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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Cole, Banumathi K. Beydoun, Hind Lieb, David C. Haynes, Bronson A. Dobrian, Anca D. Fontana, Mark A. Brotman, Joshua J. Aye, Myo S. Hatcher, Margaret A. Wohlgemuth, Stephen D. Nadler, Jerry L. |
| Description | Author Affiliation: Lieb DC ( Departments of Internal Medicine (D.C.L., B.K.C., J.L.N.) and Physiological Sciences (J.J.B., M.A.H., M.S.A., B.A.H., A.D.D.) and Graduate Program in Public Health (H.B.), Eastern Virginia Medical School, Norfolk, Virginia 23507) |
| Abstract | CONTEXT: Visceral adipose tissue (VAT) is a key contributor to chronic inflammation in obesity. The 12/15-lipoxygenase pathway (ALOX) is present in adipose tissue (AT) and leads to inflammatory cascades that are causal for the onset of insulin resistance in rodent models of obesity. OBJECTIVE: The pathophysiology of the ALOX 12/15 pathway in human AT is unknown. We characterized the ALOX pathway in different AT depots in obese humans with or without type 2 diabetes (T2D). DESIGN: This study includes a cross-sectional cohort of 46 morbidly obese (body mass index >39 kg/m(2)) nondiabetic (n = 25) and T2D (n = 21) subjects. SETTING: This study was conducted at Eastern Virginia Medical School (Norfolk, Virginia) in collaboration with Sentara Metabolic and Weight Loss Surgery Center (Sentara Medical Group, Norfolk, Virginia). PATIENTS: Twenty-five obese (body mass index 44.8 ± 4.4 kg/m(2)) nondiabetic (hemoglobin A1c 5.83% ± 0.27%) and 21 obese (43.4 ± 4.1 kg/m(2)) and T2D (hemoglobin A1c 7.66% ± 1.22%) subjects were included in the study. The subjects were age matched and both groups had a bias toward female gender. MAIN OUTCOMES AND MEASURES: Expression of ALOX isoforms along with fatty acid substrates and downstream lipid metabolites were measured. Correlations with depot-specific inflammatory markers were also established. RESULTS: ALOX 12 expression and its metabolite 12(S)-hydroxyeicosatetraenoic acid were significantly increased in the VAT of T2D subjects. ALOX 15A was exclusively expressed in VAT in both groups. ALOX 12 expression positively correlated with expression of inflammatory genes IL-6, IL-12a, CXCL10, and lipocalin-2. CONCLUSIONS: ALOX 12 may have a critical role in regulation of inflammation in VAT in obesity and T2D. Selective ALOX 12 inhibitors may constitute a new approach to limit AT inflammation in human obesity. |
| ISSN | 0021972X |
| e-ISSN | 19457197 |
| DOI | 10.1210/jc.2013-4461 |
| Journal | The Journal of Clinical Endocrinology & Metabolism |
| Issue Number | 9 |
| Volume Number | 99 |
| Language | English |
| Publisher | Oxford University Press |
| Publisher Date | 2014-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Arachidonate 12-lipoxygenase Metabolism Arachidonate 15-lipoxygenase Diabetes Mellitus, Type 2 Enzymology Intra-abdominal Fat Obesity, Morbid Adolescent Genetics Biological Markers Cross-sectional Studies Immunology Fatty Acids Gene Expression Regulation, Enzymologic Hemoglobin A, Glycosylated Inflammation Lipid Metabolism Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Endocrinology Discipline Metabolism |
| Content Type | Text |
| Resource Type | Article |
| Subject | Biochemistry (medical) Biochemistry Clinical Biochemistry Endocrinology Endocrinology, Diabetes and Metabolism |
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