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Glucose homeostasis, nutrition and infections during critical illness.
Ingels, C, Vanhorebeek, I, Van den Berghe, G
Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2018;(1):10-15
Abstract
Critical illness is a complex life-threatening disease characterized by profound endocrine and metabolic alterations and by a dysregulated immune response, together contributing to the susceptibility for nosocomial infections and sepsis. Hitherto, two metabolic strategies have been shown to reduce nosocomial infections in the critically ill, namely tight blood glucose control and early macronutrient restriction. Hyperglycaemia, as part of the endocrine-metabolic responses to stress, is present in virtually all critically ill patients and is associated with poor outcome. Maintaining normoglycaemia with intensive insulin therapy has been shown to reduce morbidity and mortality, by prevention of vital organ dysfunction and prevention of new severe infections. The favourable effects of this intervention were attributed to the avoidance of glucose toxicity and mitochondrial damage in cells of vital organs and in immune cells. Hyperglycaemia was shown to impair macrophage phagocytosis and oxidative burst capacity, which could be restored by targeting normoglycaemia. An anti-inflammatory effect of insulin may have contributed to prevention of collateral damage to host tissues. Not using parenteral nutrition during the first week in intensive care units, and so accepting a large macronutrient deficit, also resulted in fewer secondary infections, less weakness and accelerated recovery. This was at least partially explained by a suppressive effect of early parenteral nutrition on autophagic processes, which may have jeopardized crucial antimicrobial defences and cell damage removal. The beneficial impact of these two metabolic strategies has opened a new field of research that will allow us to improve the understanding of the determinants of nosocomial infections, sepsis and organ failure in the critically ill.
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Insulin resistance - "the good or the bad and ugly".
Szosland, K, Lewinski, A
Neuro endocrinology letters. 2018;(5):355-362
Abstract
Insulin resistance (IR) is a state of decreased sensitivity or responsiveness of target tissues to metabolic actions of circulating insulin. IR can be selective, involving only certain aspects of insulin action, i.e. only its impact on hepatic glucose disposal. Plasma insulin concentration is a continuous variable, dependent upon several physiological stimuli, thus the thresholds used to diagnose IR are arbitrary. Insulin resistance (impaired insulin action) may occur due to derangements on three levels: pre-receptor (antibodies against insulin, defected insulin molecule), receptor (defects of insulin receptor, anti-receptor antibodies) and post-receptor (disregulated intracellular pathways). The aim of the study has been promoting the opinion that IR itself cannot be considered only a harmful phenomenon. Detrimental effect is rather chronic hyperinsulinemia related to IR. IR appears important physiological mechanism responsible for adaptation to various stresses: physical, as well as emotional/physiological. Diurnal, seasonal, age-related, pregnancy-associated, and illness-induced fluctuations in food intake and energy expenditure necessitate homeostatic versatility, including the capacity to vary insulin sensitivity, so as to optimize partitioning between tissues of a variable nutrient supply. IR has positively been selected during evolution for the short-lived energy-consuming activation of the brain or immune system. Physiologic situations that require organisms to reserve priority nutrient access for an emerging metabolic requirement, for example immune system activation or foetal development, promote the decrease of systemic insulin sensitivity, reducing nutrient uptake by non-priority tissues and reserving glucose for priority cells. It has been suggested that IR is a mechanism of antioxidant defence in conditions of nutrient energy excess.
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DIABETIC KETOACIDOSIS: A COMMON DEBUT OF DIABETES AMONG AFRICAN AMERICANS WITH TYPE 2 DIABETES.
Vellanki, P, Umpierrez, GE
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2017;(8):971-978
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Abstract
OBJECTIVE More than half of African Americans (AA) with a new diagnosis of diabetic ketoacidosis have clinical and metabolic features of type 2 diabetes during follow-up. This particular presentation of diabetes has been termed as ketosis-prone type 2 diabetes (KPDM) or atypical diabetes. METHODS We review the epidemiology, diagnosis, pathophysiology, and acute and long-term management of AA with KPDM and compare these similarities to patients with type 2 diabetes. RESULTS In contrast to the long-term insulin requirement of auto-immune type 1 diabetes, patients with KPDM are able to discontinue insulin after a few months of therapy and maintain acceptable glycemic control for many years on either diet or oral agents. Patients with KPDM have significant impairment of both insulin secretion and insulin action at presentation; however, at the time of near-normoglycemia remission, insulin secretion and action improve to levels similar to hyperglycemic patients with ketosis-resistant type 2 diabetes. In the long term, however, patients with KPDM have a decline in β-cell function similar to patients with type 2 diabetes. Recent studies indicate that treatment with metformin and dipeptidyl peptidase-4 inhibitors can prolong the period of near-normoglycemia remission for several years compared to placebo therapy. CONCLUSION KPDM is a unique but common presentation of newly diagnosed African Americans with type 2 diabetes. ABBREVIATIONS A(+/-) = auto-antibody positive/negative AA = African Americans DKA = diabetic ketoacidosis FFA = free fatty acids G6PD = glucose-6-phosphate dehydrogenase GAD-65 = 65-kDA glutamic acid decarboxylase HBA1c = glycated hemoglobin A1c HHV8 = human herpes virus 8 HLA = human leukocyte antigen KPDM = ketosis-prone type 2 diabetes.
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Medical Nutrition Therapy Is Effective in the Management of Hypoglycemia Caused by Insulin Antibodies: A Case Report and Literature Review.
Li, R, Mao, J, Yu, K, Wang, L, Hu, M, Xu, L
Journal of the American College of Nutrition. 2016;(1):86-90
Abstract
Autoimmune antibodies, induced by exogenous insulin preparations, may result in labile glucose control and frequent hypoglycemia in some rare cases. In addition to insulin cessation, immune suppressants and/or plasmapheresis have been used as the primary remedies for these patients. Some previous studies also indicate that the condition tends to remit spontaneously after discontinuation of insulin exposure. Because of this, the clinical importance of nutritional interventions and behavioral approaches, which may play a role in ameliorating the symptoms, should also be emphasized. Herein, we report on a 64-year-old man with hypoglycemia induced by insulin antibodies (IAs), whose hypoglycemic symptoms significantly improved after the implementation of nutrition therapy. This rare case expands our knowledge of the management of hypoglycemia, and for the first time highlights the significance of nutritional and lifestyle intervention in treatment of IA-induced hypoglycemia.
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Lessons from type 1 diabetes for understanding natural history and prevention of autoimmune disease.
Simmons, K, Michels, AW
Rheumatic diseases clinics of North America. 2014;(4):797-811
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Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disorder resulting from immune-mediated destruction of insulin-producing beta cells within the pancreatic islets. Prediction of T1D is now possible, as having 2 or more islet autoantibodies confers a 100% risk of diabetes development. With the ability to predict disease development, clinical trials to prevent diabetes onset have been completed and are currently under way. This review focuses on the natural history, prediction, and prevention trials in T1D. We review the lessons learned from these attempts at preventing a chronic autoimmune disease and apply the paradigm from T1D prevention to other autoimmune disorders.
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Primary and secondary prevention of Type 1 diabetes.
Skyler, JS
Diabetic medicine : a journal of the British Diabetic Association. 2013;(2):161-9
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Since type 1 diabetes is an immunologically mediated disease, immune intervention should alter the natural history of the disease. This article reviews prevention studies undertaken either prior to any evidence of autoimmunity (primary prevention) or after the development of islet autoantibodies (secondary prevention). Most immune intervention studies have been conducted in recent-onset type 1 diabetes (tertiary prevention), and these are not reviewed herein. The goal of primary and secondary intervention is to arrest the immune process and thus prevent or delay clinical disease. Primary prevention studies have been conducted in infants with high genetic risk. Interventions tested include several dietary manipulations, including infant formulas free of either cow's milk or of bovine insulin, infant formula supplemented with the omega-3-fatty acid docosahexaenoic acid, delayed introduction of gluten-containing foods, and vitamin D supplementation. Secondary prevention studies have been conducted in both children and adults with diabetes autoantibodies. Interventions tested include nicotinamide, insulin injections, oral insulin, nasal insulin, glutamic acid decarboxylase, and cyclosporine. Underway are secondary prevention studies with teplizumab and with abatacept.
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Insulin therapy in preterm newborns.
Beardsall, K, Dunger, D
Early human development. 2008;(12):839-42
Abstract
The perinatal period is known to be a critical period for pancreatic development, and the impact of prematurity on the development of insulin secretion and sensitivity is poorly defined. Premature infants are at risk of hyperglycaemia which is a marker of relative insulin deficiency which impacts on anabolism both directly and indirectly by regulation of insulin like growth factors. The use of insulin in preterm infants and prevention of hyperglycaemia could also effect immune function, lipid metabolism, growth and IGF-I generation leading to improved short term clinical outcomes such as retinopathy of prematurity. It may also have longer term health effects however the outcomes of clinical trials are currently awaited.
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Hyperglycemia in the critically ill.
Digman, C, Borto, D, Nasraway, SA
Nutrition in clinical care : an official publication of Tufts University. 2005;(2):93-101
Abstract
Hyperglycemia is frequently seen in acutely ill patients and has historically been viewed as a normal response to stress. Treatment is often not initiated unless blood glucose exceeds 200 to 250 mg/dL. Recent evidence suggests that hyperglycemia is associated with worse outcomes within the population of medical and surgical intensive care units. Hyperglycemia in this population of patients develops from increased gluconeogenesis and insulin resistance. Although the specific mechanisms by which hyperglycemia contributes to poor outcomes are as yet unknown, disruption of normal mitochondrial respiration, direct glucose toxicity, accumulation of asymmetric dimethylarginine, and impairment of immune cell function are among the possibilities implicated. Studies demonstrate that intensive insulin therapy to achieve euglycemia reduces mortality and morbidity in critically ill patients. In addition to recognizing and treating hyperglycemia, it is as important to identify other frequently overlooked factors that contribute to hyperglycemia, such as medications, intravenous fluids, and enteral and parenteral nutrition.
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Anabolic strategies in critical illness.
Hadley, JS, Hinds, CJ
Current opinion in pharmacology. 2002;(6):700-7
Abstract
Critical illness precipitates a marked catabolic response, with protein wasting and loss of lean body mass. Prolongation of this response leads to impaired immunity, poor wound healing, loss of intestinal barrier function and muscle weakness, thereby increasing morbidity and perhaps mortality. Conventional nutritional support only partially ameliorates this process. Disappointingly, specific anabolic and anticatabolic strategies have so far met with only limited success, although recent findings, in particular studies demonstrating the potential value of aggressive insulin therapy and the administration of growth hormone secretagogues, have been encouraging.