The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Hypothalamic mechanisms in cachexia
Open accessAbstract
The role of nutrition and balanced metabolism in normal growth, development, and health maintenance is well known. Patients affected with either acute or chronic diseases often show disorders of nutrient balance. In some cases, a devastating state of malnutrition known as cachexia arises, brought about by a synergistic combination of a dramatic decrease in appetite and an increase in metabolism of fat and lean body mass. Other common features that are not required for the diagnosis include decreases in voluntary movement, insulin resistance, and anhedonia. This combination is found in a number of disorders including cancer, cystic fibrosis, AIDS, rheumatoid arthritis, renal failure, and Alzheimer's disease. The severity of cachexia in these illnesses is often the primary determining factor in both quality of life, and in eventual mortality. Indeed, body mass retention in AIDS patients has a stronger association with survival than any other current measure of the disease. This has led to intense investigation of cachexia and the proposal of numerous hypotheses regarding its etiology. Most authors suggest that cytokines released during inflammation and malignancy act on the central nervous system to alter the release and function of a number of neurotransmitters, thereby altering both appetite and metabolic rate. This review will discuss the salient features of cachexia in human diseases, and review the mechanisms whereby inflammation alters the function of key brain regions to produce stereotypical illness behavior.
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Cites
Principles of interleukin (IL)-6-type cytokine signalling and its regulation
HEINRICH, P. C., BEHRMANN, I., HAAN, S., HERMANNS, H. M., MÜLLER-NEWEN, G., & SCHAPER, F. (2003) · Biochemical Journal · doi:10.1042/bj20030407 · Cited by 3,272 · cited 1×
“Receptor binding stimulates gp130-mediated activation of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway [157], the same pathway activated by the binding of leptin to its receptor [158].”
Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure
Levine, B., Kalman, J., Mayer, L., Fillit, H. M., & Packer, M. (1990) · New England Journal of Medicine · doi:10.1056/nejm199007263230405 · Cited by 2,582 · cited 1×
“Indeed, elevated circulating levels of TNF-α and IL-6 in patients with cardiac cachexia are the strongest predictor for pathological weight loss [27,28].”
Anatomy and regulation of the central melanocortin system
Cone, R. D. (2005) · Nature Neuroscience · doi:10.1038/nn1455 · Cited by 1,583
IKKβ/NF-κB Activation Causes Severe Muscle Wasting in Mice
Cai, D., Frantz, J. D., Tawa, N. E., Melendez, P. A., Oh, B.-C., Lidov, H. G. W., Hasselgren, P.-O., Frontera, W. R., Lee, J., Glass, D. J., et al. (2004) · Cell · doi:10.1016/j.cell.2004.09.027 · Cited by 1,367
Interleukin-6-deficient mice develop mature-onset obesity
Wallenius, V., Wallenius, K., Ahrén, B., Rudling, M., Carlsten, H., Dickson, S. L., Ohlsson, C., & Jansson, J.-O. (2002) · Nature Medicine · doi:10.1038/nm0102-75 · Cited by 1,213
Elmquist, J. K., Elias, C. F., & Saper, C. B. (1999) · Neuron · doi:10.1016/s0896-6273(00)81084-3 · Cited by 1,160
Cerebrospinal fluid leptin levels: Relationship to plasma levels and to adiposity in humans
Schwartz, M. W., Peskind, E., Raskind, M., Boyko, E. J., & Porte, D. (1996) · Nature Medicine · doi:10.1038/nm0596-589 · Cited by 1,014
STAT3 signalling is required for leptin regulation of energy balance but not reproduction
Bates, S. H., Stearns, W. H., Dundon, T. A., Schubert, M., Tso, A. W. K., Wang, Y., Banks, A. S., Lavery, H. J., Haq, A. K., Maratos-Flier, E., et al. (2003) · Nature · doi:10.1038/nature01388 · Cited by 1,010 · cited 2×
“This process is dependent on gp130-mediated activation of JAK2/STAT3 signaling, which is known to underlie the induction of POMC mRNA expression by leptin, suggesting that LIF may activate hypothalamic POMC neurons in a similar manner [160,175].”
Murakami, M., Naraba, H., Tanioka, T., Semmyo, N., Nakatani, Y., Kojima, F., Ikeda, T., Fueki, M., Ueno, A., Oh-ishi, S., et al. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m003505200 · Cited by 964
Broberger, C., Johansen, J., Johansson, C., Schalling, M., & Hökfelt, T. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.25.15043 · Cited by 798
Cited by
Cancer Cachexia: Mediators, Signaling, and Metabolic Pathways
Fearon, K. C. H., Glass, D. J., & Guttridge, D. C. (2012) · Cell Metabolism · doi:10.1016/j.cmet.2012.06.011 · Cited by 1,205
Neurobiology of food intake in health and disease
Morton, G. J., Meek, T. H., & Schwartz, M. W. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3745 · Cited by 748
Understanding cachexia as a cancer metabolism syndrome
Porporato, P. E. (2016) · Oncogenesis · doi:10.1038/oncsis.2016.3 · Cited by 562
Inter-tissue communication in cancer cachexia
Argilés, J. M., Stemmler, B., López-Soriano, F. J., & Busquets, S. (2019) · Nature Reviews Endocrinology · doi:10.1038/s41574-018-0123-0 · Cited by 305
Malnutrition, fatigue, frailty, vulnerability, sarcopenia and cachexia: overlap of clinical features
Jeejeebhoy, K. N. (2012) · Current Opinion in Clinical Nutrition and Metabolic Care · doi:10.1097/mco.0b013e328352694f · Cited by 226
Metadata
- Authors
- Grossberg, A. J., Scarlett, J. M., & Marks, D. L.
- Venue
- Physiology & Behavior
- Publisher
- Elsevier BV
- Published
- 2010-07
- Volume
- 100
- Issue
- 5
- Pages
- 478-489
- ISSN
- 0031-9384 (ISSN-L)
- OpenAlex
- W1990411503
- Cited by
- 160
- References
- 35
- FWCI
- 4.42
- Type
- journal article
- Language
- en
- Open access
- green
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