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Increasing leptin sensitivity increases blood pressure in mice on a TH2 responsive background only
Author(s) -
Chantemele Eric J Belin
Publication year - 2012
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.26.1_supplement.1128.6
Subject(s) - leptin , endocrinology , medicine , cytokine , inflammation , t cell , aldosterone , secretion , tumor necrosis factor alpha , biology , chemistry , immune system , immunology , obesity
Besides inducing sympatho‐activation, leptin promotes T cell‐mediated pro‐inflammatory cytokines release. Since T cells play a key role in hypertension we hypothesized that increasing leptin sensitivity via protein tyrosine phosphatase 1B (PTP1B) deletion or increasing leptin concentration would promote inflammation and hypertension through a T cell dependent mechanism. PTP1B was deleted in mice on either a TH1 (C57) or a TH2 (Balb/C) T cell background. Blood pressure (BP) recording showed that PTP1B deletion and leptin infusion elevated BP in TH2 responsive mice only. As reflected by the BP response to ganglionic blockade, sympathetic tone was increased in response to PTP1B deletion and leptin in TH2 mice. Plasma aldosterone levels, indexes of the activation of the renin‐angiotensin‐aldosterone system were also increased in response to leptin and PTP1B deletion in TH2 mice. PTP1B deletion suppressed TH2‐derived anti‐inflammatory cytokine secretion (IL‐10, IL‐4) and increased TH1‐derived inflammatory cytokines (IL‐6, TNFα) production in TH2 mice. IL‐10 and TNFα secretion were not affected by PTP1B deletion in mice on TH1 responder background but levels of TH1 derived pro‐inflammatory cytokines (IL‐6, INFγ) were reduced. Taken together these data suggest that T cell background might influence BP response to leptin likely by controlling the inflammatory response to leptin.