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)

Central obesity is frequently associated with adipose tissue inflammation and hepatic insulin resistance. To identify potential individual mediators in this process, we used in vitro systems and assessed if insulin resistance in liver cells could be induced by secreted products from adipocytes preexposed to an inflammatory stimulus. Conditioned medium from 3T3-L1 adipocytes pretreated without (CM) or with TNFalpha (CM-TNFalpha) was used to treat Fao hepatoma cells. ELISAs were used to assess the concentration of several inflammatory mediators in CM-TNFalpha. CM-TNFalpha-treated Fao cells exhibited about 45% diminution in insulin-stimulated phosphorylation of insulin receptor, insulin receptor substrate proteins, protein kinase B, and glycogen synthase kinase-3 as compared with CM-treated cells, without changes in the total abundance of these protein. Insulin increased glycogenesis by 2-fold in CM-treated Fao cells but not in cells exposed to CM-TNFalpha. Expression of IL-1beta mRNA was elevated 3-fold in TNFalpha-treated adipocytes, and CM-TNFalpha had 10-fold higher concentrations of IL-1beta but not TNFalpha or IL-1alpha. IL-1beta directly induced insulin resistance in Fao, HepG2, and in primary rat hepatocytes. Moreover, when TNFalpha-induced secretion/production of IL-1beta from adipocytes was inhibited by the IL-1 converting enzyme (ICE-1) inhibitor II (Ac-YVAD-CMK), insulin resistance was prevented. Furthermore, liver-derived cells treated with IL-1 receptor antagonist were protected against insulin resistance induced by CM-TNFalpha. Finally, IL-1beta secretion from human omental fat explants correlated with body mass index (R(2) = 0.639, P < 0.01), and the resulting CM induced insulin resistance in HepG2 cells, inhibitable by IL-1 receptor antagonist. Our results suggest that adipocyte-derived IL-1beta may constitute a mediator in the perturbed cross talk between adipocytes and liver cells in response to adipose tissue inflammation.
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PMID:Interleukin-1beta may mediate insulin resistance in liver-derived cells in response to adipocyte inflammation. 2066 63

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

Low grade inflammation has been linked to risk of type 2 diabetes and atherosclerotic vascular diseases. Obesity and, in particular, abdominal obesity increase the risk of diabetes and atherosclerotic vascular diseases. One of the mechanisms could be low grade inflammation and vascular endothelial dysfunction. Permanent weight reduction is the first line of treatment both for obese individuals at increased risk of diabetes and for newly onset type 2 diabetes. Weight reduction lowers the level of several inflammatory factors in the body while increasing the level of adiponectin. Besides weight reduction the quality of diet and physical activity also modifies low grade inflammation. Based on the literature survey and our own studies in humans, it is possible to have dietary patterns that reduce inflammatory stress in the body and improves vascular endothelial dysfunction. There is strong evidence to suggest that IL-1 Ra is a very sensitive marker of low grade inflammation in obesity and related phenotypes; however, its level is markedly lowered by weight reduction and by choosing foods that have been shown to reduce inflammatory stress in the body.
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PMID:Diet, inflammation and prediabetes-impact of quality of diet. 2450 May 60