Alterations in carbohydrate metabolism during stress: a review of the literature.

Sepsis is a highly lethal and urgent unmet medical need. It is the result of a complex interplay of several pathways, including inflammation, immune activation, hypoxia, and metabolic reprogramming. Specifically, the regulation and the impact of the latter have become better understood in which the highly catabolic status during sepsis and its similarity with starvation responses appear to be essential in the poor prognosis in sepsis. It seems logical that new interventions based on the recognition of new therapeutic targets in the key metabolic pathways should be developed and may have a good chance to penetrate to the bedside. In this review, we concentrate on the pathological changes in metabolism, observed during sepsis, and the presumed underlying mechanisms, with a focus on the level of the organism and the interplay between different organ systems.

https://www.embopress.org/doi/pdf/10.15252/emmm.201708712

Reprogramming of basic metabolic pathways in microbial sepsis: therapeutic targets at last?

To get insight in the endocrine and metabolic responses in children with meningococcal sepsis 26 children were studied the first 48 h after admission. On admission there was a significant difference in cortisol/ACTH levels between nonsurvivors (n = 8) and survivors (n = 18). Nonsurvivors showed an inadequate cortisol stress response in combination to very high ACTH levels, whereas survivors showed a normal stress response with significantly higher cortisol levels (0.62 vs. 0.89 μmol/L) in combination with moderately increased ACTH levels (1234 vs. 231 ng/L). Furthermore, there was a significant difference between nonsurvivors and survivors regarding pediatric risk of mortality score (31 vs. 17), TSH (0.97 vs. 0.29 mE/L), T3 (0.53 vs. 0.38 nmol/L), reverse T3 (rT3) (0.75 vs. 1.44 nmol/L), C-reactive protein (34 vs. 78 mg/L), nonesterified fatty acids (0.32 vs. 0.95 mmol/L), and lactate (7.3 vs. 3.2 mmol/L). In those who survived, the most important changes within 48 h were seen in a normalization of cortis...

/pdf/endocrine-and-metabolic-responses-in-children-with-w9umsevbne.pdf

Endocrine and Metabolic Responses in Children with Meningoccocal Sepsis: Striking Differences between Survivors and Nonsurvivors

Sepsis is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. Contrary to the older definitions, the current one not only focuses on inflammation, but points to systemic disturbances in homeostasis, including metabolism. Sepsis leads to sepsis-induced dysfunction and mitochondrial damage, which is suggested as a major cause of cell metabolism disorders in these patients. The changes affect the metabolism of all macronutrients. The metabolism of all macronutrients is altered. A characteristic change in carbohydrate metabolism is the intensification of glycolysis, which in combination with the failure of entering pyruvate to the tricarboxylic acid cycle increases the formation of lactate. Sepsis also affects lipid metabolism—lipolysis in adipose tissue is upregulated, which leads to an increase in the level of fatty acids and triglycerides in the blood. At the same time, their use is disturbed, which may result in the accumulation of lipids and their toxic metabolites. Changes in the metabolism of ketone bodies and amino acids have also been described. Metabolic disorders in sepsis are an important area of research, both for their potential role as a target for future therapies (metabolic resuscitation) and for optimizing the current treatment, such as clinical nutrition.

/pdf/metabolic-alterations-in-sepsis-3e1jhn4u47.pdf

Metabolic Alterations in Sepsis

Context: Sepsis-induced hypoglycemia is a well known, but rare, event of unknown origin. Objective: The aim of the study was to obtain insight into the mechanism of sepsis-induced hypoglycemia, focusing on glucose kinetics and insulin sensitivity measured with stable isotopes by using the model of human endotoxemia. Design: Glucose metabolism was measured during two hyperinsulinemic [insulin levels of 100 pmol/liter (low-dose clamp) and 400 pmol/liter (medium-dose clamp)] euglycemic (5 mmol/liter) clamps on two occasions: without or with lipopolysaccharide (LPS). Setting: The study was conducted at the Academic Medical Center, Metabolic and Clinical Research Unit (Amsterdam, The Netherlands). Participants: Eighteen healthy male volunteers participated in the study. Intervention: A hyperinsulinemic euglycemic (5 mmol/liter) clamp with LPS (two groups of six subjects; insulin infusion at rates of either 10 or 40 mU · m−2 · min−1) or without LPS (n = 6; both insulin infusions in same subjects). Main Outcome ...

Early endotoxemia increases peripheral and hepatic insulin sensitivity in healthy humans

A unique case report with sequential measurements of the plasma concentrations of glucoregulatory hormones, interleukin-6 and tumor necrosis factor during development of hypoglycemia in fatal meningococcemia is presented. Hormonal explanations for hypoglycemia like hyperinsulinemia or defective hypoglycemic counterregulation were excluded. Plasma concentrations of interleukin-6 and tumor necrosis factor were skyhigh. The putative relation between cytokines and hypoglycemia in sepsis is discussed.

Hypoglycemia, hormones and cytokines in fatal meningococcal septicemia.

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Hypoglycemia, hormones and cytokines in fatal meningococcal septicemia.