If diabetic patients are in a state of high blood sugar for a long time, they are still prone to diabetes-related complications even if their blood sugar levels are reduced. Sustained high blood sugar is the root cause of the development of diabetic complications. Why do complications occur after blood sugar is lowered? Is it because high blood sugar "hangs around"? Another interesting phenomenon is that when the blood sugar of diabetic patients drops to a lower level, , even after blood sugar rebounds, the therapeutic effects of lowering blood sugar continue to exist. Why is this? It seems that it’s not just high blood sugar that “hangs around”! In fact, there is another protagonist - "metabolic memory"! Also called "glycemic blot".
The "metabolic memory" effect is the bridge between diabetes and its complications, posing new challenges to blood sugar management in patients with type 2 diabetes. At first glance, Xiaonuo and my friends were frightened to death by the content of the previous article. However, as long as we read the following content carefully, we will see that there is a bright future, and efforts to lower blood sugar will not be in vain! Friends are welcome to share their opinions. own point of view. Why did it come about? Many scholars have studied the mechanism of the "metabolic memory" effect: in 2000, Italian scholars proposed the "unified mechanism theory", pointing out that oxidative stress induced by high sugar is a factor in diabetic vascular complications, β-cell dysfunction and insulin resistance. common pathogenesis. Ceriell proposed the "metabolic memory" theory and believed that oxidative stress is a central link in various factors related to "metabolic memory". Oxidative stress may be involved in the polyol pathway, glycation end product (AGE) formation, protein kinase C ( PKC) pathway activation, hexosamine pathway, gene expression and other pathways ultimately lead to vascular endothelial dysfunction.
So far, this theory is still the most well-known mechanism hypothesis in studying the mechanism of "metabolic memory", and its connotation has been continuously expanded through more new research discoveries, and the mechanisms involved have become increasingly complex. Clinical Evidence DCCT Study This study included a total of 1441 patients with type 1 diabetes, who were randomized to receive intensive or conventional treatment, with an average follow-up of 6.5 years. After the study ended, in order to continue to study the long-term impact of intensive treatment, especially the subsequent impact on diabetes complications , the EDIC observational study continued. In the DCCT study, the treatment of patients in the intensive treatment group remained unchanged, while patients in the conventional treatment group were switched to an intensive treatment plan and continued to be followed for 10 years. During the EDIC stage, the glycated hemoglobin (HbA1c) gap (7% vs. 9%) between the two treatment groups gradually disappeared, and finally remained at around 8%. However, the risk of diabetic complications in the intensive treatment group was still significantly lower than that in the conventional treatment group (retina The risk of disease is reduced by 70%, the risk of diabetic nephropathy is reduced by 53% to 86%, and the risk of neuropathy is reduced by 31%).
This phenomenon is called a "metabolic memory" effect, and its effects last for at least 10 years. In addition, the "metabolic memory" effect also occurs in macrovascular disease. In the EDIC study, the risk of accompanying cardiovascular events was reduced by 58% in the intensive treatment group. UKPDS study The UK Prospective Diabetes Study (UKPDS) included a total of 4209 newly diagnosed patients with type 2 diabetes, who were randomly divided into two groups: intensive and conventional treatment. Some overweight or obese patients received intensive treatment with metformin. After 20 years of treatment, it was found that compared with conventional treatment, intensive treatment can significantly improve microvascular (risk of retinopathy reduced by 68%, risk of proteinuria reduced by 74%) and macrovascular complications (HbA1c decreased by 1% corresponding to The risk was reduced by 14% for myocardial infarction, 12% for stroke, 16% for heart failure, and 21% for all diabetes-related endpoints). After the 20-year treatment period, an additional 10 years of follow-up was conducted. The difference in baseline HbA1c between the original intensive and conventional treatment groups (7.9% vs. 8.5%) disappeared after 1 year of follow-up. After that, HbA1c levels were similar between the two groups, but After 10 years of follow-up, compared with the conventional treatment group, patients in the intensive treatment group had a 9% lower risk of diabetes-related endpoints, a 24% lower risk of microvascular disease, a 15% lower risk of myocardial infarction, and a 13% lower risk of all-cause death.
VADT study The Veterans Diabetes Study (VADT) included 1,791 patients with type 2 diabetes and were randomized to receive intensive or conventional treatment for 5.6 years. After 3 years of follow-up, the difference in HbA1c levels between the intensive treatment and conventional treatment groups decreased from 1.5% to 0.2 %-0.3%. Observing the data results after 9.8 years, the risk of first major cardiovascular event in the intensive treatment group was significantly reduced (8.6 fewer major vascular events per 1000 patient-years, and the exposure hazard ratio was reduced by 17%. Both the UKPDS and VADT studies have shown that "metabolic memory" The existence of the "effect" also proves that intensive treatment to lower blood sugar in patients with type 2 diabetes can reduce the risk of complications and bring long-term benefits. Clinical response through early and strict blood sugar control can effectively inhibit the "metabolic memory" effect and delay diabetes. The occurrence and development of complications. In animal experiments, some researchers compared the establishment of a diabetes model with no treatment, and observed the effects of intensive treatment immediately and treatment initiated two and a half years later on diabetic retinopathy. The results showed that animals that received intensive treatment immediately Retinopathy was suppressed, while retinal capillary aneurysms and other vascular damage developed in untreated animals, which did not develop retinopathy for 2.5 years without treatment, and which still developed retinopathy in animals that were switched to intensive treatment for 2.5 years.
Such results indicate that early intervention and treatment can change the metabolic state and prevent the adverse effects caused by the "metabolic memory" effect. On the contrary, if late intervention treatment is affected by the "metabolic memory" effect, it will not be able to change adverse outcomes. The "China Guidelines for the Prevention and Treatment of Type 2 Diabetes" clearly recommends: When a combination of multiple oral hypoglycemic drugs still fails to achieve blood glucose levels, insulin treatment should be initiated promptly to avoid adverse outcomes caused by long-term exposure to high blood sugar.
Early intensive treatment of newly diagnosed type 2 diabetes patients can induce long-term remission of the condition. Within 1 year after intensive treatment, the percentage of patients who can control their blood sugar with lifestyle intervention alone reaches 45% to 51%. At the same time, these patients have significant improvement in beta cell function. improve. Intensive insulin therapy is accompanied by long-term benefits, helping to reduce the risk of diabetic complications. All in all, oxidative stress triggered by high blood sugar will trigger a "metabolic memory" effect. Avoiding long-term exposure to high blood sugar can inhibit the "metabolic memory" effect and reduce the occurrence and development of diabetic complications. Early and timely insulin treatment can improve β-cell function, delay the progression of diabetes, reduce the occurrence of complications, and has a better economic benefit ratio.
