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Inflammation and sexual dimorphism in development of insulin resistance: a dual animal model comparison
Author(s) -
Wintrob Zachary A.P.,
Oppong Emmanuel K.,
Tse Yu C.,
Welt Jeffery M.,
Boateng Hans R.,
Drumea Ioana,
Martorana Michael,
Irlam John,
LeVea Charles M.,
Faitar Silviu L.,
Ceacareanu Alice C.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.918.2
Subject(s) - insulin resistance , adipokine , leptin , medicine , endocrinology , adiponectin , adipose tissue , inflammation , sexual dimorphism , insulin , obesity
Severe combined immunodeficiency (SCID) and immunocompetent BALBc mice strains may constitute resourceful model‐candidates for revealing inflammation‐mediated mechanisms involved in high fat diet (HFD) induced insulin resistance (IR). This study included 32 animals in groups of 4 for all combinations of male (M), female (F), BALBc, SCID, low fat diet (LFD, 4.1% fat), and HFD (35% fat) for a total of 21 weeks. All groups switched to 10% fat, between week 12 and 15. Biweekly fasting levels of adipokines, inflammatory cytokines and growth factors were assessed. IR was verified by glucose tolerance test at week 13. By week 13 the HFD‐SCID‐F neither gained weight, nor developed IR; HFD‐BALBc‐F gained weight but did not develop IR, while all HFD‐Ms both gained weight and developed IR. Ultimately the HFD‐SCID‐F gained ~4g and had low insulin levels, while all other HFD groups gained ~10g and had 4–7 fold higher fasting insulin. Adiponectin (ADP) spiked at 3 weeks and remained elevated in HFD‐BALBc‐F. Switching food resulted in upward‐trending insulin reversing only in BALBc‐M and upward‐trending leptin decreased in all but SCID‐F. Liver pathology associated fatty liver disease with IR in HFD. Concomitant evaluation of these models suggests a combined contribution of inflammation and sexual dimorphism in developing IR. Further research may clarify whether ADP is a mediator of this mechanism.