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The in vivo Effects of Glucose and Lipid on the Granulocytes and Monocytes of Type 2 Diabetic Male Subjects
Author(s) -
Horvath Peter,
Oliver Stacy R.,
Zaldivar Frank P.,
RadomAizik Shlomit,
Galassetti Pietro R.
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.684.3
Subject(s) - cd14 , innate immune system , monocyte , medicine , endocrinology , cd16 , immune system , type 2 diabetes , integrin alpha m , hyperlipidemia , flow cytometry , diabetes mellitus , immunology , chemistry , cd8 , cd3
Atherosclerosis/cardiovascular disease are major causes of morbidity/mortality in type 2 diabetes (T2D), and have been associated with activation of innate immune cells, their diapedesis to the arterial intima, formation of the atherosclerotic plaque and release of thrombotic factors. While in T2D immune cell activation likely depends on dysregulated metabolic conditions, we have limited knowledge of the interaction between individual metabolic factor typical of T2D (hyperglycemia, hyperlipidemia), innate immune cell activation, and the progression of atherosclerosis. We therefore measured by flow cytometry cell surface expression of CD11b, CD14, CD16, CD62L and CD66b, known markers of granulocyte (Gc) and monocyte (Mc) activation, in 5 T2D subjects, during 4‐h i.v. infusions of glucose and lipids, performed separately or simultaneously. We hypothesized that both glucose and lipids would increase Gc/Mc surface marker expression, and simultaneous infusion would have a synergistic effect. Surprisingly, though, glucose only had little effect, while lipids, alone or combined with glucose, increased expression of several markers (such as CD11b in Gc, see figure, and in Mc). Our results suggest lipids may be stronger acute contributors to innate cell activation than glucose per se, possibly helping shape preventive dietary guidelines in T2D. Supported by NIH Grants P01HD048721 and UL1RR031985