Efficacy of Physiologic Insulin Resensitization as a Treatment for Insulin Resistance Pathophysiology | Chapter 1 | Recent Updates in Disease and Health Research Vol. 6

 

Diabetes was the eighth leading cause of death in the United States in 2021 based on the 103,294 death certificates in which diabetes was listed as the underlying cause of death. The prevalence of Type 2 diabetes mellitus (T2DM) has increased from 2.5% of the US population in 1990 and rose to 11.6% of the total US population, or 38.4 million people, in 2021. This chapter has three purposes such as exploring insulin resistance pathophysiology, addressing the role of the insulin receptor (InsR) in the regulation of glucose homeostasis; and reviewing literature for clinical outcomes and molecular mechanisms that support the use of Physiologic Insulin Resensitization (PIR) as an effective treatment to address IR, of which diabetes and its complications are the most common diagnoses. Insulin resistance is the primary cause of type 2 diabetes. Insulin resistance leads to increasing insulin secretion, leading to beta-cell exhaustion or burnout. This triggers a cascade leading to islet cell destruction and the long-term complications of type 2 diabetes. Concurrent with insulin resistance, the regular bursts of insulin from the pancreas become irregular. This has been treated by the precise administration of insulin more physiologically. There is consistent evidence that this treatment modality can reverse the diabetes-associated complications of neuropathy, diabetic ulcers, nephropathy, and retinopathy and that it lowers HbA1c. Using physiologic insulin resensitization is a logical clinical solution to restore physiologic insulin function. The study also suggests that the complications, hospitalizations, medication costs, and emergency room visits may be reduced using physiologic insulin resensitization.

 

 

Author(s) Details:-

 

Frank Greenway
Clinical Trials Unit, Pennington Biomedical Research Center, Baton Rouge, Louisiana, USA.

 

Brian Loveridge
Wellcell Global, Houston Texas, USA.

 

Richard Marchase
Wellcell Global, Houston Texas, USA.

 

Zach Villaverde
Wellcell Global, Houston Texas, USA.

 

Carol Wilson
Wellcell Global, Houston Texas, USA.

 

Michael Alexander
Department of Surgery, University of California Irvine, Irvine, California, USA.

 

Scott A. Hepford
Wellcell Global, Houston Texas, USA.

 

Jonathan R. T. Lakey
Department of Surgery, University of California Irvine, Irvine, California, USA and Department of Biomedical Engineering, University of California Irvine, Irvine, California, USA.

 

Please see the link here:  https://doi.org/10.9734/bpi/rudhr/v6/3199G