- Home
- A-Z Publications
- Annual Review of Nutrition
- Previous Issues
- Volume 19, 1999
Annual Review of Nutrition - Volume 19, 1999
Volume 19, 1999
- Review Articles
-
-
-
TRANSGENIC MODELS OF GROWTH HORMONE ACTION
Vol. 19 (1999), pp. 437–461More Less▪ AbstractA growth-promoting principle of the pituitary gland was discovered in 1921, and bovine growth hormone (GH) was isolated in 1944. Since then, the structure of GH as it relates to its biological activities has been an exciting research topic. Equally fascinating is the relationship between GH structure and its metabolic activities. In attempts to define some of these activities, several investigators have used GH transgenic mice as models. In this review we summarize what is known about the molecular mechanisms of GH action. We then describe some of the GH transgenic models and point out potential targets for nutrition research.
-
-
-
-
REGULATION OF FATTY ACID OXIDATION IN SKELETAL MUSCLE
Vol. 19 (1999), pp. 463–484More Less▪ AbstractResearchers using animals are beginning to elucidate the control of fatty acid metabolism in muscle at the molecular and enzymatic level. This review examines the physiological data that has been collected from human subjects in the context of the proposed control mechanisms. A number of factors, including the availability of free fatty acids and the abundance of fatty acid transporters, may influence the rate of muscle fatty acid oxidation. However, the predominant point of control appears to be the rate at which fatty acyl–coenzyme A is transported into the mitochondria by the carnitine palmitoyl transferase system. In turn, evidence suggests that the intracellular concentration of malonyl–coenzyme A in muscle is an important regulator of carnitine palmitoyl transferase–I activity. Malonyl–coenzyme A is increased by glucose, which is likely the mechanism whereby glucose intake suppresses the transfer of fatty acids into the mitochondria for subsequent oxidation. In contrast, malonyl–coenzyme A levels decrease during exercise, which enables increased fatty acid oxidation. However, for any given carnitine palmitoyl transferase–I activity, there may be an effect of free fatty acid availability on fatty acid oxidation, particularly at low levels of free fatty acids. Nonetheless, the rate of glucose or glycogen metabolism is probably the primary regulator of the balance between glucose and fatty acid oxidation in muscle.
-
-
-
CHARACTERIZATION OF GLYCOSYLPHOSPHATIDYLINOSITIOL-ANCHORED, SECRETED, AND INTRACELLULAR VERTEBRATE MONO-ADP-RIBOSYLTRANSFERASES1
Ian J. Okazaki, and Joel MossVol. 19 (1999), pp. 485–509More Less▪ AbstractMono-ADP-ribosylation is a posttranslational modification of proteins in which the ADP-ribose moiety of nicotinamide adenine dinucleotide is transferred to an acceptor amino acid. Five mammalian ADP-ribosyltransferases (ART1–ART5) have been cloned and expression is restricted to tissues such as cardiac and skeletal muscle, leukocytes, brain, and testis. ART1 and ART2 are glycosylphosphatidylinositol (GPI)-anchored ectoenzymes. ART5 appears not to be GPI-linked and may be secreted. In skeletal muscle and lymphocytes, ART1 modifies specific members of the integrin family of adhesion molecules, suggesting that ADP-ribosylation affects cell-matrix or cell-cell interactions. In lymphocytes, ADP-ribosylation of surface proteins is associated with changes in p56lck tyrosine kinase-mediated signaling. The catalytic sites of bacterial toxins and vertebrate transferases have conserved structural features, consistent with a common reaction mechanism. ADP-ribosylation can be reversed by ADP-ribosylarginine hydrolases, resulting in the regeneration of free arginine. Thus, an ADP-ribosylation cycle may play a regulatory role in vertebrate tissues.
-
-
-
METABOLIC ENGINEERING WITH RECOMBINANT ADENOVIRUSES
Vol. 19 (1999), pp. 511–544More Less▪ AbstractFuel homeostasis in mammals is accomplished by the interplay between tissues and organs with distinct metabolic roles. These regulatory mechanisms are disrupted in obesity and diabetes, leading to a renewed emphasis on discovery of molecular and pharmacologic methods for reversing metabolic disorders. In this chapter, we review the use of recombinant adenoviral vectors as tools for delivering metabolic regulatory genes to cells in culture and to tissues of intact animals. Included are studies on the use of these vectors for gaining insights into the biochemical mechanisms that regulate glucose-stimulated insulin secretion from pancreatic islet β-cells. We also highlight their use for understanding the function of newly discovered genes that regulate glycogen metabolism in liver and other tissues, and for evaluating “candidate” genes such as glucose-6-phosphatase, which may contribute to development of metabolic dysfunction in pancreatic islets and liver. Finally, we discuss the use of adenoviral and related vectors for causing chronic increases in the levels of circulating hormones. These examples serve to highlight the power of viral gene transfer vectors as tools for understanding metabolic regulatory mechanisms.
-
-
-
DIETARY FACTORS IN HUMAN COLORECTAL CANCER
Vol. 19 (1999), pp. 545–586More Less▪ AbstractColorectal cancer is a significant cause of mortality in Western societies. The progression of the disease from normal colonic epithelium to the acquisition of the malignant phenotype is accompanied by numerous genetic and epigenetic alterations. Compelling experimental and epidemiological evidence indicates that diet and nutrition are key factors in the modulation of colorectal cancer. A salient case in point is the recent observation that a dietary regimen based on a Western-style diet provokes in the rodent colon the appearance of preneoplastic lesions in the absence of any genotoxic insult. This review mainly describes dietary factors that inhibit the development and progression of colorectal cancer. Much is unknown about the precise mechanisms of action of chemically disparate nutrients and how they interfere with the development and progression of this disease. Current knowledge about this important issue is summarized. We believe that continuing scrutiny and precise assessment of the benefits (and potential risks) of nutrients in the treatment and prevention of colorectal cancer will prove significant to controlling this devastating disease.
-
Previous Volumes
-
Volume 44 (2024)
-
Volume 43 (2023)
-
Volume 42 (2022)
-
Volume 41 (2021)
-
Volume 40 (2020)
-
Volume 39 (2019)
-
Volume 38 (2018)
-
Volume 37 (2017)
-
Volume 36 (2016)
-
Volume 35 (2015)
-
Volume 34 (2014)
-
Volume 33 (2013)
-
Volume 32 (2012)
-
Volume 31 (2011)
-
Volume 30 (2010)
-
Volume 29 (2009)
-
Volume 28 (2008)
-
Volume 27 (2007)
-
Volume 26 (2006)
-
Volume 25 (2005)
-
Volume 24 (2004)
-
Volume 23 (2003)
-
Volume 22 (2002)
-
Volume 21 (2001)
-
Volume 20 (2000)
-
Volume 19 (1999)
-
Volume 18 (1998)
-
Volume 17 (1997)
-
Volume 16 (1996)
-
Volume 15 (1995)
-
Volume 14 (1994)
-
Volume 13 (1993)
-
Volume 12 (1992)
-
Volume 11 (1991)
-
Volume 10 (1990)
-
Volume 9 (1989)
-
Volume 8 (1988)
-
Volume 7 (1987)
-
Volume 6 (1986)
-
Volume 5 (1985)
-
Volume 4 (1984)
-
Volume 3 (1983)
-
Volume 2 (1982)
-
Volume 1 (1981)
-
Volume 0 (1932)