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.
Malonyl-CoA can be formed within the mitochondria, peroxisomes, and cytosol of mammalian cells. Besides being an intermediate in the pathways of de novo fatty acid biosynthesis and fatty acid elongation, malonyl-CoA has an important signaling function through its allosteric inhibition of carnitine palmitoyltransferase 1, the enzyme that normally exerts flux control over mitochondrial β-oxidation. Malonyl-CoA is rapidly turned over in mammalian cells, and the activities of acetyl-CoA carboxylase and malonyl-CoA decarboxylase are important determinants of its cytosolic concentration. It is now recognized that malonyl-CoA participates in a diverse range of physiological or pathological responses and systems. These include the ketogenic response of the liver to fasting and diabetes, carbohydrate versus fat fuel selection in muscle tissues, metabolic changes in muscle during contracture, alterations in fatty acid metabolism during cardiac ischemia and postischemic reperfusion, stimulation of B cell insulin secretion by glucose, and the hypothalamic control of appetite.
Fasting or malnutrition (FM) has dramatic effects on small intestinal mucosal structure and transport function. Intestinal secretion of ions and fluid is increased by FM both under basal conditions and in response to secretory agonists. Intestinal permeability to ions and macromolecules may also be elevated by FM, which increases the potential for fluid and electrolyte losses and for anaphylactic responses to luminal antigens. Mucosal atrophy induced by FM reduces total intestinal absorption of nutrients, but nutrient absorption normalized to mucosal mass may actually be enhanced by a variety of mechanisms, including increased transporter gene expression, electrochemical gradients, and ratio of mature to immature cells. These observations underscore the value of enteral feeding during health and disease.
We are becoming increasingly aware of inherited genetic abnormalities as causes of disease. However, alterations in gene expression can also contribute to other disease processes. Recently it has been suggested that our environment may alter such genes and thus be a direct influence on disease. Diet is a potent mechanism for altering the environment of cells of most organs, particularly the gastrointestinal tract. This review addresses the influence of nutritional factors on intestinal gene regulation. These influences include insulin, which is not a dietary component but responds to dietary changes, and butyrate, a short chain fatty acid produced by normal intestinal flora. Manipulation of diet may be a means of treating intestinal disorders. Nutritional treatment therefore is also discussed in the light of its effect on gene expression.
In light of the well-documented health benefits of physical activity and the fact that the majority of adult men and women are inactive, promoting regular physical activity is a public health priority. This chapter reviews current research findings regarding the determinants of exercise behavior. It also discusses the implications of this knowledge for individual and public health recommendations and intervention strategies for promoting physical activity. The discussion is predicated on the belief that physical activity is a complex, dynamic process. During their lives, individuals typically move through various phases of exercise participation that are determined by diverse factors. This chapter discusses physical activity determinants in two broad categories: individual characteristics, including motivations, self-efficacy, exercise history, skills, and other health behaviors; and environmental characteristics such as access, cost, and time barriers and social and cultural supports.
Understanding the molecular mechanisms that inform how diet and dietary supplements influence health and disease is an active research area. One such mechanism concerns the role of diet in modulating the activity and function of microRNAs (miRNAs). miRNAs are small noncoding RNA molecules that are involved in posttranscriptional gene silencing and have been shown to control gene expression in diverse biological processes including development, differentiation, cell proliferation, metabolism, and inflammation as well as in human diseases. Recent evidence described in this review highlights how dietary factors may influence cancer, cardiovascular disease, type 2 diabetes mellitus, obesity, and nonalcoholic fatty liver disease through modulation of miRNA expression. Additionally, circulating miRNAs are emerging as putative biomarkers of disease, susceptibility, and perhaps dietary exposure. Research needs to move beyond associations in cells and animals to understanding the direct effects of diet and dietary supplements on miRNA expression and function in human health and disease.
The fields of immunology and metabolism are rapidly converging on adipose tissue. During obesity, many immune cells infiltrate or populate in adipose tissue and promote a low-grade chronic inflammation. Studies to date have suggested that perturbation of inflammation is critically linked to nutrient metabolic pathways and to obesity-associated complications such as insulin resistance and type 2 diabetes. Despite these advances, however, many open questions remain including how inflammatory responses are initiated and maintained, how nutrients impact the function of various immune populations, and how inflammatory responses affect systemic insulin sensitivity. Here we review recent studies on the roles of various immune cells at different phases of obesity and discuss molecular mechanisms underlying obesity-associated inflammation. Better understanding of the events occurring in adipose tissue will provide insights into the pathophysiological role of inflammation in obesity and shed light on the pathogenesis of obesity-associated metabolic syndrome.
Norman I. Krinsky, John T. Landrum, Richard A. Bone
▪ Abstract The macular region of the primate retina is yellow in color due to the presence of the macular pigment, composed of two dietary xanthophylls, lutein and zeaxanthin, and another xanthophyll, meso-zeaxanthin. The latter is presumably formed from either lutein or zeaxanthin in the retina. By absorbing blue-light, the macular pigment protects the underlying photoreceptor cell layer from light damage, possibly initiated by the formation of reactive oxygen species during a photosensitized reaction. There is ample epidemiological evidence that the amount of macular pigment is inversely associated with the incidence of age-related macular degeneration, an irreversible process that is the major cause of blindness in the elderly. The macular pigment can be increased in primates by either increasing the intake of foods that are rich in lutein and zeaxanthin, such as dark-green leafy vegetables, or by supplementation with lutein or zeaxanthin. Although increasing the intake of lutein or zeaxanthin might prove to be protective against the development of age-related macular degeneration, a causative relationship has yet to be experimentally demonstrated.
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