Obesity is a major risk factor for many pathologies including type 2 diabetes and cardiovascular disease and is characterised by an excessive accumulation of white adipose tissue (WAT) which stores excess energy as triglyceride. Conversely, brown adipose tissue plays a role in increasing energy expenditure through uncoupling protein 1 (UCP1). Several compounds have been shown to induce brown-like adipocytes within WAT in a process known as browning. The stimulation of browning in human adipose tissue is a potential novel therapeutic for obesity and diabetes. High throughput phenotypic screening using human adipocytes is an effective method to assess the effects of multiple compounds that can induce browning. However, many pathways in addition to UCP1 can improve adipocyte health, such as insulin signalling, inflammation and adipokine release for systemic benefits on metabolic health. Assessing gene expression changes across multiple pathways provides a comprehensive assessment of adipocyte browning and function. Here, we used a high throughput Openarray qPCR with a panel of 52 genes involved in diverse gene expression pathways including adipocyte browning, mitochondrial function, fatty acid metabolism and adipogenesis on human white adipocytes. We successfully used this high throughput platform to profile adipocytes treated with a diverse selection of 25 literature supported browning agents including small-molecule drugs, metabolites and peptides, some of which have not previously been investigated in human adipocytes. We show differential gene expression signatures and clustering across browning agents with effects on multiple pathways with a subset of compounds. For example, forskolin increased genes involved in mitochondrial pathways including UCP1 (33 fold, p<0.05), CKMT2 (6 fold, p<0.05), CKMT1b (7.7 fold, p<0.05) as well as adipokine genes such as adiponectin (3.7 fold, p<0.05) and leptin (3.6 fold, p<0.05). Peroxisome proliferator activated receptor gamma coactivator 1 alpha (PGC1α) gene expression was unaltered by forskolin treatment. In contrast, lactate did not significantly increase UCP1 (p>0.05) but increased the mitochondrial genes PGC1α (2.8-fold, p<0.05) and CKMT2 (3.3 fold, p<0.05) as well as the adipokine adiponectin (3.3 fold, p<0.05). Differences between individual browning agents may allow combination approaches providing additive or synergistic effects between compounds to further enhance adipocyte health and energy expenditure. The functional effect of gene expression changes in response to diverse browning agents were confirmed by cellular respiration and metabolic flux analysis.