PMID- 27026807
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160330
LR  - 20181113
IS  - 2052-4897 (Print)
IS  - 2052-4897 (Electronic)
IS  - 2052-4897 (Linking)
VI  - 4
IP  - 1
DP  - 2016
TI  - A role of the adaptive immune system in glucose homeostasis.
PG  - e000136
LID - 10.1136/bmjdrc-2015-000136 [doi]
LID - e000136
AB  - 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.
FAU - Bronsart, Laura L
AU  - Bronsart LL
AD  - Department of Biology , Stanford University , Stanford, California , USA.
FAU - Contag, Christopher H
AU  - Contag CH
AD  - Departments of Pediatrics, Radiology, Microbiology & Immunology , Stanford 
      University , Stanford, California , USA.
LA  - eng
GR  - R24 DK096465/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20160215
PL  - England
TA  - BMJ Open Diabetes Res Care
JT  - BMJ open diabetes research & care
JID - 101641391
PMC - PMC4800071
OTO - NOTNLM
OT  - Glucose Tolerance
OT  - Inflammation
OT  - Insulin Resistance
OT  - Type 2 Diabetes
EDAT- 2016/03/31 06:00
MHDA- 2016/03/31 06:01
PMCR- 2016/02/15
CRDT- 2016/03/31 06:00
PHST- 2015/07/21 00:00 [received]
PHST- 2015/11/03 00:00 [revised]
PHST- 2015/11/06 00:00 [accepted]
PHST- 2016/03/31 06:00 [entrez]
PHST- 2016/03/31 06:00 [pubmed]
PHST- 2016/03/31 06:01 [medline]
PHST- 2016/02/15 00:00 [pmc-release]
AID - bmjdrc-2015-000136 [pii]
AID - 10.1136/bmjdrc-2015-000136 [doi]
PST - epublish
SO  - BMJ Open Diabetes Res Care. 2016 Feb 15;4(1):e000136. doi: 
      10.1136/bmjdrc-2015-000136. eCollection 2016.