Dietary Fat

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References

Arreaza-Plaza CA, Bosch V, Otayek MA. Lipid transport across the intestinal epithelial cell. Effect of colchicine. Biochim Biophys Acta 1976 May 27;431(2):297-302
Abstract: Rats injected with colchicine (0.5 mg/100 g of body weight) 1 h before ingestion of a margarine emulsion (1 g in 2 ml of saline) do not show the rise in plasma triacylglycerol concentration found in controls during the subsequent hours. The effect of colchicine is more dramatic when the experiment is performed after prior administration of Triton WR-1339, a substance known to inhibit the catabolism of lipoproteins. Colchicine-treated rats also showed a five-fold increase in the content of triacylglycerol in proximal jejunum, when compared to controls. These results are consistent with the idea that colchicine interferes with the intracellular phase of fat absorption, suggesting that the microtubular-microfilamentous system could be involved in the release of chylomicrons from the intestinal cell into the circulation.

Buist RA. Drug-nutrient interactions - an overview. Intl Clin Nutr Rev 1984;4(3):114. (Review)

Faloon WW, Paes IC, Woolfolk D, Nankin H, Wallace K, Haro EN. Effect of neomycin and kanamycin upon intestinal absortion. Ann N Y Acad Sci. 1966 Jun 14;132(2):879-887.

Faloon WW. Metabolic effects of nonabsorbable antibacterial agents. Am J Clin Nutr. 1970 May;23(5):645-651.

Glickman RM, Perrotto JL, Kirsch K. Intestinal lipoprotein formation: effect of cholchicine. Gastroenterology 1976 Mar;70(3):347-352.
Abstract: The possibility that microtubules might be involved in intestinal lipoprotein formation or secretion was studied by determining the effect of colchicine, a known microtubule inhibitor, on intestinal lipid absorption. The effect of colchicine (0.5 mg per 100 g) in the lymphatic absorption of [14C]oleic acid was studied in rats with indwelling mesenteric lymph cannulas. Colchicine-treated animals showed a marked delay as well as a decrease in the lympatic absorption of [14C]oleic acid. Chylomicrons from colchicine-treated animals showed no difference in apoprotein content when examined on sodium dodecyl sulfate polyacrylamide gels. Micellar lipid absorption was next studied from in situ jejunal loops in animals pretreated with colchicine. Colchicine administration was associated with a 3-fold increase in residual mucosal lipid when compared with controls. Thin layer chromatography of residual lipid demonstrated that residual lipid was largely present as triglyceride, suggesting that the impairment in lipid transport induced by colchicine was at a site distal to triglyceride resynthesis. Electron microscopic examination of intestine from colchicine-treated animals revealed that most residual lipid was present within the endoplasmic reticulum and Golgi in numerous particles the size of chylomicrons (0.2 to 0.4 mu). These results suggest that the impairment in lipid transport induced by colchicine is distal and, in part, may represent an "exit block". These results suggest a possible role for microtubules in intestinal lipid transport. However, further studies are required to demonstrate directly the participation of microtubules in chylomicron secretion.

Hardison WG, Rosenberg IH.  The effect of neomycin on bile salt metabolism and fat digestion in man. J Lab Clin Med. 1969 Oct;74(4):564-573.

Hill FW. An investigation of the effects of oral neomycin on intestinal absorption and serum cholesterol levels in the dog. Br Vet J. 1973 Jul-Aug;129(4):337-344.

Holt GA. Food and Drug Interactions. Chicago: Precept Press, 1998.

Kendall MJ, Chan K. Drug-induced malabsorption. Xenobiotica 1973 Nov;3(11):727-744. (Review)

Longstreth GF, Newcomer AD. Drug-induced malabsorption. Mayo Clin Proc 1975 May;50(5):284-293.

Miura S. [Study on the fat absorption and transportation into intestinal lymph of rats--effect of colchicine on the absorption of long chain fatty acids and the role of intestinal alkaline phosphatase]. Nippon Shokakibyo Gakkai Zasshi. 1980 Apr;77(4):572-82. [Article in Japanese]

Nesbitt LT Jr. Minimizing complications from systemic glucocorticosteroid use. Dermatol Clin 1995 Oct;13(4):925-939. (Review)
Abstract: For proper use of systemic GCS, a basic knowledge of the normal HPA axis, as well as knowledge of the pharmacology, clinical usage guidelines, and adverse reactions of these agents is imperative. Both short-term (acute) and long-term side effects should be well known by the physician. The pros and cons of oral and parenteral therapy for various disorders and in various situations should be recognized. For long-term therapy, an intermediate-acting agent such as prednisone in single, early morning doses is most commonly used to minimize suppression of the HPA axis. Alternate-morning doses produce even less suppression if the disease process will respond. A through patient history, including general medical history and medications the patient is taking, is important to anticipate any potential problems. Weight and blood pressure should be checked initially and every 1 to 3 months thereafter. Blood glucose, electrolytes, and lipid studies, including triglycerides, should be done approximately every 6 months. An ophthalmology examination should be performed every year, and stool examination for occult blood and chest radiography can be obtained as indicated. Bone density studies might be necessary in patients who are at high risk for osteoporosis. Specific acute situations may dictate other studies. The patient on long-term GCS should be kept as active as possible, as mild-to-moderate exercise helps prevent certain side effects, such as osteoporosis. The dose of oral GCS is best given with food to prevent gastrointestinal irritation, and agents to decrease gastric acidity might be needed in certain situations. Exposure to infections should be prevented, where possible, and treatment initiated at the first sign of systemic or cutaneous infection. Pain should be evaluated early, especially abdominal pain or bone pain; MRI is indicated if aseptic necrosis of bone is suspected. Both trauma and severe sun exposure should be avoided. Consultation with other specialists is strongly recommended when the situation dictates. Diet is one of the most important strategies to minimize side effects from long-term GCS therapy. Vegetable protein should be increased in the diet, and fats and carbohydrates limited. Adequate calcium is imperative, and calcium supplementation is recommended for high-risk osteoporosis patients. Small amounts of vitamin D may be necessary to increase absorption of calcium. Restriction of sodium is also important, as is maintainance of dietary potassium. Supplemental potassium may be necessary in some patients, and a thiazide diuretic might be useful in patients with hypertension, edema, or osteoporosis. Vitamin C can be given to promote wound healing. A good doctor-patient relationship is important in managing the patient on long-term GCS. The patient must return for regular visits and be encouraged to promptly report any adverse reactions to the physician. If these criteria are maintained and the strategies noted previously are followed, problems from long-term therapy with GCS will be minimized.

Pavelka M, Gangl A. Effects of colchicine on the intestinal transport of endogenous lipid. Ultrastructural, biochemical, and radiochemical studies in fasting rats. Gastroenterology. 1983 Mar;84(3):544-555.
Abstract: The involvement of microtubules in the transepithelial transport of exogenous lipid in intestinal absorptive cells has been suggested. Using electronmicroscopic, biochemical, and radiochemical methods, we have studied the effects of the antimicrotubular agent colchicine on the intestinal mucosa and on the intestinal transport of endogenous lipid of rats in the fasting state. After colchicine treatment, the concentration of triglycerides in intestinal mucosa of rats fasted for 24 h doubled, and electron microscopic studies showed a striking accumulation of lipid particles in absorptive epithelial cells of the tips of jejunal villi. These findings suggest that colchicine interferes with the intestinal transepithelial transport of endogenous lipoproteins. Additional studies, using an intraduodenal pulse injection of [14C]linoleic acid, showed that colchicine does not affect the uptake of fatty acids by intestinal mucosa. However, it had divergent effects on fatty acid esterification, enhancing their incorporation into triglycerides relative to phospholipids, and caused a significant accumulation of endogenous diglycerides, triglycerides, and cholesterol esters within the absorptive intestinal epithelium. Detailed ultrastructural and morphometric studies revealed a decrease of visible microtubules, and a displacement of the smooth and rough endoplasmic reticulum and Golgi apparatus. Furthermore, it is shown that after colchicine treatment, microvilli appear at the lateral plasma membrane of intestinal absorptive cells, a change not previously reported to our knowledge. Thus, our study shows that (a) colchicine causes significant changes in enterocyte ultrastructure and (b) colchicine perturbs the reesterification of absorbed endogenous fatty acids and their secretion in the form of triglyceride-rich lipoproteins from the enterocyte.

Pavelka M, Gangl A. [Ultrastructure of small intestine epithelial cells following administration of colchicine--studies in fasting condition and during fat absorption]. Verh Anat Ges. 1978;(72):687-689. [Article in German]

Pronsky Z. Powers and Moore's Food-Medications Interactions. Ninth Edition. Food-Medication Interactions. Pottstown, PA, 1991.

Race TF, Paes IC, Faloon WW. Intestinal malabsorption induced by oral colchicine. Comparison with neomycin and cathartic agents. Am J Med Sci 1970 Jan;259(1):32-41.

Rachmilewitz D, Karmeli F. Colchicine and intestinal transport. Gastroenterology. 1982 Jul;83(1 Pt 1):159-60. (Letter)

Ratnaike RN, Jones TE. Mechanisms of drug-induced diarrhoea in the elderly. Drugs Aging 1998 Sep;13(3):245-253.

Robinson C, Weigly E. Basic Nutrition and Diet Therapy. New York: MacMillan, 1984.

Roe DA. Diet and Drug Interactions. New York: Van Nostrand Reinhold, 1989.

Roe DA. Drug-induced Nutritional Deficiencies. 2nd ed. Westport, CT: Avi Publishing, 1985, 159-160.

Roe DA. Risk factors in drug-induced nutritional deficiencies. In: Roe DA, Campbell T, eds. Drugs and Nutrients: The Interactive Effects. New York: Marcel Decker, 1984: 505-523.

Trovato A, Nuhlicek DN, Midtling JE. Drug-nutrient interactions. Am Fam Physician 1991 Nov;44(5):1651-1658.(Review)

Wallace SL. Mechanism of action of colchicine. Arthritis Rheum. 1965 Oct;8(5):744-748.

Werbach MR. Foundations of Nutritional Medicine. Tarzana, CA: Third Line Press, 1997, 223-224. (Review).