Physiologic Insulin Resensitization as a Treatment Modality for Insulin Resistance Pathophysiology

Abstract

Prevalence of type 2 diabetes increased from 2.5% of the US population in 1990 to 10.5% in 2018. This creates a major public health problem, due to increases in long-term complications of diabetes, including neuropathy, retinopathy, nephropathy, skin ulcers, amputations, and atherosclerotic cardiovascular disease. In this review, we evaluated the scientific basis that supports the use of physiologic insulin resensitization. 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. In conclusion, physiologic insulin resensitization has a persuasive scientific basis, significant treatment potential, and likely cost benefits.

Keywords: CKD; PIR; cardiovascular disease; chronic kidney disease; diabetes; insulin infusion; insulin resistance; metabolic disorder; nephropathy; neuropathy; obesity; physiologic insulin resensitization; retinopathy; treatment modality.

Figure 1

A three-minute moving average (continuous line) of the fasting plasma insulin, C-peptide and glucose concentrations taken at one-minute intervals. The dashed line shows the “unsmoothed” data. Smoothing reduces the rapid fluctuations, which are probably due to “noise,” and also blunts the amplitude. The simultaneous insulin and C-peptide cycles disappear after 50 min. Reproduced from [13].