Related Experiment Video
Updated: Jun 2, 2026
12:08
Improving IV Insulin Administration in a Community Hospital
Published on: June 11, 2012
Insulin resistance in critical illness
Archana Dhar1, Leticia Castillo
1Division of Critical Care, Department of Pediatrics, Children's Medical Center, University of Texas Southwestern, Dallas, USA.
Current Opinion in Pediatrics
|April 22, 2011
Summary
Inflammation and immune responses in critically ill children can lead to insulin resistance, a crucial adaptive mechanism. Understanding these interactions improves metabolic and immune support for better patient outcomes.
Area of Science:
- Pediatric critical care medicine
- Immunology
- Metabolic disorders
Background:
- Metabolic and immune systems are intricately linked in inflammatory processes.
- Dysregulation contributes significantly to pathology in pediatric intensive care units.
- Insulin's role in maintaining metabolic function is critical.
Purpose of the Study:
- To review current understanding of inflammation, immunity, and insulin resistance.
- To explore the interplay between metabolic and immune systems in critically ill children.
- To provide a basis for improved metabolic and immune support.
Main Methods:
- Literature review of current concepts.
- Analysis of mechanisms linking inflammation, immunity, and insulin resistance.
- Focus on pediatric intensive care unit settings.
Main Results:
- Inflammation triggered by infection (sepsis) or injury (systemic inflammatory response syndrome) involves pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs).
- Nutrient-sensing pattern recognition receptors, activated by fatty acids, initiate inflammatory cascades impacting insulin signaling and causing insulin resistance.
- Lipotoxicity is increasingly recognized as a key factor in the development of insulin resistance.
Conclusions:
- Insulin resistance serves as an adaptive response, prioritizing energy for immune functions during infection or injury.
- Enhanced comprehension of the metabolism-inflammation-immunity nexus is vital.
- This understanding will facilitate optimized metabolic and immune interventions for critically ill children.
Related Concept Videos
01:24Type II Diabetes II: Pathophysiology
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
01:19Type I Diabetes III: Clinical Manifestations
Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
01:16Insulin: Dosing Regimen and Adverse Effects
Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
01:15Hypoglycemia and Glucagon
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin and C-peptide are co-secreted in...