linoleic-acid and Diarrhea

Goldberger discovered human pellagra was a non-infectious disease, affecting mostly the small and the timid in overcrowded institutions. Symptoms were diarrhoea, dermatitis and dementia. The staff and older children escaped the disease. They ate the meat and left the small and timid with the gravy. The 'Goldberger syndrome' is observed during competitive feeding of livestock, in ketotic animals and in the zinc depleted which are lethargic and pick all day at their feed. The pellagra preventative factor was later found to be nicotinic acid, derived from the amino acid tryptophan. Deficiencies of copper, magnesium, vitamin B6 (activated by a zinc kinase) inhibit the conversion of tryptophan to nicotinic acid. Stresses, including liver diseases, malabsorption, iron overload, porphyria, marasmus, cold stress, pregnancy, lactation, antibiotics and sulfa drugs, all increase dietary needs of nicotinic acid. Elevated free fatty acids and ketone bodies in the blood are associated with ketosis, zinc depletion and the pre-diabetic state. There is a diminished uptake of glucose by the tissues, a condition also found in parturient paresis of dairy cows when elevated hydrocortisone promotes insulin resistance and hyperglycaemia. This defect in insulin response leads to a diabetic-like state. The major predisposing factor in parturient paresis of dairy cows is hypocalcaemia. Gut absorption of dietary calcium may not meet the primary demands of lactation initiation until bone calcium mobilisation is established.

Topics: Animals; Cattle; Cattle Diseases; Diarrhea; Endorphins; Female; Hypocalcemia; Linoleic Acid; Linoleic Acids; Metabolic Diseases; Pellagra; Pregnancy; Pregnancy Complications; Receptors, Cell Surface

The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly impaired 90 min after the administration of linoleic acid micelles in the cholera toxin-treated rats. This reduction of linoleic acid absorption in the cholera toxin-treated rats was not found at 180 min. We could not find any mucosal accumulation of labeled linoleic acid or disturbance of triglyceride formation in the intestinal mucosa as compared with that of controls. The amount of linoleic acid transported into the intestinal lymph was delayed and reduced in cholera toxin-treated rats. Furthermore, the absorption of the medium-chain-length fatty acid, octanoic acid, was unchanged in the cholera toxin-treated rats. These results suggest that intestinal secretion induced by cholera toxin may delay the mucosal uptake and lymphatic transport of long-chain fatty acids. Cholera toxin may not affect triglyceride formation in the epithelial cells.

Topics: Animals; Caprylates; Cholera Toxin; Diarrhea; Fatty Acids; Intestinal Absorption; Intestinal Mucosa; Jejunum; Linoleic Acid; Linoleic Acids; Lymph; Male; Rats; Rats, Inbred Strains; Time Factors