycomic and glycoproteomic data resources, were extensively reviewed, addressing problems in accessing and integrating data due to inconsistencies in the identification and representation of glycans, as well as the poor inter-linkage between databases. The focus is provided on graphic and text-based glycan structural notations, exploiting available tools to interconvert these encoding formats, in order to improve inter-linkage and interoperability among various glycomic databases. Next, metabolic modelling of parasitic cells using omics data (e.g. transcriptomics, proteomics, and glycomics) is used to understand the metabolism and the role of carbohydrates at the systems level. To explore the metabolism of human protozoan parasites, a constraint-based metabolic model of L. major, iAC560, was used as a case-study and extended to include pathways for the metabolism of lipids and larger fatty acids, and biosynthesis of carbohydrates. Flux Balance Analyses (FBA) was used to simulate the metabolism of Leishmania at promastigote (glucoserich environment) and amastigote (amino acid, amino sugar, and lipid-rich environment) conditions. Also, the model helped to assess active and inactive metabolic pathways to synthesize sugar nucleotides, which are essential precursors in the biosynthesis of glycans and glycoconjugates in promastigote and amastigote stages. Furthermore, in order to improve metabolic predictions, Gene Inactivity Moderated by Metabolism and Expression (GIMME) algorithm was used with flux-based simulations to improve the consistency between predicted fluxes and gene expression data of L. major in promastigote stage. The implementation of GIMME improved flux distribution across various pathways and helped to understand metabolism of Leishmania promastigote stage. Gene deletion analysis using the ext-iAC560 model allowed to predict 53 potential drug target genes in L. major. Many of these genes had been already characterized as essential in other protozoan species, while 10 genes (e.g. LmjF35.5330, LmjF36.2540, LmjF32.1960, LmjF33.0680, LmjF28.1280, LmjF21.1430, LmjF09.1040, LmjF06.1070, and LmjF06.0350 in promastigote stage and amastigote stage, and LmjF36.6950 in only amastigote stage) are predicted as novel drug targets. More than 70% of predicted essential genes showed lethal phenotype by preventing biosynthesis of more than two cellular building blocks. Predicted novel essential genes are associated with lipid and fatty acid biosynthesis, but essentiality in human protozoan parasites or closely related species has not been tested. Searches in literature and chemical databases (e.g. DrugBank and TDR Target) found that around 80% of the predicted essential genes have enzyme-based inhibitors in parasitic and non-parasitic species. Most of these enzyme-based inhibitors were not tested in Leishmania species; however, molecules such as Carbamide phenylacetate, CDV, Terbinafine, and 4-(dimethylaminomethyl)-2,6-di(propan-2- yl)ph enol, which are tested against essential genes in other protozoan species are of major interest, as these are more likely to have similar responses in Leishmania.