What Is Glucose Homeostasis?

Glucose transporters (GLUTs) are a family of transmembrane proteins that regulate the entry of extracellular glucose into cells and are involved in the processes of glucose metabolism, inflammatory response and immune response.

Glucose transporter

The metabolism of glucose depends on the uptake of glucose by the cell. However, glucose cannot enter the cell freely through the lipid bilayer structure of the cell membrane. The uptake of glucose by the cell requires glucose transporters on the cell membrane. ) The transfer function can be realized.

Glucose transporters exist in various tissues and cells of the body. They are divided into two categories: one is the sodium-dependent glucose transporter (SGLT), which actively transports glucose against the concentration gradient; the other is the glucose transporter that facilitates diffusion (GLUT), transport glucose along a concentration gradient in a manner that facilitates diffusion, and does not consume energy during the transport process.

Glucose transporters are synthesized intracellularly and cannot be replenished exogenously!

1. Glucose transporter and diabetic retinopathy

Diabetic retinopathy (DR) is one of the most common and serious microvascular complications of diabetes.

It has been confirmed that the glucose transporter (GLUT) is a carrier of glucose passing through the blood-retinal barrier. It exists on vascular endothelial cells of the inner retinal barrier and pigment epithelial cells of the outer barrier. Its function is to transport circulating glucose to tissues. Is an important factor in maintaining a retinal glucose supply balance. Glucose transporters function abnormally, the glucose metabolism is disturbed, and glucose accumulation in the retinal cells accelerates the synthesis of advanced glycation end products and non-enzymatic glycosylation of proteins, leading to damage to endothelial cells and pericytes and the blood-retinal barrier Damaged and caused microvascular disease.

2. Glucose transporters and diabetic cardiomyopathy

Diabetic cardiomyopathy is a disorder of the metabolism and structure of myocardial tissue caused by diabetes. It is mainly characterized by pathological changes of myocardial cells and microvasculature, which are mainly manifested as cardiac diastolic and systolic dysfunction.

Myocardial glucose transporters mainly exist in the myocardial cell membrane, and a small amount exists in the intracellular membrane. Under normal circumstances, when myocardial glucose intake increases, insulin can translocate the glucose transporter from the inner cell membrane to the myometrium and cell membrane. The number of transporters assists myocardial glucose uptake, accelerates glucose transport, and forms a dynamic supply balance of myocardial glucose.

However, the blood glucose of patients with diabetes is too high. On the one hand, glucose transporters are affected by environmental changes, their activity is weakened, and the transport system appears to have defects in operation. This reduces the transmembrane transport of glucose, which directly affects myocardial glucose uptake and utilization. Insufficient utilization of insulin will hinder the translocation and aggregation of glucose transporters, and the number of glucose transporters that can function can be significantly reduced; the decrease in the number and quality of glucose transporters leads to an imbalance in the energy metabolism of myocardial cells and eventually causes diabetes cardiac disease.

3. Glucose transporters and diabetic nephropathy

The exact pathogenesis of diabetic nephropathy has not yet been elucidated. Most people believe that hyperglycemia and cell metabolic disorders are a basic pathophysiological change caused by diabetes and tissue and organ damage.

Glucose transporters are mainly distributed in renal tissues in vascular smooth muscle cells, mesangial cells, and thick sections of ascending branch of renal tubule.

Mesangial cells cultured in vitro have confirmed that the renal glucose transporter is the main glucose uptake protein transported by the kidney, the functional status of the renal glucose transporter is the key to renal glucose uptake, and the renal glucose transport is impaired. Hypertrophy of mesangial cells, increased extracellular matrix, thickened glomerular basement membrane, and proteinuria appear. Therefore, glucose transporter translocation disorder is a key factor in the occurrence and development of diabetic nephropathy.