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- Volume 17, 1997
Annual Review of Nutrition - Volume 17, 1997
Volume 17, 1997
- Review Articles
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ROLE OF NUTRITION IN PREVENTION OF THE PROGRESSION OF RENAL DISEASE
Vol. 17 (1997), pp. 435–455More Less▪ AbstractIn rats with renal disease, low-protein diets slow the decline in renal function, histologic damage, and mortality. Low-protein (and phosphorus) diets can also ameliorate uremic symptoms, secondary hyperparathyroidism, and metabolic acidosis in patients with chronic renal failure. Albeit controversial, evidence also suggests that dietary protein restriction can slow the rate of progression of renal failure and the time until end-stage renal failure. These dietary regimens appear to be safe and patients with chronic renal failure are able to activate normal compensatory mechanisms designed to conserve lean body mass when dietary protein intake is restricted. When low-protein diets are prescribed, patients should be closely monitored to assess dietary compliance and to ensure nutritional adequacy. Evidence that the spontaneous intake of dietary protein decreases in patients with progressive chronic renal failure who consume unrestricted diets should not be construed as an argument against the use of low-protein diets. Rather, it is a persuasive argument to restrict dietary protein intake in order to minimize complications of renal failure while preserving nutritional status.
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HORMONAL REGULATION OF HUMAN MUSCLE PROTEIN METABOLISM
Vol. 17 (1997), pp. 457–485More Less▪ AbstractA continuous turnover of protein (synthesis and breakdown) maintains the functional integrity and quality of skeletal muscle. Hormones are important regulators of this remodeling process. Anabolic hormones stimulate human muscle growth mainly by increasing protein synthesis (growth hormone, insulin-like growth factors, and testosterone) or by decreasing protein breakdown (insulin). Unlike in growing animals, insulin's main anabolic effect on muscle protein in adult humans is an inhibition of protein breakdown. Protein synthesis is stimulated only in the presence of a high amino acid supply. A combination of the stress hormones (glucagon, glucocorticoids, and catecholamines) cause muscle catabolism, but the effects of the individual hormones on human muscle and their mechanisms of action remain to be clearly defined. Although thyroid hormone is essential during growth, both an excess and a deficiency cause muscle wasting by yet unknown mechanisms. A greater understanding of the regulation of human muscle protein metabolism is essential to elucidate mechanisms of muscle wasting.
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ROLE OF BLOOD FLOW IN THE REGULATION OF MUSCLE
GLUCOSE UPTAKEVol. 17 (1997), pp. 487–499More Less▪ AbstractInsulin vasodilates skeletal muscle vasculature via an endothelium-derived nitric oxide–dependent mechanism. Data suggests that insulin interacts directly with the endothelium to cause nitric oxide release. This insulin-mediated increase in muscle perfusion accounts for ∼30% of insulin's overall action to stimulate muscle glucose uptake, suggesting a role for insulin and glucose delivery as a determinant of insulin action. Hindlimb perfusion experiments, where perfusion rate is fixed, suggest that changes in distribution of microcirculatory perfusion can modulate substrate uptake. The potential role of insulin to enhance flow through capillary networks that are efficient at nutrient transfer to tissue (nutritive flow) relative to non-nutritive flow is discussed.
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COMPARATIVE NUTRITION
OF IRON AND COPPERVol. 17 (1997), pp. 501–526More Less▪ AbstractThe suggestion from nutritional studies with mammals of a link between iron and copper metabolism has been reinforced by recent investigations with yeast cells. Iron must be in the reduced ferrous (FeII) state for uptake by yeast cells, and reoxidation to ferric (FeIII) by a copper oxidase is part of the transport process. Thus, yeast cells deficient in copper are unable to absorb iron. In an analogous way, animals deficient in copper appear to be unable to move FeII out of cells, probably because it cannot be oxidized to FeIII. Invertebrate animals use copper and iron in ways very similar to vertebrates, with some notable exceptions. In the cases where vertebrates and invertebrates are similar, the latter may be useful models for vertebrate metabolism. In cases where they differ (e.g. predominance of serum ferritin in insects, oxygen transport by a copper protein in many arthropods, central importance of phenoloxidase, a copper enzyme in arthropods), the differences may represent processes that are exaggerated in invertebrates and thus more amenable to study in these organisms. On the other hand, they may represent processes unique to invertebrates, thus providing novel information on species diversity.
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Human Body Composition: Advances in Models and Methods
Vol. 17 (1997), pp. 527–558More Less▪ AbstractThe field of human body composition research is reaching a mature stage in its development: The three interconnected areas that define body composition research—models and their rules, methodology, and biological effects—are well-defined and are actively investigated by scientists in diverse disciplines from many different nations; and methods are available for measuring all major atomic, molecular, cellular, and tissue-system level body composition components in research, clinical, and epidemiological settings. This review summarizes main body composition research concepts, examines new component-measurement methodologies, and identifies potential areas of future research.
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APPLICATIONS OF MASS ISOTOPOMER ANALYSIS
TO NUTRITION RESEARCHVol. 17 (1997), pp. 559–596More Less▪ AbstractInvestigations into regulating metabolic pathways with stable isotopes have, over the past decade, undergone major development with the use of nuclear magnetic resonance and mass spectrometry in studying labeling patterns of newly synthesized biomolecules. In this review, we concentrate on investigations of mass isotopomer distribution (MID) measured by mass spectrometry. We review the applications of MID to analytical problems, in particular the possibility of amplifying the measurement of low isotopic enrichments by incorporating multiple molecules or atoms of a primary analyte into the molecule of a secondary analyte, the MID of which is assayed. We also review new information on the regulation of intermediary metabolism gathered from the analysis of MID patterns of synthesized compounds. Lastly, we review the applications of MID to the synthesis of polymeric molecules, with emphasis on the validity of these techniques. A number of these techniques are applicable to investigations of nutrient metabolism in health and disease.
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Why Do We Eat? A Neural Systems Approach1
Vol. 17 (1997), pp. 597–619More Less▪ AbstractNeuroregulators found at various brain sites are involved in controlling food intake, a behavior that occurs for many reasons. Different neuroregulators may affect different stimuli that impact eating behavior. For example, neuropeptide Y may initiate feeding for energy needs, opioid peptides may provide the rewarding aspects of eating, and corticotropin releasing factor may affect stress-induced eating. We know that the neural networks regulating feeding also impact other components of energy balance. Neuropeptide Y not only increases eating, it also decreases energy expenditure in brown fat and increases enzymatic activity associated with fat storage in white fat, resulting in a more obese animal. What the sites of action are of these neuroregulators and how they interact with regulators at other sites are of utmost importance. Different regions of the brain, together with the periphery, communicate via signals acting in coordinated fashion, which leads to the final outcome: eating less or more and expending less or more energy.
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Previous Volumes
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Volume 44 (2024)
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Volume 43 (2023)
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Volume 42 (2022)
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Volume 41 (2021)
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Volume 40 (2020)
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Volume 39 (2019)
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Volume 38 (2018)
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Volume 37 (2017)
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Volume 36 (2016)
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Volume 35 (2015)
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Volume 34 (2014)
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Volume 33 (2013)
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Volume 32 (2012)
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Volume 31 (2011)
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Volume 30 (2010)
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Volume 29 (2009)
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Volume 28 (2008)
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Volume 27 (2007)
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Volume 26 (2006)
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Volume 25 (2005)
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Volume 24 (2004)
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Volume 23 (2003)
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Volume 22 (2002)
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Volume 21 (2001)
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Volume 20 (2000)
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Volume 19 (1999)
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Volume 18 (1998)
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Volume 17 (1997)
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Volume 16 (1996)
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Volume 15 (1995)
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Volume 14 (1994)
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Volume 13 (1993)
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Volume 12 (1992)
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Volume 11 (1991)
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Volume 10 (1990)
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Volume 9 (1989)
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Volume 8 (1988)
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Volume 7 (1987)
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Volume 6 (1986)
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Volume 5 (1985)
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Volume 4 (1984)
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Volume 3 (1983)
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Volume 2 (1982)
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Volume 1 (1981)
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Volume 0 (1932)