Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although increased dietary fat or cholesterol has been reported to be a risk factor for the development of certain cancers, the effect of the serum lipid level on tumor metastasis has not been well documented. Fasting serum levels of total cholesterol (TC) and triglycerides (TG) were examined in 54 patients with superficial esophageal cancer (SEC) invading lamia musucularis or submucosal layer who underwent esophagectomy with classical lymphadenectomy. The association between lymph node metastasis and the preoperative serum lipid levels as well as the pathological findings was retrospectively analyzed. The levels of TC and TG were significantly higher in 18 node-positive than in 36 node-negative patients (TC: 205.4+/-38.9 vs. 174.5+/-26.8 mg/dl, P<0.01; TG: 152.0+/-68.5 vs. 88.7+/-28.6 mg/dl, P<0.001). Patients with hypercholesterolemia (TC >/= 220 mg/dl) and hypertriglyceridemia (TG >/= 150 mg/dl) showed extremely high rates of nodal metastasis (80 and 91%, respectively), that were significantly higher than those of patients with normal lipid levels (P<0.01 and P<0.001). When hyperlipidemia was defined as the presence of either hypertriglyceridemia or hypercholesterolemia, hyperlipidemia was an independent risk factor for nodal metastasis in SEC. Elevated serum lipid levels might bring favorable circumstances for the development of lymph node metastasis in the early stage of EC. Hyperlipidemia might prompt us to perform more studies to investigate possible metastasis.
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PMID:Hyperlipidemia is a risk factor for lymphatic metastasis in superficial esophageal carcinoma. 1510 44

An increased risk of colorectal cancer (CRC) is associated with a western style diet, particularly hyperlipidemia. The expression of G-protein coupled receptor 40 (GPR40), a membrane-bound receptor for long-chain fatty acids (LCFAs), was examined in 36 cases of subserosal-invading CRC and compared with clinicopathological parameters as well as triglyceride (TG) and low-density lipoprotein (LDL) levels in the blood. All patients with CRC expressed GPR40, which was positively associated with blood TG levels (P<0.0001) but not with blood LDL levels. GPR40 expression was positively associated with nodal metastasis, distant metastasis (particularly to the liver), stage and poor prognosis. Patients with high GPR40 expression and high TG levels had comparatively worse survival outcomes compared with patients with low GPR40 expression and low TG levels. The results of the present study suggest that activation of GPR40 may be associated with the progression and prognosis of CRCs. High levels of GPR40 and/or concurrent high levels of GPR40 and TG may be a risk for CRC progression.
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PMID:Expression of long-chain fatty acid receptor GPR40 is associated with cancer progression in colorectal cancer: A retrospective study. 2980 99

Our understanding of the role of the vascular endothelium has evolved over the past 2 decades, with the recognition that it is a dynamically regulated organ and that it plays a nodal role in a variety of physiological and pathological processes. Endothelial cells (ECs) are not only a barrier between the circulation and peripheral tissues, but also actively regulate vascular tone, blood flow, and platelet function. Dysregulation of ECs contributes to pathological conditions such as vascular inflammation, atherosclerosis, hypertension, cardiomyopathy, retinopathy, neuropathy, and cancer. The close anatomic relationship between vascular endothelium and highly vascularized metabolic organs/tissues suggests that the crosstalk between ECs and these organs is vital for both vascular and metabolic homeostasis. Numerous reports support that hyperlipidemia, hyperglycemia, and other metabolic stresses result in endothelial dysfunction and vascular complications. However, how ECs may regulate metabolic homeostasis remains poorly understood. Emerging data suggest that the vascular endothelium plays an unexpected role in the regulation of metabolic homeostasis and that endothelial dysregulation directly contributes to the development of metabolic disorders. Here, we review recent studies about the pivotal role of ECs in glucose and lipid homeostasis. In particular, we introduce the concept that the endothelium adjusts its barrier function to control the transendothelial transport of fatty acids, lipoproteins, LPLs (lipoprotein lipases), glucose, and insulin. In addition, we summarize reports that ECs communicate with metabolic cells through EC-secreted factors and we discuss how endothelial dysregulation contributes directly to the development of obesity, insulin resistance, dyslipidemia, diabetes mellitus, cognitive defects, and fatty liver disease.
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PMID:Emerging Roles of Vascular Endothelium in Metabolic Homeostasis. 3035 49