Advanced Glycation End Products and the Kidney – Dr. Calvin Hirsch

Dr. Calvin Hirsch

June 10, 2022

Advanced Glycation End Products and the Kidney - Dr. Calvin Hirsch

According to Dr. Calvin Hirsch, if you’ve been reading up on the latest developments in diabetes research, you’ve probably heard about advanced glycation end products, or AGEs. But what is AGE and what role does it play in the complications associated with diabetes? This article aims to fill that void. Learn about the role of AGEs in diabetic complications and how AGEs are caused. You’ll also learn more about the FEEL receptor, an endocytic receptor.

AGEs – Dr. Calvin Hirsch

The role of RAGE in aging is unclear, but researchers have suggested that AGEs cause cellular damage by triggering the formation of extracellular matrix glycation. Moreover, RAGE can induce inflammation and oxidative stress in the body. Thus, inhibiting RAGE can improve the functions of the microglia, a type of immune cell, and help them clear plaques.

In addition to reducing dietary AGEs, eating more fruits and vegetables can also help reduce AGE levels. Many fruits and vegetables contain phenolic acids, which inhibit AGE formation. The phenolic acid present in pomegranates helps to protect the body from the negative effects of AGEs. However, consuming deep-fried eggs can damage your health, as they lose their nutritional value. Also, deep-fried eggs may be served with processed meat or cheese.

AGE receptors

Dr. Calvin Hirsch pointed out that, SR-AI scavenging receptors have been identified as critical for the regulation of AGEs in the body. AGEs are environmental xenobiotics found in tobacco smoke. Tobacco smoke induces high levels of free radicals in the body, which are difficult for the body to detoxify. These free radicals are capable of causing numerous damage to the cells and tissues of the body. AGEs have a direct effect on the kidney.

AGEs cause inflammation in the body, and interaction with AGE receptors leads to oxidative stress and inflammatory reactions. Furthermore, they cause the formation of blood clots in the arteries. Therefore, the combination of AGEs and AGE receptors has emerged as a new therapeutic target.

AGE-mediated glycation – Dr. Calvin Hirsch

Advanced glycation end products (AGEs) are nonenzymatic modifications of proteins and lipids. In addition to causing molecular rearrangements and producing reactive oxygen species, AGEs have several other harmful effects. Their biochemistry summarizes the mechanisms of glycation stress, the importance of AGE inhibitors, and the development of AGE therapies. This review discusses the glycation process and AGEs as a pathophysiologic risk factor for vascular disease.

AGEs accumulate in neurons and other neural tissues. This results in protein dysfunction and the aggregation of harmful protein oligomers. These oligomers may initiate neurodegenerative diseases. The AGEs also interact with RAGE and other cell surface receptors. Exogenous AGEs are often present in the environment, and these compounds interact with the RAGE in the body to cause aging and damage.

AGE-mediated glycation in diabetic complications

Dr. Calvin Hirsch described that, AGEs form a nonenzymatic process in the presence of glucoses and interact with cellular surface receptors. This interaction leads to increased expression of cellular adhesive proteins and the generation of reactive oxygen species. In addition, these products can stimulate the production of inflammatory cytokines, cause inflammation, and alter the extracellular matrix. Therefore, these substances may be responsible for the development of diabetic retinopathy (DR).

Over-nutrition promotes the formation of AGEs. It results in insulin resistance, increased OS, and b-cell injury. Most people consume a diet that is high in animal foods and subjected to heat. This diet is full of oxidant AGEs, which contribute to the damage that occurs to beta cells. Therefore, diabetes patients are at high risk for developing type 2 diabetes.

AGE-mediated glycation in alcohol-mediated tissue injuries

One of these mechanisms involves the formation of AGE-protein adducts in cells. When AGEs accumulate in tissues, they activate certain cellular proteins, including microglial cells in the brain and Kupffer cells in the liver. AGEs may also contribute to the pathophysiology of various tissues and organs.

This oxidative stress can lead to a series of cellular damages, such as DNA damage. Eventually, the damage induced by alcohol-mediated tissue injuries may lead to the death of the affected cells. AGE-mediated glycation is associated with an increased risk for various diseases, including diabetes mellitus.