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Type 2 diabetes affected 10.5% of the US population in 2018 compared to 2.5% in 1990 (Greenway et al., 2022). Due to an increase in long-term diabetic consequences such as neuropathy, retinopathy, nephropathy, skin ulcers, amputations, and atherosclerotic cardiovascular disease, this poses a severe threat to public health. We examined the scientific evidence for physiologic insulin resensitization in this review. Type 2 diabetes is mainly brought on by insulin resistance (Greenway et al., 2022). Beta-cell burnout or exhaustion results from increased insulin secretion caused by insulin resistance. This starts a chain of events that eventually destroys islet cells and causes type 2 diabetes with long-term consequences. The regular blasts of insulin from the pancreas become erratic along with insulin resistance. The precise delivery of insulin has been used to treat this better effectively. Consistent evidence supports the ability of this therapy to reduce HbA1c and reverse the neuropathy, diabetic ulcers, nephropathy, and retinopathy consequences of diabetes. In summary, physiologic insulin resensitization has a robust scientific foundation, promising therapeutic promise, and potential financial advantages.
One of the most critical medical issues of the twenty-first century is type 2 diabetes mellitus (T2D). In industrialized countries, over-intake of relatively cheap, calorie-dense, insufficiently satiating, and highly delicious food has resulted in extraordinary rises in obesity. Diabetes and prediabetes are more common than 50% of the population in the US (Najjar & Perdomo, 2019). Obesity is a significant risk factor for T2D, and rates of T2D prevalence have paralleled those of obesity, even though only a small percentage of obese persons get the disease. Fasting hyperglycemia, which characterizes type 2 diabetes, is primarily a result of insulins ineffective glucose-lowering activity (Loveridge et al., 2021). Therefore, it is crucial to comprehend how insulin works if we are to continue developing potential therapeutic approaches to treat T2D.
Although numerous somatic cell types express insulin receptors, the direct actions of insulin on skeletal muscle, the liver, and white adipocytes represent insulins role in glucose homeostasis. Since these tissues play different roles in maintaining metabolic homeostasis, tissue-specific insulin signal transduction pathways are required. For instance, insulin increases glucose transport and net glycogen synthesis in skeletal muscle, promoting glucose storage and use. Insulin enhances lipogenic gene expression, lowers gluconeogenic gene expression, and accelerates glycogen production in the liver. Insulin reduces lipolysis in white adipocyte tissue (WAT) while boosting glucose transport and lipogenesis. Despite these various impacts, all insulin-responsive cells share striking similarities in the proximal elements involved in insulin signal transduction (Petersen & Shulman, 2018). Different distal effectors are responsible for multiple physiological responses to insulin in various cell types. Insulin has significant indirect effects on target tissues in addition to these direct actions. Since these indirect effects of insulin are integrated and context-specific, they are more challenging to simulate in cultured cells and, as a result, need to be understood more than insulins direct, cell-autonomous actions.
The effect of insulin on WAT lipolysis to lower hepatic acetyl-CoA level and, consequently, allosterically lower pyruvate carboxylase activity illustrates indirect insulin action. This mechanism permits insulin to inhibit WAT lipolysis, which in turn inhibits hepatic gluconeogenesis along with the inhibition of glycerol turnover. Other significant mechanisms of indirect insulin action include insulin action in the central nervous system (CNS), which inhibits glucagon secretion through paracrine signaling in the pancreatic islet. An individual is deemed insulin resistant when more significant circulating insulin levels are required to provide the integrated glucose-lowering response mentioned above. Prediabetes, lipodystrophy, polycystic ovarian syndrome, and nonalcoholic fatty liver disease are a few clinical conditions associated with higher fasting plasma insulin concentrations. One of the primary mechanisms for the emergence of overt T2D is this increased workload on the endocrine pancreas and the ensuing cell decompensation (Well Cell Global, 2022). However, prospective human studies that found insulin resistance to be the strongest predictor of a future T2D diagnosis have underlined the significance of insulin resistance in the pathophysiology of T2D. Insulin resistance affects how distinct insulin target tissues function because different cell types respond to insulin differently.
Normal secretion of insulin follows a physiological pattern controlled by a pancreatic neural network that links cells in the islets of Langerhans. Numerous insults that cause inflammation in this network can result in dysfunctional insulin rhythmicity. Beta cells produce insulin asynchronously when standard patterns of insulin production are thrown off. Constant receptor exposure causes a negative feedback loop that lowers the responsiveness of the insulin receptor (Street et al., 2022). The absence of physiological peaks and troughs also brings on refractory delays in receptor activity. Last, disturbed pulsation causes unopposed glucagon levels, which lower insulin receptor transcription. It makes sense to use physiologic insulin resensitization to regain normal insulin function. The efficacy of the case studies and clinical trials examined in this research need to be revised to support the claim that this bio-imitating physiologic insulin administration method is generally adequate. Random clinical trials are required. Additionally, they show that physiologic insulin resensitization can improve several undesirable symptoms of diabetes and so seems to deal with the underlying causes of IR. They also propose that physiologic insulin resensitization may reduce problems, hospitalizations, prescription expenses, and emergency department visits.
References
Greenway, F., Loveridge, B., Grimes, R. M., Tucker, T. R., Alexander, M., Hepford, S. A., Fontenot, J., Nobles-James, C., Wilson, C., Starr, A. M., Abdelsaid, M., Lewis, S. T., & T. Lakey, J. R. (2022). Physiologic Insulin Resensitization as a Treatment Modality for Insulin Resistance Pathophysiology. International Journal of Molecular Sciences, 23(3). Web.
Loveridge, B., Tucker, T., & Lewis, S. (2021). Dynamic Diabetes Solutions: Physiologic Insulin Resensitization. Int J Diabetes Metabolic Synd, 1(1), 15. Web.
Najjar, S. M., & Perdomo, G. (2019). Hepatic Insulin Clearance: Mechanism and Physiology. Physiology, 34(3), 198215. Web.
Petersen, M. C., & Shulman, G. I. (2018). Mechanisms of Insulin Action and Insulin Resistance. Physiological Reviews, 98(4), 21332223. Web.
Street, M. E., Moghetti, P., & Chiarelli, F. (2022). The Multiple Functions of Insulin Put into Perspective: From Growth to Metabolism, and from Well-Being to Disease. International Journal of Molecular Sciences, 24(1), 200. Web.
Well Cell Global. (2022). Well Cell Global Physiologic Insulin Resensitization. Well Cell Global | Scott Hepford. Web.
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