Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolactin responses to provocative thyrotropin-releasing factor (TRH) stimulation were evaluated in 43 chronic alcoholic men were divided into groups for analysis based on the presence or absence of gynecomastia and the histologic appearance of their livers as determined by percutaneous liver biopsy. Compared to the normal volunteers, alcoholics with reversible liver disease (fatty liver) had reduced basal prolactin levels and exaggerated TRH responses. In contrast, alcoholics with cirrhosis and gynecomastia had markedly elevated basal prolactin levels and reduced responses to TRH. The results of this study combined with previously reported findings in cirrhotic men provide a basis for a possible explanation for the signs of feminization frequently found in alcoholic men.
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PMID:Hyperprolactinemia and thyrotropin-releasing factor (TRH) responses in men with alcoholic liver disease. 10 34

Oestrone (E1), oestradiol (E2), testosterone (T), androstenedione (A) and cortisol (F) as well as LH and the percentage of binding of E1, E2, T and F in plasma were measured and compared in normal young and old male subjects and in male patients with fatty liver, chronic hepatitis and cirrhosis of the liver. The alterations seen were most marked in the cirrhotic patients, but were partially also found in patients with fatty liver and in normal old subjects: a definite increase in E1, a smaller increase in E2, a decrease in T and a rise in LH. F remained unchanged. The ratios of E2/T and E1/T were higher in cirrhotic patients than in healthy young subjects. As the percentage of bound T in plasma rose, the oestrogen/androgen imbalance was greater in patients with liver disease and in old subjects than the ratio of total hormone plasma concentration indicates. The biological relevance of the extremely high E1 plasma concentrations in patients with cirrhosis of the liver is not known. It is suggested that the combination of elevated E1 and E2 and reduced T, which is strongly bound by increased sexual hormone binding globulin (SHBG) may be responsible for gynaecomastia and hypogonadism in chronic liver diseases. As similar alterations of steroid plasma concentrations and their binding to plasma proteins are found both in patients with liver disease and in old men, these changes may be caused by the same mechanism: namely an altered liver function.
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PMID:Steroid hormones and their binding in plasma of male patients with fatty liver, chronic hepatitis and liver cirrhosis. 117 87

The insulin resistance syndrome (syndrome X, metabolic syndrome) has become the major health problem of our times. Associated obesity, dyslipidemia, atherosclerosis, hypertension, and type 2 diabetes conspire to shorten life spans, while hyperandrogenism with polycystic ovarian syndrome affect the quality of life and fertility of increasing numbers of women. Whereas a growing number of single genetic diseases affecting satiety or energy metabolism have been found to produce the clinical phenotype, strong familial occurrences, especially in racially prone groups such as those from the Indian subcontinent, or individuals of African, Hispanic, and American Indian descents, together with emerging genetic findings, are revealing the polygenetic nature of the syndrome. However, the strong lifestyle factors of excessive carbohydrate and fat consumption and lack of exercise are important keys to the phenotypic expression of the syndrome. The natural history includes small for gestational age birth weight, excessive weight gains during childhood, premature pubarche, an allergic diathesis, acanthosis nigricans, striae compounded by gynecomastia, hypertriglyceridemia, hepatic steatosis, premature atherosclerosis, hypertension, polycystic ovarian syndrome, and focal glomerulonephritis appearing increasingly through adolescence into adulthood. Type 2 diabetes, which develops because of an inherent and/or an acquired failure of an insulin compensatory response, is increasingly seen from early puberty onward, as is atheromatous disease leading to coronary heart disease and stroke. A predisposition to certain cancers and Alzheimer's disease is also now recognized. The looming tragedy from growing numbers of individuals affected by obesity/insulin resistance syndrome requires urgent public health approaches directed at their early identification and intervention during childhood. Such measures include educating the public on the topic, limiting the consumption of sucrose-containing drinks and foods with high carbohydrate and fat contents, and promoting exercise programs in our nation's homes and schools.
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PMID:Insulin resistance syndrome in children. 1518 Oct 20