糖尿病 z-bo 2020-10-08 328

　　Type 2 diabetic patients are three times more likely to have fractures than non-diabetic patients. With the rapid increase in the number of diabetes patients in the United States, the bone fragility of type 2 diabetes patients is increasing, but this is a little-known public health problem. Low bone density is usually the cause of weak bones, but this is not the case for patients with type 2 diabetes, who usually have normal or very high bone density. However, they still suffered shocking fractures.

　　In Lamya Karim's Bone Biomechanics Laboratory, researchers tried to understand the internal microstructure of the bones of diabetic patients and figure out what went wrong. They believe that they have discovered one of the biological mechanisms of bone fragility in diabetic patients.

　　The bones are still alive

　　Bones are living organs. They provide the structure and protection of the body, including the living space of the bone marrow that produces blood cells, and provide stable minerals, including calcium and phosphorus.

　　If injured, bones can be repaired naturally. Or, through medical intervention, anyone who encounters difficulties can prove this. But what you may not know is that bones are always in a repaired state through a process called "remodeling."

　　Every day, physical exercise wears the bones in the form of microcracks, and the body usually repairs. The process of bone healing involves breaking down the minerals and proteins in the damaged area and replacing them with new healthy proteins.

　　Protein crosslinking

　　These fresh proteins are composed of amino acids and can react naturally with carbohydrates in the body. Imagine how a cut apple slowly turns yellow in the air. The chemical reactions of amino acids and sugars in the body are similar. This process is called non-enzymatic glycosylation and occurs in tissues throughout the body, including bones. Just like

　　Apple turns brown, non-enzymatic saccharification also turns the protein brown and forms small chemical bridges called crosslinks. Everyone has sugar in their body, so everyone is connected to each other. They form naturally, but non-enzymatic cross-linking is not good for you.

　　This is harmful because it hardens the attached protein and prevents it from bending under the pressure of daily walking. This stiffness sounds good, but you need to bend or bend the bone slightly to prevent microcracks from forming. Non-enzymatic cross-linking actually makes bones more fragile.

　　Generally, the human body can easily control crosslinking by disassembling and eliminating crosslinking. However, the bones of patients with type 2 diabetes are different. Research by Karim Lab and other researchers found two disturbing factors.

　　First of all, people with type 2 diabetes have high levels of sugar in their bodies. They believe that the bones of diabetic patients have more bridges than normal healthy bones because sugar is the fuel for the chemical reactions that form bridges. Karim and his colleagues believe that the accumulation of these bridges may be one of the causes of bone weakness in diabetic patients. The second factor is the lower level of bone remodeling in patients with type 2 diabetes. This means that the ability to dismantle the bridge is reduced. The researchers believe that this further promotes a large number of cross-links in the bone tissue of diabetic patients. Cross-linking has also been found in diabetic patients in other organs, causing complications such as blood vessel damage, kidney damage and poor eye health. Generally speaking, the study of bone cross-linking is a relatively new research field, even newer in the bones of diabetic patients.

　　Karim Lab

　　Karim’s team consists of biomedical engineers, mechanical engineers, civil engineers, chemists and doctors who use diabetic bones from patients and cadavers to study cross-linking and microfractures. I'm. In one study, they recruited diabetic patients undergoing hip replacement treatment and collected hip specimens that were discarded during surgery. They found that hard, dense bones formed from shells tend to have more crosslinks and weaker mechanical properties than non-diabetic patients. They also simulated the high sugar content in corpse bones. The bones no longer exist, but their protein structure is intact. When they cultured these bone samples in a sugar solution, the sugar could still react with the amino acids in the skeletal protein to produce crosslinks. Recently, researchers have used this technique to prove that bone samples exposed to a high-sugar environment have more bridges, are weaker, and are more prone to microcracks.

　　Karim and his colleagues are currently investigating different types of cross-linking measurements, and will look more closely at the location and manner of micro-breaks. They hope to be able to predict how a patient's fracture will occur. In addition, they are testing various compounds that can destroy bone bridges and prevent their formation, hoping that their work will help in the future treatment and better care of diabetic patients.