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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A balanced intake of alimentary lipids is necessary for calcium and phosphorus absorption, as for growth and calcification of bone. In lipid deprivation or excess, important disorders of phospho-calcic metabolism appear particularly in young growing subjects. The qualitative content of ingested fats has, too, a great influence : lipids containing short and medium-chain fatty acids, essential fatty acids and oleic acid stimulate calcium absorption. An excess of long chain and saturated lipids, or intake of erucic acid depress calcium absorption and retention. These facts are possible pathophysiological mechanisms in human disorders: The so-called humanized milks are close to human milk regarding their capacity of stimulation of phospho-calcic absorption and growth. In these milks, oleic and linoleic triglyceride level must be increased. In adult pathology, lipidic deficiency of steatorrhea is partially responsible for calcium and vitamin D malabsorption. Conversely, lipid-calcium interactions are not one-way, and an elevated dietary calcium depresses saturated lipid absorption, and has a hypolipemic action interesting in prevention of atherosclerosis of aged patients.
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PMID:[Lipid calcium interactions in experimental and human nutrition (author's transl)]. 77 52

The intestine synthesizes very low density lipoproteins (VLDL) and chylomicrons (CM) to transport fat and fat-soluble vitamins into the blood. VLDL assembly occurs constitutively whereas CM assembly is a characteristic property of the enterocytes during the postprandial state. The secretion of CM is specifically inhibited by Pluronic L81. CM are very heterogeneously-sized particles that consist of a core of triglycerides (TG) and cholesterol esters and a monolayer of phospholipids (PL), cholesterol and proteins. The fatty acid composition of TG, but not PL, in CM mirrors the fatty acid composition of fat in the diet. CM assembly is deficient in abetalipoproteinemia and CM retention disease. Abetalipoproteinemia results due to mutation in the mttp gene and is characterized by the virtual absence of apoB-containing lipoproteins in the plasma. Patients suffer from neurologic disorders, visual impairment, and exhibit acanthocytosis. CM retention disease, an inherited recessive disorder, is characterized by chronic diarrhea with steatorrhea in infancy, abdominal distention and failure to thrive. It is caused by a specific defect in the secretion of intestinal lipoproteins; secretion of lipoproteins by the liver is not affected. Besides human disorders, mice that do not assemble intestinal lipoproteins have been developed. These mice are normal at birth, but defective in fat and fat-soluble vitamin absorption, and fail to thrive. Thus, fat and fat-soluble vitamin transport by the intestinal lipoproteins is essential for proper growth and development of neonates. Recently, differentiated Caco-2 cells and rabbit primary enterocytes have been described that synthesize and secrete CM. These cells can be valuable in distinguishing between the two different models proposed for the assembly of CM. In the first model, the assembly of VLDL and CM is proposed to occur by two 'independent' pathways. Second, CM assembly is proposed to be a product of 'core expansion' that results in the synthesis of lipoproteins of different sizes. According to this model, intestinal lipoprotein assembly begins with the synthesis of 'primordial' lipoprotein particles and involves release of the nascent apoB with PL derived from the endoplasmic reticulum (ER) membrane. In addition, TG-rich 'lipid droplets' of different sizes are formed independent of apoB synthesis. The fusion of lipid droplets and primordial lipoproteins results in the formation of different size lipoproteins due to the 'core expansion' of the primordial lipoproteins.
Atherosclerosis 2000 Jan
PMID:A proposed model for the assembly of chylomicrons. 1058 Jan 65

We report the clinical phenotype in three kindreds with familial heterozygous hypobetalipoproteinemia (FHBL) carrying novel truncated apolipoprotein Bs (apoBs) of different sizes (apoB-8.15, apoB-33.4 and apoB-75.7). In D.A. kindred, we found three carriers of a C-deletion in exon 10 leading to the synthesis of apoB-8.15 not detectable in plasma. They showed steatorrhea and fatty liver. In N.L. kindred, the proband is heterozygous for a nonsense mutation in exon 26, leading to the formation of apoB-33.4. He had premature cerebrovascular disease and fatty liver; two apoB-33.4 carriers in this kindred showed only fatty liver. In B.E. kindred, the proband is heterozygous for a T-deletion in exon 26, which converts tyrosine at codon 3435 into a stop codon, resulting in apoB-75.7. The proband, a heavy alcohol drinker, had steatohepatitis, whereas his teetotaller daughter, an apoB-75.7 carrier, had no detectable fatty liver. This study suggests that: i) fatty liver invariably develops in FHBL carriers of short and medium-size truncated apoBs (< apoB-48), but its occurrence needs additional environmental factors in carriers of longer apoB forms; ii) intestinal lipid malabsorption develops only in carriers of short truncated apoBs, which are not secreted into the plasma; and iii) cerebrovascular disease due to premature atherosclerosis may occur even in FHBL subjects.
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PMID:Phenotypic expression of familial hypobetalipoproteinemia in three kindreds with mutations of apolipoprotein B gene. 1159 Feb 10

Pancreatic exocrine insufficiency (PEI) is one of the long-term consequences of chronic pancreatitis (CP). Majority of patients with PEI were undiagnosed or undertreated. Inadequately treated or subclinical severe PEI causes malnutrition and may pose the patients at risk of premature atherosclerosis and cardiovascular events. Indication of pancreatic enzyme replacement therapy (PERT) is patients with severe PEI, as indicated by the presence of steatorrhea, diarrhea, weight loss, fecal fat > 7 g/day, (13) C-mixed triglyceride breath test < 29%, fecal elastase < 100 ug/g stool, imaging or endoscopic findings of pancreatic ductal dilatation or calculi, and eight endosonographic criteria of CP. The mainstay treatment of PEI is PERT. Dietary fat restriction is unnecessary. PERT with lipase > 40,000 U per meal is recommended. Enteric-coating may be preferred to conventional enzymes because of the availability of high-dose preparations and no need of acid suppression co-therapy. Administration of enzymes with meals is proven to be the most effective regimen. Response to PERT should be measured by the improvement of patients' symptoms, nutritional status, and, in selected cases, by fecal fat or (13) C-mixed triglyceride breath test. Patients unresponsive to PERT should be checked for compliance, increase the dose of lipase to 90,000 units/meal or co-therapy with proton pump inhibitor. In patient with previous gastrointestinal surgery that may interfere enzyme-food mixing, opening the capsules and administering the enzyme granules with meals. Finally, search for small intestinal bacterial overgrowth syndrome and other causes of small bowel malabsorption.
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PMID:Maldigestion from pancreatic exocrine insufficiency. 2425 13