Progress in food & nutrition science最新文献

Dietary fiber consumption has been associated with a decrease in diabetes and atherosclerotic diseases in population surveys. The contribution of soluble fiber (compared to insoluble fiber) to each of these problems has been investigated in several ways. This paper reviews the role which soluble fiber consumption plays in carbohydrate and lipid metabolism. The effects of specific fibers on glucose and insulin responses are examined; possible mechanisms responsible for the described effects are discussed. Epidemiologic evidence that consumption of foods containing soluble fiber contributes to decreased atherosclerotic disease is reviewed. Studies of administration of soluble fiber to hyperlipidemic males and females and normolipidemic subjects are examined with respect to changes in plasma lipids. Soluble fiber appears to play an important role in preventing and possibly treating diabetes and hyperlipidemia, diseases common to Westernized countries.

The prevalence of obesity is increasing in the developed as well as underdeveloped countries. Obesity in women is associated with reproductive disorders. The levels of estrone and androgens are higher in obese women along with a reduction in the levels of sex hormone binding globulin ( SHBG ). The pituitary secretion of hormones is altered either due to a deficient peripheral feedback regulation or a concomitant central defect in the obese. Luteinizing hormone ( LH ) level may increase in some of the obese subjects. The secretion of LH in response to luteinizing hormone releasing hormone ( LHRH or GnRH ), clonidine and naloxone may be altered in obese women. The levels of circulating prolactin may fall along with a delay in the nocturnal surge of the hormone. The secretion of prolactin in response to thyrotropin releasing hormone ( TRH ), insulin-induced hypoglycemia, arginine and chlorpromazine is altered. Similarly growth hormone secretion in response to growth hormone releasing hormone ( GHRH ), clonidine, naloxone and arginine is also altered in obesity. The literature suggests an alteration in the autonomic nervous system activity and the metabolism of carbohydrates and fats in the obese. Steroid hormones could affect the distribution of fat in the various regions of the body, and the distribution of body fat is linked with the severity of hyperandrogenism and metabolic disorders in obese subjects. However, it is heartening to note that many of the endocrinological and reproductive disorders are reversible with weight reduction in the obese subjects.

It is well recognized that the absorption, retention and metabolism of most essential minerals can be markedly influenced by the presence of antinutrient factors in the diet (i.e. fiber and phytate). However, in addition, interactions can also occur between essential minerals. Indeed, under some circumstances, these interactions can be profound and have significant implications for human health. Interactions between essential minerals can be broadly classified as direct or indirect. Direct interactions are generally competitive phenomena that occur during the intestinal absorption and/or during the tissue utilization of a mineral. Indirect interactions occur when one of the minerals is involved in the metabolism of the other mineral, or when a deficiency or toxicity of one of the minerals results in hormonal changes or tissue damage which affects the metabolism of the other mineral. In this review we have focused our comments on direct interactions between essential minerals, and we present suggested levels at which an excess of a mineral (coined "X") can significantly alter the metabolism of another mineral (coined "Y") for several of the known competitive interactions. This level is characterized as the lowest X/Y ratio of the dietary intakes which has been shown to produce negative consequences on the metabolism of the element Y (assuming the intake of Y is physiological). Moreover, the importance of the physiological status of the animal with regard to the determination of these ratios is discussed. The calculated X/Y ratio at which interactions may be predicted to occur is generally higher than the ratio calculated for most minerals using typical dietary intakes of X and Y in Western-type diets. However, ratios which might be predicted to result in negative interactions do occur in select food products, and can be reached as a consequence of supplementation (either through food enrichment or therapeutic use of supplements). In fact, considering the ready availability of dietary supplements, such interactions may become commonplace. Finally, the interactions between essential and non-essential minerals (heavy metals) are briefly discussed, as are indirect mineral interactions.

Changing the concentration or the type of fat intake impacts several aspects of the immune response involving lymphocytes, monocytes, and neutrophils. An increase in the intake of fat inhibited immune response in humans and in several animal models. Polyunsaturated fatty acids (PUFA) of N-6 type lowered immune response in several animal models, but a moderate increase in the consumption of N-6 PUFA by humans did not have any detectable adverse effect on the immune response. In humans, several indices of immune response were inhibited by the N-3 PUFA, but in animals both inhibition and stimulation were found, depending upon the species, the fatty acids used and the index being examined. Whether the absolute amounts or the ratios between individual fatty acids or fatty acid classes are critical in determining their effects on immune response need to be investigated. Manipulation of fat intake has already found limited success in managing some of the disorders of the immune system and further use of this treatment is anticipated.

While epidemiologic and concordant experimental data indicate a direct relationship between dietary fat (and presumably caloric) intake and the development of colon cancer, the effect of dietary cholesterol on this disease is still not clear. However, there appears to be a developing literature concerning an inverse relationship between serum and plasma cholesterol levels, and the risk for colon cancer. Findings that low serum cholesterol levels are apparent as early as ten years prior to the detection of colon cancer implies that sub clinical disease is probably not involved initially in this process. The possibility of low serum cholesterol as a bio-marker was considered in epidemiologic studies which focused upon obese men with lower than normal serum cholesterol levels who were found to be at increased risk to colon cancer. While the relationship between low serum cholesterol and colonic or intestinal cholesterol metabolism is presently not understood, current genetic studies provide a promising though as yet unexplored potential association. Alterations which occur during the developmental progression of colonic cancer include changes in chromosome 5, which also carries two genes vital to the biosynthesis and regulation of systemic and cellular cholesterol metabolism, 3-hydroxy-3-methylglutaryl coenzyme A synthase, and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCoA R). Regulation of cholesterol metabolism in intestinal cells in vivo and in vitro varies from that seen in normal fibroblasts or hepatocytes in terms of exogenous sources of cholesterol and how these sources regulate internal synthesis. Colonic cancer cells have been used to assess small bowel enterocyte cholesterol metabolism, which has been possible because of their ability to differentiate in culture, however information regarding true colonic enterocyte cholesterol metabolism is relatively scarce. Colonic cancer cells have been shown to possess a diminished or nonexistent ability to use low density lipoprotein to support cellular growth, unlike normal fibroblasts. Diminished low density lipoprotein (LDL) receptor (LDL-R) activity is a significant alteration in a metabolic pathway with such fundamental ties to cellular growth and activation (via mevalonate effects on isoprenylation of G-proteins for example), that it is selected for in the development of certain tumors--among them human colonic carcinomas. It would be expected that such a loss would provide a growth advantage to the tumor cell. Preliminary investigation of this hypothesis has shown that LDL will inhibit the proliferative capacity of certain human colonic adenocarcinomas, and that these cells possess a high rate of cholesterol synthesis relative to fibroblasts.(ABSTRACT TRUNCATED AT 400 WORDS)

Vitamin K is an essential cofactor necessary for the production of clotting factors II, VII, IX, and X in humans and has recently been found to be an essential factor for many other proteins in the body. There are two sources of this essential vitamin, including vitamin K1, or phylloquinone which is primarily found in green leafy vegetables and vitamin K2 or menaquinone which is synthesized by certain intestinal bacteria. The precise contribution of the bacterially synthesized menaquinone to overall vitamin K requirements in man is unknown. This paper reviews the available literature regarding the production and liberation of menaquinones from bacteria, the animal experiments which have been done to examine the absorption of menaquinones and the indirect and direct evidence in humans regarding utilization of menaquinones. The preponderance of the evidence suggests that bacterially synthesized menaquinones, particularly in the ileum can and do play a significant role in contributing to vitamin K requirements in humans to prevent clinically significant coagulopathy, especially during periods of episodic dietary lack of the vitamin.

Zinc is a metal with great nutritional importance, particularly during periods of rapid growth due to its intervention in cellular replication as well as in the development of the immune response. A review of studies by several authors trying to determine the normal behaviour of zinc during pregnancy and early infancy is done, in an attempt to establish adequate circulating levels, in order to be able to identify zinc deficiency correctly and provide appropriate treatment. However, the information is very contradictory and no real conclusion can be reached.

The incidence of iron deficiency anemia, rickets, and zinc deficiency is very high in Chinese preschool children and a method for prevention is urgently needed. From our studies, it can be seen that a soft drink powder is a convenient vehicle for the supplementation of iron, zinc, calcium, vitamin D, riboflavin, and ascorbic acid. Table salt is also a good, low-cost carrier for iron and zinc, and cow's milk can only be used for the enrichment of vitamins A and D. In our study the therapeutic dose of iron was lower than 3 mg/kg body weight recommended by the WHO Expert Committee. As ascorbic acid can enhance the absorption of iron in the body, so 300 mg vitamin C was added to 100 g of soft drink powder containing 100 mg of elemental iron. Ten g of powder is not only enough for the prevention of iron deficiency anemia but it can also cure iron deficiency anemia within 3 months. One hundred mg of iron in 100 g of table salt is an adequate level, because an adult or a child taking 10 or 5 g of salt will receive 10 and 5 mg of elemental iron respectively. This dosage is adequate for the prevention of anemia. From our results, 10 mg of zinc daily is enough for the prevention and treatment of zinc deficiency in preschool children. Four hundred IU of vitamin D (from fortified soft drink powder or enriched fresh cow's milk) orally-administered daily, is a good way to prevent rickets in infants and young children.

This paper reviews the evidence that certain dietary components can affect intestinal absorption of magnesium. Increased intakes of protein and fructose improve apparent magnesium absorption (magnesium intake minus fecal excretion) in humans, whereas a lowering effect occurs with consumption of cellulose and phytate. Although dietary concentrations of lactose, fat, calcium and phosphate have clear effects on magnesium absorption in experiments with rats, the impact of these nutrients on magnesium absorption in humans remains unsettled. Mechanisms underlying the effects of dietary components on magnesium absorption in humans are generally poorly understood. A change in magnesium absorption not necessarily results in a change in magnesium retention. When consuming practical diets, the fall of apparent magnesium absorption caused by phytate and cellulose is generally compensated by increased magnesium intake due to high magnesium concentrations in phytate- and cellulose-rich products. Furthermore, to maintain homeostasis, urinary magnesium excretion will be raised after stimulation of apparent magnesium absorption and it will be lowered after impairment of apparent magnesium absorption. Thus, the effects of dietary components on magnesium absorption probably are critically important only at low intakes of magnesium. At low magnesium intakes, differences in magnesium absorption may be expected to influence magnesium retention and thus can either induce or abolish magnesium deficiency.