Fat deficiency syndrome

Arachidonic acid, biosynthesis, VIII, 63 deficiency, effect on skin, VI, 139 fat deficiency syndrome and, VIII, 59, 61... 

Hexahydroxystearic acid, fat deficiency syndrome and, VIII, 59 Hexestrol,... 

Thomasson (1953) noted that ordinary linolenic acid (9,12,16-octa-decatrienoic acid), formerly considered as possessing biopotency equal to that of linoleic acid, under certain conditions, is actually practically inactive (9%) when tested by the new bio-assay method of the author on the other hand, y-linolenic acid (6,9,12-octadecatrienoic acid) is considered to possess 100% biopotency as compared with linoleate. The conjugated trienoic acid, a-elaeostearic acid (9,11,13-octadecatrienoic acid), was reported by Burr, Burr, and Miller (1932) to be ineffective in counteracting the fat-deficiency syndrome confirmatory negative results have... 

The dog represents a species which is readily susceptible to the fat-deficiency syndrome. Because of the convenient size of this species, which will enable a clinical study to be made on one animal over a period of time, considerable work has been reported on EFA deficiency in these animals. Hansen and Wiese (1943) first demonstrated that the symptoms of fat deficiency in the dog are similar to those produced by fat-free diets in other species. It has been suggested that dietary fat may supply a factor necessary for the maturation of epithelial, sebaceous, and sudoriparous cells. The fat-deficiency symptoms in the dog were found to respond quickly to a diet containing fresh lard to the extent of 29% of the total calories (Hansen and Wiese, 1943, 1951). 

In spite of the unequivocal relationship between the skin symptoms and the blood level of EFA in man, it has not been possible to produce the fat-deficiency syndrome in man experimentally by diet. In a single experiment on a normal male subject maintained on a fat-free regimen for six months. Brown et al, (1938) were unable to observe the appearance of any of the classical symptoms of fat deficiency. However, a 50% reduction in plasma linoleate and plasma arachidonate occurred, which was completely out of proportion to the extent of decrease of other blood lipids. In spite of this single negative result on man, it would seem to the reviewers that the proof of the requirement of EFA by man is unequivocal. Because of the greater life span, or because of the lower requirement for EFA, the fat-deficiency syndrome cannot be initiated as... 

The low capillary resistance of the fat-deficient rat could be restored to normal by the administration of small amounts of linseed oil or of linoleic acid itself. It would appear that one must consider decreased capillary resistance (or increased capillary permeability) as an additional manifestation of the fat-deficiency syndrome in rats and also in man. 

Less than 50 per cent of female rats fed a completely fat-free diet show regular ovulation (29). If the ovulating females are bred to normal males they may gain weight and produce litters. The young are underweight and of reduced viability. The reproductive capacity of rats showing the fat-deficiency syndrome can be restored by a few drops of com oil, olive oil, and the like. Linolenic or linoleic acid (30), and also arachidonic acid (31) prevent and cure the fat deficiency syndrome. There is no proof that withdrawal of carbohydrate interferes with normal reproduction in the rat (9). 

Water-soluble vitamins removed by hemodialysis (HD) contribute to malnutrition and vitamin deficiency syndromes. Patients receiving HD often require replacement of water-soluble vitamins to prevent adverse effects. The vitamins that may require replacement are ascorbic acid, thiamine, biotin, folic acid, riboflavin, and pyridoxine. Patients receiving HD should receive a multivitamin B complex with vitamin C supplement, but should not take supplements that include fat-soluble vitamins, such as vitamins A, E, or K, which can accumulate in patients with renal failure. 

It should be noted that deficiency states for some vitamins (e.g., pantothenic acid) are practically unknown in human beings. In such cases, deficiency states may be simulated by feeding the subject an appropriate vitamin antagonist. In another series of situations, vitamin deficiencies can be brought about by interfering with their absorption intentionally or may be the result of a disease process. Thus, fat-soluble vitamin deficiency may develop in cases of fat malabsorption syndromes (steatorrhea) sprue, pancreatic insufficiency, and bile duct obstruction. 

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. 

Vitamin K is absorbed by the small intestines, where it enters the lymph packaged in chylomiciions. A deficiency in vitamin K can occur in adults and children suffering from fat malabsorphon syndromes, such as cystic fibrosis. 

Persons at risk for EFA deficiency tend to be the same as those at risk for vitamin E deficiency. Some signs are shared by both defidencies. Premature infants may be at risk for EFA deficiency because of their low stores of lipids and their rapid growth, especially when they are fed diets that do not contain EFAs. For example, fats have been omitted from diets used to feed preterm infants (to avoid a variety of complications). EFA deficiency may develop later in life with fat malabsorption syndromes, EFA deficiency has presented in adults fed by total parenteral nutrition for longer periods, where EFAs had not been included in the liquid diet. 

Common problems in the past were fat overload syndrome, metabolic acidosis, hyperglycemia, and hypertriglyceridemia (6). These problems are now rare. Increasing efforts have been made to avoid adverse effects such as central venous catheter infection and hepatic dysfunction. Major developments in the future are likely to be achieved with the identification of nutrients, hormones, or other active compounds that can positively influence outcome beyond the safe provision of 40 essential nutrients in proper amounts, which is what principally has been achieved to date (7). Liver damage is still a major problem. The most common micronutrient deficiency is of thiamine. 

Burr GO, Brown JB, Kass JP, Lundberg WO. Comparative curative values of unsat urated fatty acids in fat deficiency. Proc Soc Exp Biol Med 1940 44 242-244. Clarke SD. Polyunsaturated fatty acid regulation of gene transcription A molecular mechanism to improve the metabolic syndrome. J Nutr 2001 131 1129-1132. Cuthbertson WFJ. Essential fatty acid requirements in infancy. Am J Clin Nutr 1976 ... 

Fat(s), see also under Fatty acids animal, as source of vitamin D, VI, 90 deficiency, syndrome, VIII, 58ff. essential fatty acids and, VIII, 59, 60, 61... 

Symptoms of deficiency. In humans rare and mostly resulting from fat malabsorption syndromes, liver disease, and antibiotic therapy that inhibits microbial vitamin K2 synthesis in the gut. 

Symptoms of deficiency. In humans generally not due to dietary insufficiency but due to fat malabsorption syndromes or genetic abnormalities. Symptoms are difficult to categorize, e.g., reproduction disorders, abnormalities of muscles, liver, bone marrow, brain functions. At cellular level increased oxidation of cell membranes. 

Human milk is the primary agent for infant nutriture and thereby guides the composition of manufactured infant formula and milk substitutes. The reported concentration of biotin in human milk is variable with lactation (and unfortunately between analytical methods), but is more than sufficient to supply the newborn infant with the RDI of 5-6pg/day, as evidenced by the absence of reported deficiency syndromes in breast-fed babies. Interestingly, most biotin in milk is present in a free form and therefore unbound with any macromolecules. As expected, when milk is separated into its fat and aqueous fractions, the water-soluble biotin is found predominantly in the skim-milk phase. Biotin has some lipophilidty and so a small percentage is carried into the cream as part of the fat-globule membrane. The total concentration of human milk is not large and somewhat similar to bovine milk. With respect to breast milk substitutes, it is necessary to ensure the biotin status remains comparable, thus international guidelines recommend 0.4-2.4pg/100 kJ of reconstituted or ready-to-feed infant formula. 

By feeding a diet composed of 16% casein, approximately 4% salts and vitamins and the remainder sucrose. Burr and Burr were able to induce a dietary deficiency syndrome which they later traced to the absence of linoleic acid. The principal deficiency symptoms were a diminished growth rate and a scaly dermatitis seen principally on the feet and tail. An example of a fat deficient rat is shown in Figure 1. Most of the organs of the body are affected by the deficiency and aberrations in structure or function of many tissues have been observed. Reproduction is impaired, the liver becomes fatty., kidney function is impaired, the electrocardiogram is abnormal, and the permeability of the skin toward water is much increased- This leads to evaporative loss of water and of heat from the body accounting for an increased food consumption and a diminished caloric efficiency. 

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