Changes in red cell insulin receptors during recovery from severe malnutrition

H M Payne-Robinson1, H G Coore, M H Golden

  • 1Department of Biochemistry, University of the West Indies, Kingston, Jamaica.

Insights

Malnourished children showed reduced red blood cell insulin binding and receptor affinity. Nutritional recovery, particularly with increased protein and energy intake, improved both insulin binding and affinity, suggesting a link to carbohydrate intolerance during malnutrition.

Area of Science:

  • Endocrinology
  • Nutritional Science
  • Pediatrics

Background:

  • Severe malnutrition impacts metabolic processes, including insulin signaling.
  • Understanding insulin receptor dynamics during recovery is crucial for pediatric nutrition.

Purpose of the Study:

  • To investigate red cell insulin binding characteristics in malnourished Jamaican children during different recovery phases.
  • To examine the relationship between nutritional intake, weight gain, and insulin receptor parameters.

Main Methods:

  • Studied 13 children (4-24 months) across malnutrition, early recovery, late recovery, and anthropometric recovery phases.
  • Measured red cell-specific insulin binding (SB), insulin receptor affinity (K), receptor number (S), plasma insulin (IN), plasma glucose (G), weight gain rate (RW), energy intake (EN), and protein intake (PR).
  • Utilized analyses of variance and multiple regression for longitudinal and cross-sectional analyses.

Main Results:

  • Red cell insulin binding (SB) and receptor affinity (K) were significantly lower in malnourished (MAL) children compared to recovery phases (GI, GII).
  • Insulin receptor number (S) was high in malnutrition and decreased with recovery, though not significantly.
  • Plasma insulin (IN) increased during recovery, and SB was positively associated with protein and energy intake, and receptor number.

Conclusions:

  • Severe malnutrition is associated with low red cell insulin receptor affinity.
  • Nutritional rehabilitation, especially increased protein and energy intake, enhances insulin receptor affinity and specific binding.
  • The observed negative correlation between insulin binding and glucose during malnutrition may indicate carbohydrate intolerance.

Related Concept Videos

Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: 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...
Type I Diabetes II: Pathophysiology01:26

Type 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...
Type I Diabetes III: Clinical Manifestations01:19

Type 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...
Type II Diabetes II: Pathophysiology01:24

Type 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.