Despite decades of research, the causes and biology of schizophrenia remain unknown. The condition is associated with metabolic symptoms such as hyperinsulinemia, dyslipidaemia, type 2 diabetes (T2DM), and obesity. These sensations are a prevalent side effect of the new antipsychotic medications. Nevertheless, metabolic dysfunction in schizophrenia has been studied before the antipsychotic phase, and it has also been documented in patients with first- onset schizophrenia prior to antipsychotic treatment. We investigate the evidence for metabolic abnormalities in schizophrenia patients, both in the central and peripheral nervous systems. Post-mortem brain tissue molecular analysis indicated alterations in glucose metabolism and insulin signalling pathways, whereas blood-based molecular profiling revealed hyperinsulinemia and abnormalities in insulin and co-released factor synthesis after the development of symptoms. Yet, such features are not seen in all patients with the disorder, and not all people with such defects have schizophrenia symptoms. One explanation of these facts is the presence of an underlying metabolic sensitivity in a subset of persons that interacts with environmental or hereditary factors to create the disorder's overt symptoms.