Insulin is the main metabolic regulator of fuel molecules in the diet, such as carbohydrates, lipids, and proteins. It does so by facilitating glucose influx from the circulation into the liver, adipose tissue, and skeletal myocytes. The outcome of which is subjected to glycogenesis in skeletal muscle and lipogenesis in adipose tissue, as well as in the liver. Therefore, insulin has an anabolic action while, on the contrary, hypoinsulinemia promotes the reverse process. Protein breakdown in myocytes is also encountered during the late stages of diabetes mellitus. The balance of the blood glucose level in physiological conditions is maintained by virtue of the interactive functions of insulin and glucagon. In insulin resistance (IR), the balance is disturbed because glucose transporters (GLUTs) of cell membranes fail to respond to this peptide hormone, meaning that glucose molecules cannot be internalized into the cells, the consequence of which is hyperglycemia. To develop the full state of diabetes mellitus, IR should be associated with the impairment of insulin release from beta-cells of the pancreas. Periodic screening of individuals of high risk, such as those with obesity, hypercholesterolemia, and pregnant nulliparous women in antenatal control, is vital, as these are important checkpoints to detect cases of insulin resistance. This is pivotal as IR can be reversed, provided it is detected in its early stages, through healthy dietary habits, regular exercise, and the use of hypoglycemic agents. In this review, we discuss the pathophysiology, etiology, diagnosis, preventive methods, and management of IR in brief.

Radical drug therapy for schizophrenia is usually hard to achieve with one currently available antipsychotic agent. Indeed, it is the negative symptoms of this morbidity that are a dilemma to neutralize. Most of the first-generation agents can deal with the positive symptoms of the disease to a convincing degree, but not with its negative symptoms. The creation of so-called second-generation agents aimed to treat the negative symptoms, as these invisible barriers are the real reasons that isolate psychotic individuals and hinder their integration into society. Unfortunately, these newly designed drugs, including OLZ, turned out to induce different categories of undesired effects; the most embarrassing among them are the metabolic drawbacks, such as insulin resistance, weight gain, and other subcategories of metabolic consequences. Antagonism induced at certain receptors, particularly 5-HT2C and histamine H1 receptors, is implicated particularly in these metabolic adverse effects. The choice of antipsychotics (APCs) should be tailored separately for each case, as each patient responds variably to each neuroleptic. This possibility exists due to the abundant alternatives within the currently available APC medications. This work aims to discuss the reasons behind these undesired metabolic effects, how to deal with them, how to choose the appropriate agent for each psychotic case, and how to manage intoxication using olanzapine. To address these inquiries, we carefully selected 154 relevant studies, including robust meta-analyses, from the past 20 years and analyzed them in this work.

The incidence of insulin resistance and its complications is rising across societies worldwide, making its treatment a significant economic challenge. The disease is multifactorial, and its pathophysiology varies accordingly. Genetic factors, aging, and coexisting diseases are major contributors to its development. Among the coexisting conditions are autoimmune diseases and other conditions requiring treatment with therapeutic agents, some of which can induce insulin resistance. Research indicates that the free radical theory plays a significant role in initiating this complex cycle and in shaping the full clinical picture of diabetes syndrome. In this work, we discuss the pathophysiology of insulin resistance, the role of free radicals in its etiology, and drug treatments for diseases that may contribute to insulin resistance. We also explore the antioxidant effects of vitamin D and oral hypoglycemic agents, as well as their notable adverse effects, including cobalamin (vitamin B12) deficiency. A total of 147 scientific studies, including comprehensive meta-analyses, have been selected to address these questions and have been analyzed and discussed objectively to minimize scientific bias and confusion. This narrative work will help doctors and primary health caregivers envision the dimensions of diabetes syndrome from multiple perspectives and update their knowledge about the significance of vitamin D as an effective tool to combat insulin resistance.

Radical drug therapy for schizophrenia is usually hard to achieve with one currently available antipsychotic agent. Indeed, it is the negative symptoms of this morbidity that are a dilemma to neutralize. Most of the first-generation agents can deal with the positive symptoms of the disease to a convincing degree, but not with its negative symptoms. The creation of so-called second-generation agents aimed to treat the negative symptoms, as these invisible barriers are the real reasons that isolate psychotic individuals and hinder their integration into society. Unfortunately, these newly designed drugs turned out to induce different categories of undesired effects; the most embarrassing of which is the metabolic drawbacks, such as insulin resistance, weight gain, and other subcategories of metabolic consequences. In this work, we discuss the reasons behind these undesired metabolic effects, how to deal with these, and how to choose the proper agent for each psychotic case separately. The choice of antipsychotics should be tailored separately for each case, as each patient responds variably to each neuroleptic.