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)

The seasonal variations in circulating 25-hydroxycholecalciferol (25-HCC) were studied in 102 alcoholics with fatty liver disease without histologic signs of cirrhosis and in 35 patients with alcoholic cirrhosis. The mean levels were compared with those of normal persons. Alcoholics had generally lower 25-HCC values than the controls, particularly in the summer. This was primarily explained by insufficient diet and reduced exposure to sunshine. The ability of the liver to hydroxylate in the 25-position was studied in three groups of alcoholics with 1) fatty liver disease without cirrhosis, 2) compensated cirrhosis, 3) severely incompensated liver cirrhosis. All three groups exhibited a significant increase in serum 25-HCC following the peroral administration of cholecalciferol at a dose of 1 200 U daily for 7 days. Similar rises were seen 7 days after a single injection of 10 000 U cholecalciferol. This indicates a normal intestinal absorption of vitamin D, even in advanced alcoholic liver disease, and is inconsistent with a severely damaged 25-hydroxylation capacity in these patients. Osteomalacia due to impaired liver hydroxylation of vitamin D can hardly explain the increased fracture rate and the decreased bone mass, which have been described in alcoholics.
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PMID:The hepatic conversion of vitamin D in alcoholics with varying degrees of liver affection. 91 Jun 39

Compared to enteral or hypocaloric oral nutrition, the use of PN (parenteral nutrition) is not associated with increased mortality, overall frequency of complications, or longer length of hospital stay (LOS). The risk of PN complications (e.g. refeeding-syndrome, hyperglycaemia, bone demineralisation, catheter infections) can be minimised by carefully monitoring patients and the use of nutrition support teams particularly during long-term PN. Occuring complications are e.g. the refeeding-syndrome in patients suffering from severe malnutrition with the initiation of refeeding or metabolic, hypertriglyceridemia, hyperglycaemia, osteomalacia and osteoporosis, and hepatic complications including fatty liver, non-alcoholic fatty liver disease, cholestasis, cholecystitis, and cholelithiasis. Efficient monitoring in all types of PN can result in reduced PN-associated complications and reduced costs. Water and electrolyte balance, blood sugar, and cardiovascular function should regularly be monitored during PN. Regular checks of serum electrolytes and triglycerides as well as additional monitoring measures are necessary in patients with altered renal function, electrolyte-free substrate intake, lipid infusions, and in intensive care patients. The metabolic monitoring of patients under long-term PN should be carried out according to standardised procedures. Monitoring metabolic determinants of bone metabolism is particularly important in patients receiving long-term PN. Markers of intermediary, electrolyte and trace element metabolism require regular checks.
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PMID:Complications and monitoring - Guidelines on Parenteral Nutrition, Chapter 11. 2004 74

Human and mouse alkaline phosphatases (AP) are encoded by a multigene family expressed ubiquitously in multiple tissues. Gene knockout (KO) findings have helped define some of the precise exocytic functions of individual isozymes in bone, teeth, the central nervous system, and in the gut. For instance, deficiency in tissue-nonspecific alkaline phosphatase (TNAP) in mice (Alpl (-/-) mice) and humans leads to hypophosphatasia (HPP), an inborn error of metabolism characterized by epileptic seizures in the most severe cases, caused by abnormal metabolism of pyridoxal-5'-phosphate (the predominant form of vitamin B6) and by hypomineralization of the skeleton and teeth featuring rickets and early loss of teeth in children or osteomalacia and dental problems in adults caused by accumulation of inorganic pyrophosphate (PPi). Enzyme replacement therapy with mineral-targeting TNAP prevented all the manifestations of HPP in mice, and clinical trials with this protein therapeutic are showing promising results in rescuing life-threatening HPP in infants. Conversely, TNAP induction in the vasculature during generalized arterial calcification of infancy (GACI), type II diabetes, obesity, and aging can cause medial vascular calcification. TNAP inhibitors, discussed extensively in this book, are in development to prevent pathological arterial calcification. The brush border enzyme intestinal alkaline phosphatase (IAP) plays an important role in fatty acid (FA) absorption, in protecting gut barrier function, and in determining the composition of the gut microbiota via its ability to dephosphorylate lipopolysaccharide (LPS). Knockout mice (Akp3 (-/-)) deficient in duodenal-specific IAP (dIAP) become obese, and develop hyperlipidemia and hepatic steatosis when fed a high-fat diet (HFD). These changes are accompanied by upregulation in the jejunal-ileal expression of the Akp6 IAP isozyme (global IAP, or gIAP) and concomitant upregulation of FAT/CD36, a phosphorylated fatty acid translocase thought to play a role in facilitating the transport of long-chain fatty acids into cells. gIAP, but not dIAP, is able to modulate the phosphorylation status of FAT/CD36. dIAP, even though it is expressed in the duodenum, is shed into the gut lumen and is active in LPS dephosphorylation throughout the gut lumen and in the feces. Akp3 (-/-) mice display gut dysbiosis and are more prone to dextran sodium sulfate-induced colitis than wild-type mice. Of relevance, oral administration of recombinant calf IAP prevents the dysbiosis and protects the gut from chronic colitis. Analogous to the role of IAP in the gut, TNAP expression in the liver may have a proactive role from bacterial endotoxin insult. Finally, more recent studies suggest that neuronal death in Alzheimer's disease may also be associated with TNAP function on certain brain-specific phosphoproteins. This review recounts the established roles of TNAP and IAP and briefly discusses new areas of investigation related to multisystemic functions of these isozymes.
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PMID:Multisystemic functions of alkaline phosphatases. 2386 Jun 46

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease and abnormal liver enzyme worldwide. NAFLD is reported to be associated with other extra-hepatic diseases including cardiovascular disease, diabetes mellites and thyroid gland abnormalities. Liver is also the source of many proteins involved in bone metabolism and is the regulator of several bone metabolism pathways. Although underlying pathogenesis is not clear, the association between NAFLD and low bone mineral density (BMD) in the forms of osteoporosis and osteopenia has been recently reported. This study aimed to review current evidences supporting the association between bone metabolism including low BMD and serum vitamin D level in patients with NAFLD. Epidemiolocal studies indicating lower BMD and vitamin D in patients with NAFLD have been reviewed. The main pathophysiological mechanisms including association of insulin resistance, serum adiponectin, ghrelin, osteopontin, osteoprotegerin, and osteocalcin with NAFLD and low BMD have been briefly reviewed and summarized. Results of current clinical trials investigating the role of vitamin D supplementation for treatment of hepatic steatosis and non-alcoholic steatohepoatitis (NASH) have been also summarized. As a conclusion, increasing evidences are now available suggesting low BMD in patients with NAFLD. Some of these studies showed association of NAFLD severity with low vitamin D and BMD. Screening and surveillance of skeletal system regarding osteoporosis/osteomalacia in patients with NAFLD may be considered in future strategies and guidelines for NAFLD management.
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PMID:Bone metabolism in non-alcoholic fatty liver disease: vitamin D status and bone mineral density. 2797 61