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)

Neonatal rats of the Holtzman strain, 6 days of age, were fed a myo-inositol restricted liquid formula by gastric intubation for 10 days, after which they were fed a purified myo-inositol-free diet until they were 72 days old. No differences in weight gain were observed between myo-inositol/100 ml of formula or 150 mg myo-inositol/100 g diet. Most tissues examined from rats fed the myo-inositol deprived formula and diet had lower free myo-inositol levels than the controls with the exception of the liver. Despite reduced free and lipid-bound myo-inositol in the liver, there was no evidence of fatty liver in the young rats at any age. The cerebrum and cerebellum of myo-inositol deprived rats had normal myelination and mitochondriogenesis as judged by the levels of 2',3'-cyclic nucleotide-3'-phosphohydrolase (EC 3.1.4.1) and fumarase (EC 4.2.1.2) activity, respectively.
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PMID:myo-Inositol metabolism in the neonatal and developing rat fed a myo-inositol-free diet. 18 43

Obesity and type 2 diabetes are associated with impaired mitochondrial function in adipose tissue. To study the effects of primary deficiency of mitochondrial energy metabolism in fat, we generated mice with adipose-specific deficiency of fumarate hydratase (FH), an integral Krebs cycle enzyme (AFHKO mice). AFHKO mice have severe ultrastructural abnormalities of mitochondria, ATP depletion in white adipose tissue (WAT) and brown adipose tissue, low WAT mass with small adipocytes, and impaired thermogenesis with large unilocular brown adipocytes. AFHKO mice are strongly protected against obesity, insulin resistance, and fatty liver despite aging and high-fat feeding. AFHKO white adipocytes showed normal lipolysis but low triglyceride synthesis. ATP depletion in normal white adipocytes by mitochondrial toxins also decreased triglyceride synthesis, proportionally to ATP depletion, suggesting that reduced triglyceride synthesis may result nonspecifically from adipocyte energy deficiency. At thermoneutrality, protection from insulin resistance and hepatic steatosis was diminished. Taken together, the results show that under the cold stress of regular animal room conditions, adipocyte-specific FH deficiency in mice causes mitochondrial energy depletion in adipose tissues and protects from obesity, hepatic steatosis, and insulin resistance, suggesting that in cold-stressed animals, mitochondrial function in adipose tissue is a determinant of fat mass and insulin sensitivity.
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PMID:Adipose-Specific Deficiency of Fumarate Hydratase in Mice Protects Against Obesity, Hepatic Steatosis, and Insulin Resistance. 2755 70