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Insulin & IGF1

Jul 17, 2011 | By Matthew Larson
Insulin & IGF1
Photo Credit Cameron Spencer/Digital Vision/Getty Images

Insulin and insulin-like growth factor are two common protein molecules in the body. Despite their close structural resemblance, the nature of the work performed by these two proteins is highly divergent in some cases. There are many examples, however, of similarities in the way these molecules function, almost reflecting the cellular evolution of the mechanisms of life.

Insulin in Physiology

The concentration of glucose in the bloodstream is a tightly regulated variable, with multiple organ systems interacting to precisely supply glucose to active tissues throughout the body. Insulin acts to decrease blood glucose levels by facilitating the uptake of glucose into tissues throughout the body. Think of insulin as the "key" that opens the cell's "lock" to allow entry of glucose. Insulin acts to increase glucose uptake in skeletal muscle and liver tissue for storage as glycogen complexes.

Role of Insulin in Diabetes

Type 1 and Type 2 diabetes are disorders related to the function of insulin; in Type 1, insulin is no longer produced and in Type 2, the body has become resistant to the effect of insulin. Glucose is a chemically active molecule capable of reacting with proteins in the circulation through a process known as glycosylation. Chronically elevated blood glucose levels can be assessed in diabetics by measuring the number of glycosylated hemoglobin molecules in the patient's red blood cells. Regardless of the root cause, both conditions increase the level of sugar in the bloodstream, leading to high rates of protein glycosylation throughout the circulation, which can cause long-term damage to highly vascular structures such as the capillaries supplying the kidney, retina and peripheral nerves.

Molecular Properties of IGF1

IGF1, produced by the liver in response to stimulation from growth hormones, travels systemically in the blood to induce cell growth in tissues throughout the body. The molecular structure of this hormone is similar to insulin, hence the name. This chemical plays an important role in growth during development and continues to demonstrate important effects into adulthood.

Role of IGF1 in Development

Growth factor molecules stimulate the rapid growth of cells and tissues. In doing so, these chemicals reduce the tissue's resistance to oxidative stress, an effect that shortens the life of the organism. According to a 2011 article from the journal "Best Practice and Research in Clinical Endocrinology and Metabolism," defects in IGF signaling pathways resulted in intrauterine and postnatal growth retardation, neural deafness, and intellectual deficit. The study also showed that other clinical features, including microcephaly, or small brain, and insulin resistance, were more common later in life.

IGF1 in the Cardiovascular System

According to a 2008 article from the journal "Clinical Endocrinology," there is an association between low serum IGF-1 levels and increased risk of myocardial infarction, ischemic heart disease, atherosclerosis and stroke. This correlation was observed in cases of growth hormone deficiencies, which disrupted the chemical pathways responsible for releasing IGF-1; this lead to the low serum levels seen in the patient. This study highlights the importance of normal IGF-1 levels as well as the hormonal pathways involved in its production.

Clinical Applications: Mecasermin

Also known as recombinant human insulin-like growth factor 1, mecasermin is used in the treatment of growth hormone insensitivity, a condition that results in dysfunctional growth. The drug has an "insulin-sensitizing effect" according to the 2009 article published in the journal "Advanced Therapy," which may benefit Type 1 and 2 diabetics.

Insulin and IGF1 in Alzheimer's Disease

Evidence reviewed by researchers at the Cajal Institute in Madrid Spain highlights the role of disturbed insulin and IGF-1 signaling between brain cells in developing Alzheimer's disease. The cause of this form of dementia is being explored; current theories hold that accumulation of beta amyloid protein causes deteriorating brain function in Alzheimer's patients. This 2004 article suggests that a reduction of insulin and IGF-1 sensitivity in brain cells leads to an increase in the enzymatic processes responsible for creating beta amyloid. This theory demonstrates an integral connection between these two compounds in a pathological state, emphasizing their combined importance for maintaining health.

References

Article reviewed by Libby Swope Wiersema Last updated on: Jul 17, 2011

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