Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psoriasis is a chronic, relapsing, inflammatory - proliferative disease, belonging to the group of autoimmune disorders. Although the disease process concerns mainly the skin, this is a systemic inflammation. In psoriasis there is an increased synthesis of proinflammatory proteins, such as: C-reactive protein (CRP), interleukin 1 (IL-1), IL-2, IL-6, IL-8, tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), alpha2-macroglobulin, alpha1-antitrypsin and ceruloplasmin. Many studies have shown increased incidence of the metabolic syndrome in patients with psoriasis. There is also relationship between severity of psoriasis and severity of the various components of metabolic syndrome (impaired glucose tolerance or diabetes, abdominal obesity, atherogenic dyslipidemia and hypertension). Chronic inflammation seems to be a link between psoriasis and various components of metabolic syndrome. Proinflammatory cytokines may cause atherosclerosis, insulin resistance, hypertension and type 2 diabetes. Presence of obesity and particular components of the metabolic syndrome may also play an important role in the pathogenesis of chronic kidney disease in patients with psoriasis. The primary intervention in patients with psoriasis and metabolic syndrome in order to reduce cardiovascular risk are lifestyle modifications, i.e. increased physical activity and dietary treatment of obesity, in combination with pharmacotherapy of particular components of metabolic syndrome.
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PMID:[Metabolic disorders in patients with psoriasis]. 2251 79

Midlife obesity is a risk factor of late onset Alzheimer's disease (LOAD) but why this is the case remains unknown. As systemic inflammation is involved in both conditions, obesity-related neuroinflammation may contribute to damage in limbic structures important in LOAD. Here, we investigated the hypothesis that systemic inflammation would mediate central obesity related effects on limbic tissue microstructure in 166 asymptomatic individuals (38-71 years old). We employed MRI indices sensitive to myelin and neuroinflammation [macromolecular proton fraction (MPF) and kf] from quantitative magnetization transfer (qMT) together with indices from neurite orientation dispersion and density imaging (NODDI) to investigate the effects of central adiposity on the fornix, parahippocampal cingulum, uncinate fasciculus (compared with whole brain white matter and corticospinal tract) and the hippocampus. Central obesity was assessed with the Waist Hip Ratio (WHR) and abdominal visceral and subcutaneous fat area fractions (VFF, SFF), and systemic inflammation with blood plasma concentrations of leptin, adiponectin, C-reactive protein and interleukin 8. Men were significantly more centrally obese and had higher VFF than women. Individual differences in WHR and in VFF were negatively correlated with differences in fornix MPF and kf, but not with any differences in neurite microstructure. In women, age mediated the effects of VFF on fornix MPF and kf, whilst in men differences in the leptin and adiponectin ratio fully mediated the effect of WHR on fornix MPF. These results suggest that visceral fat related systemic inflammation may damage myelin-related properties of the fornix, a key limbic structure known to be involved in LOAD.
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PMID:Sex-specific effects of central adiposity and inflammatory markers on limbic microstructure. 3073 26