In several clinical conditions, lipid digestion and absorption are impaired, resulting in the malabsorption of lipids and other nutrients and fatty stools. Abnormal lipid absorption can result in numerous problems because the body requires certain fatty acids (e.g., linoleic and arachidonic acid, precursors of prostaglandins) to function normally. These are called essential fatty acids because the human body cannot synthesize them and is, therefore, totally dependent on the diet to supply them. Recent studies suggest that the human body may also require omega-3 fatty acids in the diet during development. These include linolenic, docosahexaenoic, and eicosapentaenoic acids. Linolenic acid is abundant in plants, and docosahexaenoic and eicos-apentaenoic acids are abundant in fish. Docosahexaenoic acid is an important fatty acid present in the retina and other parts of the brain.
Pancreatic deficiency significantly reduces the ability of the exocrine pancreas to produce digestive enzymes. Because the pancreas normally produces an excess of digestive enzymes, enzyme production has to be reduced to about 10% of normal before symptoms of malabsorption develop. One characteristic of pancreatic deficiency is steatorrhea (fatty stool), resulting from the poor digestion of fat by the pancreatic lipase. Normally about 5 g/day of fat are excreted in human stool. With steatorrhea, as much as 50 g/day can be excreted.
Fat absorption subsequent to the action of pancreatic li-pase requires solubilization by bile salt micelles. Acute or chronic liver disease can cause defective biliary secretion, resulting in bile salt concentrations lower than necessary for micelle formation. The normal absorption of fat is thereby inhibited.
Abetalipoproteinemia, an autosomal recessive disorder, is characterized by a complete lack of apo B, which is required for the formation and secretion of chylomicrons and VLDLs. Apo B-containing lipoproteins in the circulation—including chylomicrons, VLDLs, and low-density lipoproteins (LDLs)—are absent. Plasma LDLs are absent because they are derived mainly from the metabolism of VLDLs. Since individuals with abetalipoproteinemia do not produce any chylomicrons or VLDLs in the small intestine, they are unable to transport absorbed fat, resulting in an accumulation of lipid droplets in the cytoplasm of enterocytes. They also suffer from a deficiency of fat-soluble vitamins.
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