Vishwanath M. Sardesai

Nutritional role of polyunsaturated fatty acids

Abstract In mammalian tissues there are four families of polyunsaturated fatty acids derived from the parent fatty acids: palmitoleic and oleic acids, which can be synthesized endogenously, and linoleic and linolenic acids, which must be obtained from the diet and are known as essential fatty acids. These four precursors are desaturated and chain elongated to form the long chain highly unsaturated fatty acids. The principal products of linoleic acid are arachidonic, with four double bonds (tetraene), and dihomogamma linolenic acids; those of linolenic acid are eicosapentaenoic and docosahexaenoic acids. These polyunsaturated acids derived from essential fatty acids when incorporated into membrane phospholipids can alter membrane fluidity, which determines the permeability of membranes and the behavior of membrane-bound enzymes and receptors. The dihomogammalinolenic, arachidonic, and eicosapentaenoic acids are also the precursors of eicosanoids, which influence many cellular processes. When the dietary amounts of linoleic and linolenic acids are inadequate, palmitoleate and oleate are desaturated and chain elongated to give rise to eicosatrienoic acids (triene). An elevated tissue triene/tetraene ratio is, therefore, used as a marker for essential fatty acid deficiency. The essential fatty acid deficiency symptoms include reduced growth rate, scaly dermatitis, impaired reproduction, and susceptibility to infection. The intake of 1 to 2% of the daily calories as linoleate and 0.2 to 0.5% as linolenate is widely acknowledged as the approximate amounts to meet the needs of essential fatty acids in humans

Natural and synthetic intense sweeteners

Abstract Two types of intense sweeteners are available: natural sweeteners of plant origin and artificial or synthetic sweeteners. The sweeteners from natural sources with potential for commercial use include perillaldehyde, stevioside, rabaudioside, glycyrrhizin, osladin, thaumatins, and monellin. The compound miraculin, although not sweet, has the property of modifying the taste of sour food into a delightfully sweet taste. The artificial sweeteners currently in use in this country are saccharin, aspartame, and acesulfame K. In addition, sucralose, alitame, and several other sugar substitutes are in various stages of development. Although these compounds provide sweetness with minimal or no calories, some studies suggest that they may induce insulin secretion and a rise in appetite. The long-term effect of these sweeteners on weight gain and insulin secretion among various groups of the population needs to be studied.

Biochemical and nutritional aspects of eicosanoids

Abstract The eicosanoids are derived from 20-carbon polyunsaturated fatty acids e.g., dihomogamma linolenic, arachidonic, eicosapentaenoic, and Mead acid, which are present as components of cell membrane phospholipids. Activation of phospholipases causes release of these fatty acids that can be metabolized either via the cyclooxygenase pathway to produce the prostanoids—prostaglandins, thromboxanes, and prostacyclins—or via the lipoxygenase pathway to form leukotrienes and lipoxins. These fatty acids can also be oxidized by the cytochrome P-450 system giving rise to several metabolites including epoxyeicosatrienoic acids. Eicosanoids are highly active substances with diverse biological actions. Because arachidonic acid is the most common fatty acid present in tissue lipids, the eicosanoids derived from it predominate in human tissues. Some of the eicosanoids formed from arachidonic acid such as thromboxane A 2 and leukotrienes have deleterious effects, while those derived from other polyunsaturated fatty acids are generally less potent or have beneficial actions. The steroidal anti-inflammatory agents, such as cortisone, block the release of precursor fatty acids and thus the formation of all eicosanoids. Non-steroidal anti-inflammatory agents such as aspirin inhibit cyclooxygenase and prevent the production of prostanoids. It is possible to modulate the precursor fatty acid component in cell membrane phospholipids by dietary means, which in turn can alter the types of eicosanoids formed endogenously. Some food constituents such as vitamin C, vitamin E, garlic, onion, ginger, and alcohol can affect the production of eicosanoids. The dietary manipulation may serve as a long-term strategy to favorably modify the endogenous eicosanoid production.

Introduction to clinical nutrition

Introduction - fundamentals of nutrition. Part 1 Essential and nonessential nutrients: digestion of macronutrients - carbohydrates, lipids and proteins requirements for energy, carbohydrates, fat and protein role of essential fatty acids eicosanoids inorganic elements - essential macromineral, essential trace minerals and ultra trace minerals vitamins - general fat soluble vitamins - A, D, E, K water soluble vitamins 1 - thiamin-B1, riboflavin-B2, niacin, pantothenic acid and biotin water soluble vitamins 2 - folic acid, vitamin-B12, pyridoxine and vitamin C-ascorbic acid vitamin-like substances. Part 2 Nutrition in the normal life cycle: nutrition during pregnancy and lactation foetal development and nutrition during infancy, childhood and adolescence nutrition and ageing. Part 3 Nutritional conditions asssociated with health: nutritional assessment obesity and eating disorders cholesterol and hyperlipidemia osteoporosis nutritional aspects of diabetes nutritional aspects of genetic disease. Part 4 Topics of general interest (special topics of practical importance): dietary fibre antioxidants and health toxicants occurring naturally in foods and additives vegetarianism and other popular nutritional practices nutritional aspects of biotransformation nutraceuticals.

The determination of glycine in biological fluids.

Abstract A colorimetric-fluorometric method for the determination of glycine in biological fluids is described. In brief, this procedure involves the degradation of glycine, in protein-free filtrates, to formaldehyde by chloramine T. The formaldehyde is then converted to 3,5-diacetyl- i ,4-dihydrolutidine by Hantzsch reaction in which acetyl acetone and ammonia are the reactants. This reaction product in low ranges (concentration of glycine from 0.1 to 3 μg), is measured fluorometrically, while in higher ranges colorimetric analysis is used. Recovery studies of glycine added to blood and urine samples have been satisfactory. Blood samples obtained from normal human subjects are found to have glycine in the range 4–16 μg/ml. From the standpoint of sensitivity, simplicity, and time required, this technique is believed to be an improvement over previously described procedures for glycine determination.

The effect of albumin resuscitation for shock on the immune response to tetanus toxoid.

A prior prospective random study showed that supplemental albumin led to a significant (P ⩽ 0.05) fall in immunoglobulin (Ig) content of IgG, IgM, and IgA; no measurement was made on the immune response to a known antigen. Therefore, the immune response to tetanus toxoid, measured by antibody precipitation, was studied in 43 nonalbumin patients and 22 albumin patients from whom frozen sera were available. The 65 patients received an average of 16 units blood during resuscitation and 0.5 ml tetanus toxoid. Using single radial immunodiffusion technique, duplicate double-blind measurements of precipitants formed by the patients tetanus toxoid antibody and purified tetanus toxoid (TTA) incorporated in 1% agarose gel were made. TTA levels in the 22 albumin patients were compared with all nonalbumin patients and with two subgroups of 22 patients—one randomly chosen; the other matched for number of transfusions. TTA was also correlated with time after injury. TTA was significantly less in albumin patients (215 ± 100 units) than in the nonalbumin patients (387 ± 233 units) and both subgroups of nonalbumin patients. TTA correlated directly with time after injury in the nonalbumin patients (slope = −0.4). Albumin resuscitation for shock results not only in a fall in Ig content but also a reduction in the immune response to tetanus toxoid.

The effect of ethyl alcohol on rat liver tryptophan oxygenase

Abstract The activity of liver tryptophan oxygenase was determined in rats administered intoxicating dose of ethanol. Following intraperitoneal injection of ethanol there was a rise in the enzyme activity reaching levels considerably above those of the control animals. Maximum enzyme activity was reached 5 hours after ethanol administration and then returned to within control levels in about 9 hours. It is suggested that the observed increase in tryptophan oxygenase in the liver may be the result of increased plasma adrenocortical hormone level following ethanol intoxication, or may be secondary to the induction of ALA (delta-aminolevulinic acid) synthetase and consequent enhanced heme production.

The effect of E. coli endotoxin on cardiac and skeletal muscle myofibrillar ATPase

Abstract It has been reported that endotoxin has a direct depressant effect on myocardial contractility. It is reasonable to assume, therefore, that endotoxin might interact with and modify the contractile protein system of the heart. The results presented herein suggest that this does in fact happen in both cardiac and skeletal muscle systems.

Protein, Nucleotide, and Porphyrin Metabolism

The relation of alcohol to protein, nucleotide, and porphyrin metabolism is obviously a two-way relationship. Thus, not only does alcohol profoundly affect the metabolism of these three major groups of substances but also, in turn, the latter play extremely significant roles in the metabolism of ethanol* itself. This interrelationship forms the basis for the presentation in this chapter.

Ethyl alcohol and liver tryptophan oxygenase.

Abstract The activity of the enzyme tryptophan oxygenase increases after an acute dose of alcohol, reaching the maximum level 5 hr after injection. This is true for both the apoenzyme and the holoenzyme. The activity comes back to near normal level 9 hr after injection. The studies using pyrazole, an inhibitor of alcohol dehydrogenase, show that approximately 60% of the increase in the enzyme activity is primarily due to a direct alcohol effect and not due to alcohol metabolism. In adrenalectomized animals, alcohol causes only a small rise—approx 12% of that seen in normal animals—in enzyme activity. These results suggest that the effect of alcohol on tryptophan oxygenase is mediated to a large extent via adrenal hormones. The increase in tryptophan oxygenase following alcohol ingestion should result in diversion of more of the plasma tryptophan to the kynurenine pathway and decrease the availability of this amino acid for cerebral serotonin formation. This effect of alcohol may be responsible for the mood changes seen after acute alcohol ingestion.