Related Experiment Video
Updated: Jul 19, 2026
08:32
Extraction of Tissue Antigens for Functional Assays
Published on: September 10, 2012
Dietary insulin as an immunogen and tolerogen
Minna Tiittanen1, Johanna Paronen, Erkki Savilahti
1Department of Viral Diseases and Immunology, Laboratory for Immunology, National Public Health Institute, Helsinki, Finland. minna.tiittanen@ktl.fi
Summary
Human insulin in breast milk may protect infants from developing an immune response to cow
Area of Science:
- Immunology
- Pediatrics
- Endocrinology
Background:
- Cow's milk (CM) formula containing bovine insulin (BI) can trigger an immune response in infants.
- The role of human insulin (HI) in breast milk in modulating this immune response is unclear.
- Maternal diabetes may influence insulin levels in breast milk.
Purpose of the Study:
- To investigate the immunomodulatory role of human insulin (HI) in breast milk.
- To assess the relationship between breast milk insulin levels and infant immune responses to insulin.
- To examine the impact of maternal diabetes on breast milk insulin concentration.
Main Methods:
- Analysis of maternal breast milk samples from 128 infants in the TRIGR pilot study.
- Measurement of insulin concentration in breast milk and IgG antibodies to BI in infant plasma.
- Comparison of immune responses in infants fed CM formula versus casein hydrolysate.
Main Results:
- Higher insulin levels were found in breast milk of mothers with type 1 diabetes.
- Breast milk insulin concentration inversely correlated with IgG antibodies to BI in infants.
- Higher breast milk insulin levels were associated with lower risk of beta-cell autoimmunity.
Conclusions:
- Human insulin (HI) in breast milk appears to be tolerogenic, potentially downregulating immune responses to dietary bovine insulin (BI).
- Bovine insulin (BI) in cow's milk (CM) formula induces a stronger IgG response than HI in breast milk.
- However, breast milk insulin did not promote tolerance in infants who developed beta-cell autoimmunity.
Related Concept Videos
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...
01:27Insulin Formulations: Types and Delivery
Insulin preparations are categorized by their duration of action into short-acting and long-acting types. Two strategies are used to modify insulin's absorption and pharmacokinetic profile: slowing the absorption post-subcutaneous injection, or altering human insulin's amino acid sequence or protein structure. These changes retain the insulin's ability to bind to the insulin receptor, but alter its behavior in solution or after injection.
Short-acting insulins are divided into rapid-acting...
Short-acting insulins are divided into rapid-acting...
01:25Insulin: Biosynthesis, Chemistry, and Preparation
The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
01:24Glucagon-like Receptor Agonists
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
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...
01:12Type I Diabetes I: Introduction
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...