Abstract:Such long-range positive correlation in glucose homeostasis may reflect pathogenic mechanisms of diabetes, i.e., the lack of the tight control in blood glucose regulation. Using modern time series analysis methods such as DFA, continuous evaluation of glucose dynamics could promote better diagnoses and prognoses of diabetes and a better understanding of the fundamental mechanism of glucose dysregulation in diabetes.
“…0.29 in healthy volunteers. All of the critically ill patients in our series had DFA values greater than those reported by Ogata et al (23,31), which supports our hypothesis that critical illness and multisystem organ dysfunction are characterized by a loss of complexity in the glycemic profile.…”
Objective: To investigate glycemic dynamics and its relation with mortality in critically ill patients. We searched for differences in complexity of the glycemic profile between survivors and nonsurvivors in patients admitted to a multidisciplinary intensive care unit.Design: Prospective, observational study, convenience sample. Settings: Multidisciplinary intensive care unit of a teaching hospital in Madrid, Spain.Patients: A convenience sample of 42 patients, aged 29 to 86 yrs, admitted to an intensive care unit with an Acute Physiology and Chronic Health Evaluation II score of >14 and with an anticipated intensive care unit stay of >72 hrs.Interventions: A continuous glucose monitoring system was used to measure subcutaneous interstitial fluid glucose levels every 5 mins for 48 hrs during the first days of intensive care unit stay. A 24-hr period (n = 288 measurements) was used as time series for complexity analysis of the glycemic profile. n recent years, there has been a growing interest in hyperglycemia associated with critical illness. Hyperglycemia in critically ill patients is a consequence of several factors, including increased cortisol, catecholamines, glucagon, growth hormone, gluconeogenesis, and glycogenolysis (1, 2). In addition, insulin resistance has been demonstrated in >80% of critically ill patients (3).
“…0.29 in healthy volunteers. All of the critically ill patients in our series had DFA values greater than those reported by Ogata et al (23,31), which supports our hypothesis that critical illness and multisystem organ dysfunction are characterized by a loss of complexity in the glycemic profile.…”
Objective: To investigate glycemic dynamics and its relation with mortality in critically ill patients. We searched for differences in complexity of the glycemic profile between survivors and nonsurvivors in patients admitted to a multidisciplinary intensive care unit.Design: Prospective, observational study, convenience sample. Settings: Multidisciplinary intensive care unit of a teaching hospital in Madrid, Spain.Patients: A convenience sample of 42 patients, aged 29 to 86 yrs, admitted to an intensive care unit with an Acute Physiology and Chronic Health Evaluation II score of >14 and with an anticipated intensive care unit stay of >72 hrs.Interventions: A continuous glucose monitoring system was used to measure subcutaneous interstitial fluid glucose levels every 5 mins for 48 hrs during the first days of intensive care unit stay. A 24-hr period (n = 288 measurements) was used as time series for complexity analysis of the glycemic profile. n recent years, there has been a growing interest in hyperglycemia associated with critical illness. Hyperglycemia in critically ill patients is a consequence of several factors, including increased cortisol, catecholamines, glucagon, growth hormone, gluconeogenesis, and glycogenolysis (1, 2). In addition, insulin resistance has been demonstrated in >80% of critically ill patients (3).
“…Experiments in vitro have provided evidence that chronic persistent hyperglycemia can reduce the mRNA expression of insulin gene in pancreatic islet β -cells (Robertson et al 2007). In addition to persistent hyperglycemia, another commonly accepted circumstance in diabetic patients is the repeated fluctuation in blood sugar (Ogata et al 2007). There are also a few published papers referring to the toxic effect of fluctuating glucose on pancreatic β -cells in vitro (Del Guerra et al 2007).…”
“…Fluctuation from hypoglycemia to hyperglycemia is a common and important phenomenon in diabetic patients, in whom the fluctuations are more severe than those in healthy individuals [16]. To induce glucotoxicity by fluctuating glucose levels, INS-1 cells and dispersed islet cells were exposed to fluctuating glucose concentrations from 2.5 mM (low glucose) for 1 h to 17 mM (high glucose) for 48 h, and from 5 mM (low glucose) for 1 h to 25 mM (high glucose) for 48 h, respectively.…”
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