Type 2 diabetes is generally recognized as a progressive process that describes the inability of the pancreas islets to produce enough insulin and the body's resistance to the effects of insulin. Recent studies have reported that the progression can be stopped in some cases by diet restriction, bariatric surgery, or short-term intensive insulin therapy. This situation, defined as type 2 diabetes remission, referred that some patients with type 2 diabetes achieving HbA1c or eHbA1c under 6.5% or FPG under 7mmol/l for a period of time without the need for glucose-lowering medication. However, diabetes remission does not occur in everyone. It is influenced by many factors, including genetics, age, weight, residue of beta-cell function, food style or physical activity, and other conditions. Therefore, the underlying mechanism is needed to be explored, especially for how to restore beta cell function as it is crucial in the remission process.
This Research Topic aims to seek possible therapeutical treatments for diabetes remission, investigate the factors that influence the efficiency of remission, and explore the mechanisms relative to the restoration of beta-cell function through basic or clinical studies in genetics, environment, inflammation, and metabolism.
Original Research, Meta-analysis, Reviews, and Mini Reviews are all welcome regarding the following sub-topics, including but not limited to:
• The relationship between beta-cell function and the percentage and duration of remission;
• The impact of different remission approaches on beta cell function;
• The genetic and ethical factors that are relative to diabetes remission;
• The cellular and molecular mechanisms of the remission with a focus on maintaining beta-cell survival and regeneration;
• The metabolic biomarkers for the prediction of diabetes remission;
• Heterogeneity of beta cell function and the potential of diabetes remission;
• Basic and clinical studies on genetic, inflammatory or metabolic beta cell dysfunction under different intensive therapy.
Type 2 diabetes is generally recognized as a progressive process that describes the inability of the pancreas islets to produce enough insulin and the body's resistance to the effects of insulin. Recent studies have reported that the progression can be stopped in some cases by diet restriction, bariatric surgery, or short-term intensive insulin therapy. This situation, defined as type 2 diabetes remission, referred that some patients with type 2 diabetes achieving HbA1c or eHbA1c under 6.5% or FPG under 7mmol/l for a period of time without the need for glucose-lowering medication. However, diabetes remission does not occur in everyone. It is influenced by many factors, including genetics, age, weight, residue of beta-cell function, food style or physical activity, and other conditions. Therefore, the underlying mechanism is needed to be explored, especially for how to restore beta cell function as it is crucial in the remission process.
This Research Topic aims to seek possible therapeutical treatments for diabetes remission, investigate the factors that influence the efficiency of remission, and explore the mechanisms relative to the restoration of beta-cell function through basic or clinical studies in genetics, environment, inflammation, and metabolism.
Original Research, Meta-analysis, Reviews, and Mini Reviews are all welcome regarding the following sub-topics, including but not limited to:
• The relationship between beta-cell function and the percentage and duration of remission;
• The impact of different remission approaches on beta cell function;
• The genetic and ethical factors that are relative to diabetes remission;
• The cellular and molecular mechanisms of the remission with a focus on maintaining beta-cell survival and regeneration;
• The metabolic biomarkers for the prediction of diabetes remission;
• Heterogeneity of beta cell function and the potential of diabetes remission;
• Basic and clinical studies on genetic, inflammatory or metabolic beta cell dysfunction under different intensive therapy.
