The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Is the Energy Homeostasis System Inherently Biased Toward Weight Gain?
Open accessAbstract
We describe a model of energy homeostasis to better understand neuronal pathways that control energy balance and their regulation by hormonal signals such as insulin and leptin. Catabolic neuronal pathways are those that both reduce food intake and increase energy expenditure (e.g., melanocortin neurons in the hypothalamic arcuate nucleus) and are stimulated by input from insulin and leptin. We propose that in the basal state, catabolic effectors are activated in response to physiological concentrations of leptin and insulin, and that this activation is essential to prevent excessive weight gain. In contrast, anabolic pathways (e.g., neurons containing neuropeptide Y) are those that stimulate food intake and decrease energy expenditure and are strongly inhibited by these same basal concentrations of insulin and leptin. In the basal state, therefore, catabolic effector pathways are activated while anabolic effector pathways are largely inhibited. The response to weight loss includes both activation of anabolic and inhibition of catabolic pathways and is, thus, inherently more vigorous than the response to weight gain (stimulation of already-activated catabolic pathways and inhibition of already-suppressed anabolic pathways). Teleological, molecular, physiological, and clinical aspects of this hypothesis are presented, along with a discussion of currently available supporting evidence.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Kopelman, P. G. (2000) · Nature · doi:10.1038/35007508 · Cited by 4,795
Coexpression of Agrp and NPY in fasting-activated hypothalamic neurons
Hahn, T. M., Breininger, J. F., Baskin, D. G., & Schwartz, M. W. (1998) · Nature Neuroscience · doi:10.1038/1082 · Cited by 1,164
Self-citationBroberger, 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
Insulin activates ATP-sensitive K+ channels in hypothalamic neurons of lean, but not obese rats
Spanswick, D., Smith, M. A., Mirshamsi, S., Routh, V. H., & Ashford, M. L. J. (2000) · Nature Neuroscience · doi:10.1038/77660 · Cited by 495
Regulation of hypothalamic proopiomelanocortin mRNA by leptin in ob/ob mice
Thornton, J. E., Cheung, C. C., Clifton, D. K., & Steiner, R. A. (1997) · Endocrinology · doi:10.1210/endo.138.11.5651 · Cited by 437
The Catabolic Action of Insulin in the Brain Is Mediated by Melanocortins
Benoit, S. C., Air, E. L., Coolen, L. M., Strauss, R., Jackman, A., Clegg, D. J., Seeley, R. J., & Woods, S. C. (2002) · The Journal of Neuroscience · doi:10.1523/jneurosci.22-20-09048.2002 · Cited by 417
Self-citation
Cited by
Adipocytes as regulators of energy balance and glucose homeostasis
Rosen, E. D., & Spiegelman, B. M. (2006) · Nature · doi:10.1038/nature05483 · Cited by 2,170
Leptin receptor signaling in POMC neurons is required for normal body weight homeostasis
Balthasar, N., Coppari, R., McMinn, J., Liu, S. M., Lee, C. E., Tang, V., Kenny, C. D., McGovern, R. A., Chua, S. C., Elmquist, J. K., et al. (2004) · Neuron · doi:10.1016/j.neuron.2004.06.004 · Cited by 935
Gonadal Hormones Determine Sensitivity to Central Leptin and Insulin
Clegg, D. J., Brown, L. M., Woods, S. C., & Benoit, S. C. (2006) · Diabetes · doi:10.2337/diabetes.55.04.06.db05-1339 · Cited by 552
Self-citationNair (2005) · doi:10.1093/ajcn/81.5.953 · Cited by 469
Coppari, R., Ichinose, M., Lee, C. E., Pullen, A. E., Kenny, C. D., McGovern, R. A., Tang, V., Liu, S. M., Ludwig, T., Chua, S. C., et al. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2004.12.004 · Cited by 457
Adaptive thermogenesis in humans
Rosenbaum, M., & Leibel, R. L. (2010) · International Journal of Obesity · doi:10.1038/ijo.2010.184 · Cited by 349
Self-citationThe defence of body weight: a physiological basis for weight regain after weight loss
Sumithran, P., & Proietto, J. (2013) · Clinical Science · doi:10.1042/cs20120223 · Cited by 310
Intranasal Insulin Reduces Body Fat in Men but not in Women
Hallschmid, M., Benedict, C., Schultes, B., Fehm, H.-L., Born, J., & Kern, W. (2004) · Diabetes · doi:10.2337/diabetes.53.11.3024 · Cited by 281
Sleep restriction leads to increased activation of brain regions sensitive to food stimuli
St-Onge, M.-P., McReynolds, A., Trivedi, Z. B., Roberts, A. L., Sy, M., & Hirsch, J. (2012) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.111.027383 · Cited by 277
Anticipatory physiological regulation in feeding biology: Cephalic phase responses
Power, M. L., & Schulkin, J. (2008) · Appetite · doi:10.1016/j.appet.2007.10.006 · Cited by 258
Oral and postoral determinants of food reward.
SCLAFANI, A. (2004) · Physiology & Behavior · doi:10.1016/j.physbeh.2004.04.031 · Cited by 218
O'Rahilly, S., & Farooqi, I. S. (2008) · Diabetes · doi:10.2337/db08-0210 · Cited by 205
Elman, I., Borsook, D., & Lukas, S. E. (2006) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301051 · Cited by 169
Energy intake in weight-reduced humans
Rosenbaum, M., Kissileff, H. R., Mayer, L. E. S., Hirsch, J., & Leibel, R. L. (2010) · Brain Research · doi:10.1016/j.brainres.2010.05.062 · Cited by 142
Self-citationDiet in the management of weight loss
Strychar, I. (2006) · Canadian Medical Association Journal · doi:10.1503/cmaj.045037 · Cited by 129
Molecular physiology of weight regulation in mice and humans
Leibel, R. L. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.245 · Cited by 120
Self-citationWarne, J. P. (2009) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2008.09.036 · Cited by 112
van den Hoek, A. M., Voshol, P. J., Karnekamp, B. N., Buijs, R. M., Romijn, J. A., Havekes, L. M., & Pijl, H. (2004) · Diabetes · doi:10.2337/diabetes.53.10.2529 · Cited by 109
Changes in gut hormones after bariatric surgery
Vincent, R. P., & Le Roux, C. W. (2008) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2007.03164.x · Cited by 100
Motivation, Readiness to Change, and Weight Loss Following Adjustable Gastric Band Surgery
Dixon, J. B., Laurie, C. P., Anderson, M. L., Hayden, M. J., Dixon, M. E., & O'Brien, P. E. (2009) · Obesity · doi:10.1038/oby.2008.609 · Cited by 90
Overweight and Obesity in ΔF508 Homozygous Cystic Fibrosis
Kastner-Cole, D., Palmer, C. N. A., Ogston, S. A., Mehta, A., & Mukhopadhyay, S. (2005) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2005.06.003 · Cited by 73
Neuroendocrine and metabolic effects of adipocyte-derived hormones
Jackson, M. B., & Ahima, R. S. (2006) · Clinical Science · doi:10.1042/cs20050243 · Cited by 68
Stealth Interventions for Obesity Prevention and Control
Robinson, T. N. (2010) · Obesity Prevention · doi:10.1016/b978-0-12-374387-9.00025-8 · Cited by 64
If Body Fatness is Under Physiological Regulation, Then How Come We Have an Obesity Epidemic?
Speakman, J. R. (2014) · Physiology · doi:10.1152/physiol.00053.2013 · Cited by 53
Heijboer, A. C., van den Hoek, A. M., Pijl, H., Voshol, P. J., Havekes, L. M., Romijn, J. A., & Corssmit, E. P. M. (2005) · Diabetologia · doi:10.1007/s00125-005-1838-8 · Cited by 43
Hooper, L. E., Foster-Schubert, K. E., Weigle, D. S., Sorensen, B., Ulrich, C. M., & McTiernan, A. (2010) · Nutrition Research · doi:10.1016/j.nutres.2010.02.002 · Cited by 36
The threshold shift paradigm of obesity: evidence from surgically induced weight loss
Ferrannini, E., Rosenbaum, M., & Leibel, R. L. (2014) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.114.090167 · Cited by 32
Self-citationChong, P., Beah, Z., Grube, B., & Riede, L. (2014) · Phytotherapy Research · doi:10.1002/ptr.5158 · Cited by 32
Metadata
- Authors
- Schwartz, M. W., Woods, S. C., Seeley, R. J., Barsh, G. S., Baskin, D. G., & Leibel, R. L.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2003-02-01
- Volume
- 52
- Issue
- 2
- Pages
- 232-238
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2107551481
- Cited by
- 351
- References
- 6
- FWCI
- 12.84
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.