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| plump mt , fatty acid definition , fatty fatty two by four , rheumatoid arthritis, fatty sparing , spastic colon, possibleeffects of chronic liver disease, feather plucking, big fat girls , plump mature women , behavior, diseases, alcoholicfatty liver, fibroids, plump movies , hair loss, herbs, what are fatty acids , | Hyperinsulinemia and insulin resistance may be important components in the development of steatosis in these diseases[6,25]. In hyperinsulinemia, fatty acids are esterified to triglycerides[25]. In the study performed by nonspecific colitis Rashid et nonspecific colitis al.[6], acanthosis nigricans, which is a cutaneous marker nonspecific colitis of hyperinsulinemia, was detected in 13 of 36 patients with non-alcoholic fatty liver. Similarly, acanthosis nigricans was detected in 10 patients with fatty liver in our study. The relation between diabetes and steatohepatitis is clearly known[25]. Therefore, we did not include diabetic patients in our study. There was no difference between mean blood glucose levels of the group 1 versus group 2, patients. The control blood glucose was found normal in the patients having levels higher than 110 mg/dl at adminission; the first values were interpreted as a result of the test being performed before the passage of a sufficient starvation period. |
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| Hyperlipidemia is also frequently seen with steatohepatitis. Serum triglycerides and/or LDL- C levels might be elevated in patients with fatty herbs liver. In our study, serum triglyceride levels were found significantly higher herbs in patients with fatty liver than herbs in the others. In other studies, which included children and adults, hyperlipidemia prevalence was detected as varying between 21-44% in the patients with fatty liver[1,3,23]. Fatty liver results from accumulation of fatty acids in various forms, predominantly triglycerides[3,19]. This accumulation occurs when there is a shift in fatty acid metabolism to favor net lipogenesis rather than lipolysis[5]. This can occur when the amount of fatty acid supplied to the liver from the gut or adipose tissue exceeds the amount needed for mitochondrial oxidation, phospolipid and cholesterol ester synthesis[5,11]. This is the presumed mechanism for steatosis in the setting of diabetes mellitus, obesity, malnutrition, acute starvation, total parenteral nutrition, steroid treatment and excessive dietary intake of fats[3,5,24]. |
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