Format

Send to

Choose Destination
BMJ Open Diabetes Res Care. 2016 Feb 15;4(1):e000136. doi: 10.1136/bmjdrc-2015-000136. eCollection 2016.

A role of the adaptive immune system in glucose homeostasis.

Author information

1
Department of Biology , Stanford University , Stanford, California , USA.
2
Departments of Pediatrics, Radiology, Microbiology & Immunology , Stanford University , Stanford, California , USA.

Abstract

OBJECTIVE:

The immune system, including the adaptive immune response, has recently been recognized as having a significant role in diet-induced insulin resistance. In this study, we aimed to determine if the adaptive immune system also functions in maintaining physiological glucose homeostasis in the absence of diet-induced disease.

RESEARCH DESIGN AND METHODS:

SCID mice and immunocompetent control animals were phenotypically assessed for variations in metabolic parameters and cytokine profiles. Additionally, the glucose tolerance of SCID and immunocompetent control animals was assessed following introduction of a high-fat diet.

RESULTS:

SCID mice on a normal chow diet were significantly insulin resistant relative to control animals despite having less fat mass. This was associated with a significant increase in the innate immunity-stimulating cytokines granulocyte colony-stimulating factor, monocyte chemoattractant protein 1 (MCP1), and MCP3. Additionally, the SCID mouse phenotype was exacerbated in response to a high-fat diet as evidenced by the further significant progression of glucose intolerance.

CONCLUSIONS:

These results support the notion that the adaptive immune system plays a fundamental biological role in glucose homeostasis, and that the absence of functional B and T cells results in disruption in the concentrations of various cytokines associated with macrophage proliferation and recruitment. Additionally, the absence of functional B and T cells is not protective against diet-induced pathology.

KEYWORDS:

Glucose Tolerance; Inflammation; Insulin Resistance; Type 2 Diabetes

Supplemental Content

Full text links

Icon for BMJ Publishing Group Icon for PubMed Central
Loading ...
Support Center