Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polyunsaturated fatty acids are known to affect plasma lipids and lipoproteins but there is no information on the effect of essential fatty acid (EFA) deficiency on lipoprotein composition. The purpose of this study was to characterize lipoproteins from 17 cystic fibrosis (CF) patients in relationship to their EFA status (eicosatrienoic/arachidonic acid ratio) and compare them with those of 10 healthy siblings (SIB) and of 10 unrelated controls. In 7 EFA-deficient (EFAD) and 10 EFA-sufficient (EFAS) patients, hypocholesterolemia was associated with a decrease of HDL-cholesterol and of LDL-cholesterol which was more marked in the EFAD group. Similarly, although triglyceride enrichment of VLDL, LDL, HDL2, and HDL3 with a concomitant reduction of cholesteryl esters from all particles except HDL2 was observed in both CF groups, it was more sizable in the EFAD patients. These changes led to an increase in the particle size of VLDL, LDL, and HDL2 whereas the distribution of HDL3 was skewed to smaller particles. Alterations in the apoprotein composition of particles were greater in EFAD than in EFAS. A decrease of total postheparin lipolytic activity was observed in the two groups of CF patients as well as in siblings. It was entirely accounted for by hepatic lipase (mumol FFA/ml per h) which was more severely diminished in EFAD (2.8 +/- 0.6) than in EFAS (4.4 +/- 0.7) and SIB (5.1 +/- 0.5). Although the two groups of CF children differed in terms of growth, severity of malabsorption, and vitamin E status, these data suggest that disturbance of lipoprotein concentration, composition, size, and metabolism (hepatic lipase) may be in part related to EFA deficiency. Further studies are necessary to explore the effect of EFA deficiency on hepatic lipase activity.
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PMID:Relationship of decreased hepatic lipase activity and lipoprotein abnormalities to essential fatty acid deficiency in cystic fibrosis patients. 276 73

Malnutrition may cause to the damage intestinal epithelium and pancreas resulting in overt signs of malabsorption syndrome. The diet protein, fats and carbohydrates stimulate secretion, CCK-P, GIP, and gastrin release and effect insulin and HGH release. The amounts of the hormones released depends on intestinal absorption and pancreas secretory function. Therefore, in undernourished children with malabsorption syndrome on impaired function of the hormonal entero-insular axis is likely. In 30 children hormonal component of malnutrition was studied. Digestion and absorption were assayed by glycemic levels and FFA, with hydroxyprolinuria studies following administration of the mixed test meal. HGH and IRI levels were measured following mixed test meal stimulation. Hormonal studies data were correlated with digestion and absorption indices. In undernourished children low levels of HGH and IRI were frequently found. In certain patients with malnutrition the administration of anabolic drugs seems to be advisable.
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PMID:[Food stimulated release of IRI and HGH in children with malabsorption (author's transl)]. 610 40

Orlistat is a specific inhibitor of pancreatic and gastric lipases leading to decreased absorption of fat. In the present study, we measured the effect of orlistat on lymphatic fat transport in rats following intake of oils very different in FA composition and TAG structure, and compared this with the transport in normal rats and rats with fat malabsorption. Rats were subjected to cannulation of the main mesenteric lymph duct, and a feeding catheter was inserted into the stomach. In addition, malabsorbing rats were cannulated in the common bile and pancreatic duct. Emulsified safflower, fish, and randomized oils were administered, and lymph was collected for 24 h and analyzed for FA composition. Administration of 25 mg orlistat together with the dietary oils resulted in very small changes from baseline lymphatic transport, indicating that inhibition of the fat absorption was almost complete and furthermore that the source of fat had no influence on the inhibitory effect of orlistat. Orlistat did not interfere with the absorption of the hydrolysis products, since high absorption of sn-2 MAG and FFA (oleic acid) mixed with orlistat was observed. The baseline lymphatic transport in the orlistat group was higher than in the malabsorbing group, but this was the result of generally lower transport of endogenous FA in the malabsorbing group, presumably caused by the absence of bile FA. The transport of FA in normal rats was several-fold higher than the transport after orlistat addition and in malabsorbing rats. Thus, this study showed that orlistat inhibited fat hydrolysis, and thereby lymphatic absorption, almost completely independently of the fat administered.
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PMID:Effect of orlistat on fat absorption in rats: a comparison of normal rats and rats with diverted bile and pancreatic juice. 1466 68

Hedgehog (Hh) signaling plays an important role in embryonic development of many tissues, including the gastrointestinal tract. Sonic Hh-and Indian Hh-deficient mice die before or soon after birth, precluding further study of this signaling pathway in the mature intestine. Maternal transfer of inactivating monoclonal antibodies to Hh proteins (anti-Hh moAb) during late stages of embryogenesis or to early postnatal mice produced intestinal villous abnormalities, progressive runting, and severe malabsorption of dietary fat. In the present study, we sought to determine the effect of inhibiting Hh signaling on weight gain and lipid absorption in adult mice. Anti-Hh moAb was administered to adult Balb/c mice fed either a low-fat, nonpurified diet or a high-fat, semipurified diet, and to adult ob/ob mice fed the low-fat, nonpurified diet. Weight gain was significantly inhibited by anti-Hh moAb treatment in Balb/C mice fed the high-fat, but not the low-fat diet and in ob/ob mice. Further analysis of adult Balb/c mice fed the high-fat diet demonstrated that although total lipid absorption was normal, the rate of triglyceride absorption was significantly delayed in mice treated with anti-Hh moAb and they had significantly increased fecal FFA excretion. Hepatic steatosis, found in high-fat fed Balb/c mice treated with the control moAb, was abrogated by anti-Hh moAb administration. These findings point to a potential role for Hh signaling pathways in diet-induced abnormalities of lipid metabolism.
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PMID:Inhibition of Hedgehog signaling protects adult mice from diet-induced weight gain. 1551 62