Annual Review of Nutrition
0199-9885
1545-4312
Mỹ
Cơ quản chủ quản: ANNUAL REVIEWS , Annual Reviews Inc.
Lĩnh vực:
Nutrition and DieteticsMedicine (miscellaneous)
Phân tích ảnh hưởng
Thông tin về tạp chí
The Annual Review of Nutrition, in publication since 1981, covers the significant developments in the field of nutrition, including energy metabolism, carbohydrates, lipids, proteins and amino acids, vitamins, minerals, nutrient transport and function, metabolic regulation, nutritional genomics, molecular and cell biology, clinical nutrition, comparative nutrition, nutritional anthropology, nutritional toxicology, nutritional microbiology, epidemiology, and public health nutrition.
Các bài báo tiêu biểu
THE MOLECULAR BIOLOGY OF METAL ION TRANSPORT IN<i>SACCHAROMYCES CEREVISIAE</i> ▪ Abstract Transition metals such as iron, copper, manganese, and zinc are essential nutrients. The yeast Saccharomyces cerevisiae is an ideal organism for deciphering the mechanism and regulation of metal ion transport. Recent studies of yeast have shown that accumulation of any single metal ion is mediated by two or more substrate-specific transport systems. High-affinity systems are active in metal-limited cells, whereas low-affinity systems play the predominant roles when the substrate is more abundant. Metal ion uptake systems of cells are tightly controlled, and both transcriptional and posttranscriptional regulatory mechanisms have been identified. Most importantly, studies of S. cerevisiae have identified a large number of genes that function in metal ion transport and have illuminated the existence and importance of gene families that play related roles in these processes in mammals.
Tập 18 Số 1 - Trang 441-469 - 1998
Metabolic Regulation and Function of Glutathione Peroxidase-1 Glutathione peroxidase-1 (GPX1) represents the first identified mammalian selenoprotein, and our understanding in the metabolic regulation and function of this abundant selenoenzyme has greatly advanced during the past decade. Selenocysteine insertion sequence–associating factors, adenosine, and Abl and Arg tyrosine kinases are potent, Se-independent regulators of GPX1 gene, protein, and activity. Overwhelming evidences have been generated using the GPX1 knockout and transgenic mice for the in vivo protective role of GPX1 in coping with oxidative injury and death mediated by reactive oxygen species. However, GPX1 exerts an intriguing dual role in reactive nitrogen species (RNS)-related oxidative stress. Strikingly, knockout of GPX1 rendered mice resistant to toxicities of drugs including acetaminophen and kainic acid, known as RNS inducers. Intracellular and tissue levels of GPX1 activity affect apoptotic signaling pathway, protein kinase phosphorylation, and oxidant-mediated activation of NFκB. Data are accumulating to link alteration or abnormality of GPX1 expression to etiology of cancer, cardiovascular disease, neurodegeneration, autoimmune disease, and diabetes. Future research should focus on the mechanism of GPX1 in the pathogeneses and potential applications of GPX1 manipulation in the treatment of these disorders.
Tập 27 Số 1 - Trang 41-61 - 2007
Mechanisms and Consequences of Lipid Peroxidation in Biological Systems
Tập 5 Số 1 - Trang 365-390 - 1985
Docosahexaenoic Acid Signalolipidomics in Nutrition: Significance in Aging, Neuroinflammation, Macular Degeneration, Alzheimer's, and Other Neurodegenerative Diseases Essential polyunsaturated fatty acids (PUFAs) are critical nutritional lipids that must be obtained from the diet to sustain homeostasis. Omega-3 and -6 PUFAs are key components of biomembranes and play important roles in cell integrity, development, maintenance, and function. The essential omega-3 fatty acid family member docosahexaenoic acid (DHA) is avidly retained and uniquely concentrated in the nervous system, particularly in photoreceptors and synaptic membranes. DHA plays a key role in vision, neuroprotection, successful aging, memory, and other functions. In addition, DHA displays anti-inflammatory and inflammatory resolving properties in contrast to the proinflammatory actions of several members of the omega-6 PUFAs family. This review discusses DHA signalolipidomics, comprising the cellular/tissue organization of DHA uptake, its distribution among cellular compartments, the organization and function of membrane domains rich in DHA-containing phospholipids, and the cellular and molecular events revealed by the uncovering of signaling pathways regulated by DHA and docosanoids, the DHA-derived bioactive lipids, which include neuroprotectin D1 (NPD1), a novel DHA-derived stereoselective mediator. NPD1 synthesis agonists include neurotrophins and oxidative stress; NPD1 elicits potent anti-inflammatory actions and prohomeostatic bioactivity, is anti-angiogenic, promotes corneal nerve regeneration, and induces cell survival. In the context of DHA signalolipidomics, this review highlights aging and the evolving studies on the significance of DHA in Alzheimer's disease, macular degeneration, Parkinson's disease, and other brain disorders. DHA signalolipidomics in the nervous system offers emerging targets for pharmaceutical intervention and clinical translation.
Tập 31 Số 1 - Trang 321-351 - 2011
REGULATION OF GENE EXPRESSION BY DIETARY FAT ▪ Abstract Dietary fat is an important macronutrient for the growth and development of all organisms. In addition to its role as an energy source and its effects on membrane lipid composition, dietary fat has profound effects on gene expression, leading to changes in metabolism, growth, and cell differentiation. The effects of dietary fat on gene expression reflect an adaptive response to changes in the quantity and type of fat ingested. Specific fatty acid–regulated transcription factors have been identified in bacteria, amphibians, and mammals. In mammals, these factors include peroxisome proliferator–activated receptors (PPARα, -β, and -γ), HNF4α, NFκB, and SREBP1c. These factors are regulated by (a) direct binding of fatty acids, fatty acyl–coenzyme A, or oxidized fatty acids; (b) oxidized fatty acid (eicosanoid) regulation of G-protein–linked cell surface receptors and activation of signaling cascades targeting the nucleus; or (c) oxidized fatty acid regulation of intracellular calcium levels, which affect cell signaling cascades targeting the nucleus. At the cellular level, the physiological response to fatty acids will depend on (a) the quantity, chemistry, and duration of the fat ingested; (b) cell-specific fatty acid metabolism (oxidative pathways, kinetics, and competing reactions); (c) cellular abundance of specific nuclear and membrane receptors; and (d) involvement of specific transcription factors in gene expression. These mechanisms are involved in the control of carbohydrate and lipid metabolism, cell differentiation and growth, and cytokine, adhesion molecule, and eicosanoid production. The effects of fatty acids on the genome provide new insight into how dietary fat might play a role in health and disease.
Tập 19 Số 1 - Trang 63-90 - 1999
Hyperhomocyst(e)inemia as a Risk Factor for Occlusive Vascular Disease
Tập 12 Số 1 - Trang 279-298 - 1992
HOMOCYSTEINE METABOLISM ▪ Abstract Homocysteine is a sulfur amino acid whose metabolism stands at the intersection of two pathways: remethylation to methionine, which requires folate and vitamin B12 (or betaine in an alternative reaction); and transsulfuration to cystathionine, which requires pyridoxal-5′-phosphate. The two pathways are coordinated by S-adenosylmethionine, which acts as an allosteric inhibitor of the methylenetetrahydrofolate reductase reaction and as an activator of cystathionine β-synthase. Hyperhomocysteinemia, a condition that recent epidemiological studies have shown to be associated with increased risk of vascular disease, arises from disrupted homocysteine metabolism. Severe hyperhomocysteinemia is due to rare genetic defects resulting in deficiencies in cystathionine beta synthase, methylenetetrahydrofolate reductase, or in enzymes involved in methyl-B12 synthesis and homocysteine methylation. Mild hyperhomocysteinemia seen in fasting conditions is due to mild impairment in the methylation pathway (i.e. folate or B12 deficiencies or methylenetetrahydrofolate reductase thermolability). Post–methionine-load hyperhomocysteinemia may be due to heterozygous cystathionine β-synthase defect or B6 deficiency. Early studies with nonphysiological high homocysteine levels showed a variety of deleterious effects on endothelial or smooth muscle cells in culture. More recent studies with human beings and animals with mild hyperhomocysteinemia provided encouraging results in the attempt to understand the mechanism that underlies this relationship between mild elevations of plasma homocysteine and vascular disease. The studies with animal models indicated the possibility that the effect of elevated homocysteine is multifactorial, affecting both the vascular wall structure and the blood coagulation system.
Tập 19 Số 1 - Trang 217-246 - 1999