Metabolic dysregulation is a common hallmark across a range of complex diseases such as cancer and diabetes. Interestingly, adipocyte metabolism is characterised by aerobic glycolysis and lipogenesis, features that are shared by cancer cells. A cell’s metabolic phenotype is rapidly regulated post-transcriptionally by metabolite levels, triggering energy storage as a substrate accumulates using allosteric regulation. This is complemented by post-translational modification of proteins via hormonal regulation. For example, classically, insulin stimulates glucose metabolism primarily by promoting glucose uptake, but our phosphoproteomics screen showed insulin signalling phosphorylates hundreds of metabolic proteins in adipocytes. We explored the implications of this by measuring acute metabolomic changes to insulin, taking a dynamic approach to traditional 13C-tracer steady-state experiments. Insulin rapidly stimulated glucose uptake (t1/2=4 min) and incorporation of 13C-glucose into central carbon metabolites. Interestingly, the flow of glucose was highly selective, favouring the pentose phosphate pathway and bifurication of the TCA cycle by pyruvate anaplerosis. This implies coordinated regulation by insulin signalling, driving glucose to quickly establish NADPH sources to support lipogenesis beyond its role as merely a carbon source. Overlaying metabolomic and phosphoproteomic data in a 'transomic analysis' revealed a majority of phosphorylation occurs very acutely (<5 min). Indeed, this activated anabolism (lipid/glycogen synthesis) before substrates accumulated, creating a demand-driven system to ‘drag’ glucose down specific pathways. This complements the supply-driven regulation of anabolism by substrate accumulation, revealing a novel role for how kinase signalling coordinates metabolism. This has implications for metabolic dysregulation in situations of overactive signalling (cancer) or nutrient oversupply (diabetes).