This is an automatically translated article.
Type 2 diabetes is caused by a combination of genetic and environmental factors that cause tissue insulin resistance and impaired beta cell function. Therefore, understanding the function of beta cells as well as the causes of beta cell dysfunction is an important condition for the prevention or treatment of type 2 diabetes.
1. Normal beta cell function
The main role of beta cells in the pancreas is to synthesize and secrete insulin to maintain blood sugar levels within the physiological range. Although several agents that stimulate insulin secretion exist such as nutrients (amino acids such as leucine, leucine-conjugated glutamine, unsaturated fatty acids), hormones, neurotransmitters, and drugs (sulfonylurea, glinides), Glucose represents the major physiological insulin secretagogue.
According to the most widely accepted hypothesis, insulin secretion is a multistep process initiated with glucose transport into beta cells. In other words, when blood sugar levels rise, usually after a meal, the normal function of beta cells is to release insulin into the bloodstream, helping to promote glucose into the cells for energy metabolism. As a result, blood sugar will drop.
In addition, scientists have demonstrated that insulin release from beta cells is fluctuating with a relatively steady flow occurring every 8 - 10 minutes. In humans, the amplitude of insulin oscillations in the portal vein is 100 times higher than in the systemic circulation, implying that the liver will preferentially extract the insulin pulse into the bloodstream. Accordingly, understanding the roles of these pathways may provide strategies for future therapies for the treatment of type 2 diabetes due to impaired beta-cell function.
2. Mechanism of causing type 2 diabetes due to impaired beta cell function
It is now accepted by scientists that for hyperglycemia to persist in type 2 diabetes, there must be pre-existing beta cell dysfunction. This change manifests itself in a number of different ways, including decreased insulin release in response to glucose-secreting stimulants, and changes in insulin secretion that fluctuate wildly in the efficiency of proinsulin-to-insulin conversion. and reduced amyloid polypeptide release from islets.
A decrease in insulin release can be demonstrated in people with type 2 diabetes after oral administration of glucose into the bloodstream. In addition to its ability to directly stimulate insulin release, glucose also regulates beta-cell responses to other secretions, such as amino acids, in individuals on a completely starch-free diet.
Two other components related to β-cell function are worth mentioning as they are both dysregulated in type 2 diabetes. The first involves insulin biosynthesis. Insulin production requires the cleavage of insulin from the larger proinsulin peptide precursor leading to the formation of insulin and C-peptide. In some healthy individuals, approximately 2% of all insulin-like immune responses are composed of intact proinsulin and cleavage-mediated proinsulin under normal conditions. In patients with type 2 diabetes, the cellular efficiency of proinsulin processing is reduced. Thus, in hyperglycemic subjects, after acute stimulation, the proportion of proinsulin-like molecules is increased but without hypoglycemic activity. However, as the need for secretion increases, the release of a beta cell granule is less mature at the time of incomplete conversion of proinsulin to insulin. As a result, blood sugar levels in the blood can no longer be controlled, so it becomes true diabetes.
3. Future ways to prevent beta cell dysfunction and prevent type 2 diabetes
Because it is clear today that the decline in beta cell function begins before a clinical diagnosis of diabetes is made, future therapeutic approaches to the disease must include early prevention.
Under the hypotheses that hyperglycemia and elevated free fatty acids contribute to beta cell dysfunction, aggressive control of these blood parameters holds the promise of improving insulin release and possibly preventing prevent disease progression. In addition, since the deposition of amyloid plaques in the islets is predicted to lead to a sustained loss of beta cell mass, it is possible that the small amount of amyloid detected in the blood is sufficient to account for the decline in beta-cell mass. Early progressive reduction in β-cell function is observed in type 2 diabetes. Therefore, inhibition of amyloidogenesis is expected to be of significance in preserving beta-cell counts, preventing decline in beta cell function will occur.
Finally, a few recent observations concern the discovery of resistin, a peptide produced and secreted by adipocytes and capable of inducing insulin resistance. This difference in peptide release may mediate changes in later beta cell function.
In summary, persistent hyperglycemia is an important contributing factor in the development of dangerous complications of type 2 diabetes. The difficulty of maintaining stable blood glucose levels is due to impaired blood sugar levels. Persistent decline in beta-cell function that begins many years before the disease is diagnosed. While there are many therapeutic options to lower plasma glucose, no breakthrough has yet to be demonstrated for diabetes by slowing the decline of beta-cell function. Therefore, genetic, physiological and immunological approaches that have to focus early on beta cells are expected to benefit latent type 2 diabetes patients in the future.
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