Dynamics Of Glucose Metabolism Research Articles

Dynamics of glucose metabolism after liver transplantation: prediabetes as a window of opportunity for patient survival and long-term kidney function.

Post-transplantation diabetes mellitus (PTDM) is a relevant complication following liver transplantation with profound impact on morbidity and mortality. To date, little is known about the evolution and dynamics of glucose metabolism and the impact of prediabetes in long-term follow-up. To address this issue, all consecutive adult liver transplant recipients (n=429) from a European university hospital transplant center between 2007 and 2017 were analyzed retrospectively. In patients without pre-existing diabetes (n=327), we conducted a longitudinal characterization of glucose metabolism. Median follow-up was 37 [9-64, IQR] months. Median prevalence of prediabetes was 39 [37-39]% and of PTDM 21 [17-22]%. Throughout follow-up, intra-individual glucose regulation of patients was highly variable, continuously fluctuating between different states of glucose metabolism (normal glucose tolerance, prediabetes, PTDM). Whereas overall survival and long-term kidney function of patients with PTDM were significantly lower than that of patients with normal glucose metabolism, prediabetes was not associated with adverse outcome. This study provides new insight into the dynamics and impact of glucose metabolism after liver transplantation. Unlike PTDM, prediabetes is not associated with adverse outcome, providing a window of opportunity for targeted intervention. The results underline the need for constant screening and intervention in posttransplant care of liver allograft recipients.

Dynamics of Glucose Metabolism After Kidney Transplantation

Background/Aims: Posttransplantation diabetes mellitus (PTDM) impacts patient and allograft survival after kidney transplantation. Prediabetes, which is an independent risk factor for PTDM, is modifiable also in a post-transplant setting. Understanding the risks and dynamics of impaired glucose metabolism after transplantation is a key component for targeted intervention. Methods: A retrospective chart analysis of all adult non-diabetic renal allograft recipients (n=251, 2007-2014) was performed. Longitudinal follow-up included fasting plasma glucose and HbA1c, as well as data on allograft function and immunosuppression at consecutive time points (months 3-6 to >5 years post transplantation). Results: Throughout follow-up, median prevalence of prediabetes and PTDM was 53.3 [52.4-55.7]% and 15.4 [15.0-16.5]%, respectively. Continuously high fluxes between states of glucose metabolism, with individual patients’ state deteriorating or improving over time, resulted in a high number of incident patients even long after transplantation. The greatest number of patients shifted between normal glucose tolerance and prediabetes, followed by those between prediabetes and PTDM. Conclusion: Prediabetes and PTDM are highly prevalent after kidney transplantation and incidences remain relevant throughout follow-up. Patient fluxes into and out of the prediabetic state show that glucose metabolism is highly dynamic after transplantation. This provides a continuous opportunity for intervention in an aim to reduce diabetes-associated complications.

A genetic perspective on glucose consumption in the cerebral cortex during human development.

As the major glucose-consuming organ in the human body, the dynamics of glucose metabolism in the brain deserve special attention. It has been shown that the brain's energy allocation as a percentage of the total energy budget of the individual peaks during childhood and declines through adolescence until reaching the stable allocation level seen in the adult. This pattern of glucose consumption has not been observed in other species, including our close primate relatives, and is therefore potentially either a driver or a consequence of human cognition. Furthermore, the allocation of glucose usage in the brain changes as the individual ages, with a surprising amount dedicated to glycolysis rather than oxidative phosphorylation pathway. This suggests that, at certain developmental stages, glucose-fuelled anabolic pathways, in addition to ATP generation, are the driving forces behind the brain's high energy requirement. In this study, we explore the most recent work pertaining to the dynamic glucose uptake and allocation of the developing human brain and investigate several genes that may play a role in regulating these processes.

A Mathematical Model For Attenuating the Spread Of Diabetes and Its Management In A Population

We study the dynamics of diabetes in a population based on the etiology of the disease. In carrying out the study, we proposed that; a population generate non-diabetic non – susceptible sub-population, and a non-diabetic susceptible sub-population, the non-diabetic susceptible sub-population can further generate a population of diabetics without complication, who can later transit to a population with diabetic complications. Based on the etiology dynamics, we proposed control measures at the point of transition from the population to non-diabetic susceptible population, and at the point of transition from diabetes without complications to diabetes with complications. For this study, we intend to look at the control measure. In this regard, we proposed a mathematical model for the dynamics of diabetes by incorporating a control parameter h, so as to investigate how to control diabetes in a population. The result of the study suggested that; we need to control the incidence of diabetes, I(t), and improve the control measure, h, for transition from diabetes without complication to diabetes with complication. Thus entailing going further in research to; Look into the dynamics of the genetics of transmission of the diabetic gene, to investigate how to reduce the spread (and hence the incidence I(t)) of diabetes, and to also look into the influence of the control factor h, on the dynamics of glucose metabolism, this will give an insight on how to manage diabetic patients.Keywords: Diabetes, Population, Genes, Genetics, Etiology.

Studies of fatty liver and kidney syndrome in chickens: dynamics of glucose metabolism.

1. Fatty liver and kidney syndrome (FLKS) was induced in a proportion of a group of 4-week-old chickens by giving a diet of meat meal and wheat; inclusion in the diet of animal tallow for 54 h substantially reduced the occurrence of FLKS. 2. Measurements of dynamic aspects of glucose metabolism were made with single injections of [2-3H]glucose which indicated that birds given the 'FLKS-inducing' diet and showing physical symptoms of FLKS had significantly lower rates of synthesis of glucose than birds given either the same diet supplemented with tallow or a commercial diet. 3. In a second series of experiments glucose metabolism was studied in birds (1) with or without physical symptoms that were given the 'FLKS-inducing' diet and (2) birds given the same diet supplemented with tallow or biotin. Affected birds fed the 'FLKS-inducing' diet had significantly lower plasma glucose concentrations, pool sizes and synthesis rates than birds fed the same diet and not showing symptoms, or birds fed the supplemented diets. 4. It is suggested that the cause of death in birds with FLKS is a low rate of gluconeogenesis during periods without feed which results in a lack of glucose to meet essential functions.

Altered glucoregulatory hormones during acute pneumococcal sepsis in the rhesus monkey.

To determine the effects of a Diplococcus pneumoniae infection upon the dynamics of glucose metabolism and the hormones responsible for its control, intravenous glucose tolerance tests (IVGTT's) were performed in monkeys during baseline control conditions and twenty-four hours after initiating infection when the monkeys were febrile. Along with plasma glucose, immunoreactive insulin and glucagon concentrations were measured sequentially through each IVGTT. Furthermore, fasting concentrations of plasma amino acids, immunoreactive growth hormone and cortisol were determined. These data reveal no differences in the fasting plasma concentrations of growth hormone and glucose, or in the disappearance rates of glucose during the two IVGTT's. There was, however, a mild relative hyperinsulinemia (p < 0.05) (following glucose) along with fasting hyperglucagonemia (p < 0.01) during infection. Of the twenty-one amino acids measured, twenty were depressed during infection; only cysteine was elevated (p < 0.05) in the infected monkeys. Although plasma cortisol levels were significantly (p < 0.05) increased above preinfection values by the stress of infection, they remained within the control range. The hyperglucagonemia and depression of the mean insulin: glucagon molaf ratio are compatible with the catabolic events occurring during a mild bacterial infection in the monkey.