The "Metabolic Memory" Theory and the Early Treatment of Hyperglycemia in Prevention of Diabetic Complications

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Term Occurence Count Dictionary
obesity 1 endocrinologydiseases
pioglitazone 1 endocrinologydiseasesdrugs
diabetes mellitus 3 endocrinologydiseases
diabetic retinopathy 1 endocrinologydiseases
hyperglycemia 15 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases

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pioglitazone 18003 stress generation. Different drugs have already shown the capacity to block AGE formation. Metformin and pioglitazone have been shown in vitro to prevent AGE formation [[52]]. ACE inhibitors and AT-1 blockers are compounds
Select Disease Character Offset Disease Term Instance
diabetes mellitus 4928 Diabetes Study (UKPDS), which emerged as important in developing the theory of “metabolic memory” in diabetes mellitus . In this trial, people who underwent intensive treatment had fewer vascular complications and fewer
diabetes mellitus 15116 have an important role in metabolic memory is low-grade inflammation. Inflammation plays a key role in diabetes mellitus and its vascular complications, and prolonged inflammation could mediate metabolic memory. Epigenetic
diabetes mellitus 15536 complications and metabolic memory. All environmental factors that promote the development and progression of diabetes mellitus trigger an inflammatory response, promoting inflammation-mediated insulin resistance and endothelial
diabetic retinopathy 3291 1987 report from Engerman et al. [[4]], who evaluated the extent of the arrest in the development of diabetic retinopathy derived from improved glycemic control. Later clinical trials in diabetes also provided a picture of
hyperglycemia 2027 in the light of this theory.1. IntroductionDiabetes mellitus is a serious illness characterized by hyperglycemia that leads to reduced life expectancy due to its specific complications. It can be controlled clinically
hyperglycemia 8385 reported in diabetes complications verified in dogs in which retinopathy continues to progress even after hyperglycemia is corrected [[4],[16]]. Brownlee has postulated that there is an excess of superoxide anion in the
hyperglycemia 8548 that there is an excess of superoxide anion in the mitochondria of endothelial cells in response to hyperglycemia , which gives rise to diabetes complications [[17]]. Considering that this overproduction of reactive
hyperglycemia 8715 Considering that this overproduction of reactive species could play a key role in the development of hyperglycemia -related diabetes complications, it is possible that the risk of complications persists even when hyperglycemia
hyperglycemia 8826 hyperglycemia-related diabetes complications, it is possible that the risk of complications persists even when hyperglycemia is reduced or normalized. To answer this question, different studies have investigated the effect of
hyperglycemia 8991 different studies have investigated the effect of re-institution of good glucose control on induced hyperglycemia . Kowluru et al. demonstrated that diabetic rats with six months of poor glycemic control followed by
hyperglycemia 9962 elevated in both urine and renal cortex [[19]]. These data all together suggest that the damage following hyperglycemia -induced oxidative stress can be prevented when good glycemic control is initiated very early, but are
hyperglycemia 11531 oxidative stress have been found to explain, at least in part, the “glycometabolic theory”. Although hyperglycemia remains a hallmark in the pathophysiology of chronic diabetes complications, it is now clear that therapies
hyperglycemia 11883 to an imbalance between oxidative stress and antioxidant capacity, which could be the link between hyperglycemia and the multiple biochemical cascades that lead to diabetes complications [[27]]. Two temporally-separated
hyperglycemia 12159 the genesis of microvascular damage. In the early years of the disease, a linear relationship between hyperglycemia , increased oxidative stress, and excessive AGE formation could be hypothesized. Later, a persistent
hyperglycemia 12361 persistent respiratory chain protein glycation and DNA damage in the mitochondria could generate a hyperglycemia -independent vicious cycle [[28]], in which oxidative stress is self-supporting, and AGEs ‘feed’
hyperglycemia 17352 changes, and chronic inflammation (Figure 1).4. Therapeutic Implications and ProspectsThe importance of hyperglycemia on the development of future complications has important therapeutic implications. An early aggressive
hyperglycemia 17608 becomes mandatory in patients with diabetes. This tight control should also include “postprandial” hyperglycemia [[47],[48]] as it is accompanied by the formation of specific reactive species [[49]] and AGEs, not
hyperglycemia 20349 successfully been tested in an in vivo trial [[61],[62]].5. ConclusionsTo conclude, we can affirm that hyperglycemia can cause early damage to cells of vasculature and target organs, favoring the future development of
hyperglycemia 20692 regarding the therapeutic management of diabetes remain unanswered. Very early aggressive treatment of hyperglycemia seems to be important in the light of this “metabolic memory”.Regarding prospective therapies, known
hyperlipidemia 18509 [[55]]. In addition, GLP1 receptor agonists have been demonstrated to decrease inflammation, postprandial hyperlipidemia , and coagulation, resulting in a beneficial effect on atherothrombosis [[56]]. Interestingly, among
obesity 16434 inflammation and oxidative stress and is a pathogenic contributor to hypertension, insulin resistance, and obesity [[44]]. Also, epigenetic mechanisms may activate inflammatory gene expression in vascular cells and

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