Critical Care |

Resistin: The Link From Fatty Inflammation to Macrophages FREE TO VIEW

Ahmad Al Hariri, MD; Betty Herndon, PhD; Agostino Molteni, MD
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University of Missouri Kansas City SOM, Kansas City, MO

Chest. 2013;144(4_MeetingAbstracts):395A. doi:10.1378/chest.1704483
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SESSION TITLE: Non Pulmonary Critical Care

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Monday, October 28, 2013 at 07:30 AM - 09:00 AM

PURPOSE: Obesity is recognized as a low grade inflammatory state, and inflammatory cytokines found in fat macrophages have body-wide clinical consequences. Our pilot effort studied obese mice for input to lung health by the systemic inflammation of obesity. Ten OB/OB mice were given TNFα receptor blocker for 60 days, leaving 10 OB/OB mice untreated. Group differences in inflammatory macrophages (mφ) in adipocytes and lung were counted (F4/80 stain). The mφ in fat decreased significantly with TNFα-r blocker treatment, those in the lung did not .

METHODS: Resistin, an adipokine with physiologic and inflammatory involvement is reported here. It induces expression of TNFα and is expressed abundantly in mouse fat cells but not human adipocytes where it occurs primarily in macrophages (F4/80 stained inflammatory mφ were counted in our pilot study). With the hypothesis that the metabolic effects of resistin relate to inflammatory mφ in both mice and humans, tissue and sera of 40 OB/OB mice were measured for resistin: 10 untreated, 10 received TNFα receptor blocker, 10 omega 3 fatty acid, 10 anti-inflammatory; the latter two treatments were added to the rodent diets.

RESULTS: Resistin in murine sera, known to be released from white fat, was significantly elevated by both TNFα-r blocker injections and the anti-inflammatory in diet (<0.001) but not by omega 3 fatty acid. Tissue homogenate showed a small increase by TNFα-r block only (p=0.42, n.s.)

CONCLUSIONS: Serum resistin increases with anti-inflammatory input in the mouse model; two types of anti-inflammatory interventions produced significant serum increases. The pilot study shows the cytokine-releasing mφ in fat (but not lung!) respond to immunosuppression. We continue considering resistin genetic similarity in mouse vs man, and the input of inflammatory mφ markers to organs of both.

CLINICAL IMPLICATIONS: Insulin resistance lacks mechanistic clarification. Resistin appears important by: Resistin contribution to murine insulin resistance; genetic similarity between human and murine resistin; resistin in organ specificity (lung, fat) of TNFα- secreting inflammatory mφ.

DISCLOSURE: The following authors have nothing to disclose: Ahmad Al Hariri, Betty Herndon, Agostino Molteni

We are using obese inbred mice and their organs and sera at necropsy are being measured for cytokines/chemokines. This is a model of human disease. Study is cleared by the University Animal care and use committee, protocol 1029.




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