The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Obesity and Hypertriglyceridemia Produce Cognitive Impairment
Open accessAbstract
Obesity is associated with cognitive impairments. Long-term mechanisms for this association include consequences of hyperglycemia, dyslipidemia, or other factors comprising metabolic syndrome X. We found that hypertriglyceridemia, the main dyslipidemia of metabolic syndrome X, is in part responsible for the leptin resistance seen in obesity. Here we determined whether triglycerides have an immediate and direct effect on cognition. Obese mice showed impaired acquisition in three different cognitive paradigms: the active avoidance T-maze, the Morris water maze, and a food reward lever press. These impairments were not attributable to differences in foot shock sensitivity, swim speed, swimming distance, or voluntary milk consumption. Impaired cognition in obese mice was improved by selectively lowering triglycerides with gemfibrozil. Injection into the brain of the triglyceride triolein, but not of the free fatty acid palmitate, impaired acquisition in normal body weight mice. Triolein or milk (97% of fats are triglycerides), but not skim milk (no triglycerides), impaired maintenance of the N-methyl-d-aspartate component of the hippocampal long-term synaptic potential. Measures of oxidative stress in whole brain were reduced by gemfibrozil. We conclude that triglycerides mediate cognitive impairment as seen in obesity, possibly by impairing maintenance of the N-methyl-d-aspartate component of hippocampal long-term potentiation, and that lowering triglycerides can reverse the cognitive impairment and improve oxidative stress in the brain.
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“Obesity and hypertriglyceridemia produce cognitive impairment in mice, including reduced lever pressing for food reward ([59](#B59)), and epidemiological studies show an association of body mass index and risk of Parkinson disease and cognitive decline ([85](#B85)).”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [59]
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Cites
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Ghrelin controls hippocampal spine synapse density and memory performance
Diano, S., Farr, S. A., Benoit, S. C., McNay, E. C., da Silva, I., Horvath, B., Gaskin, F. S., Nonaka, N., Jaeger, L. B., Banks, W. A., et al. (2006) · Nature Neuroscience · doi:10.1038/nn1656 · Cited by 828
Self-citationLower cognitive function in the presence of obesity and hypertension: the Framingham heart study
Elias, M. F., Elias, P. K., SULLIVAN, L. M., Wolf, P. A., & D’Agostino, R. B. (2003) · International Journal of Obesity · doi:10.1038/sj.ijo.802225 · Cited by 691
Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier
Banks, W. A., Coon, A. B., Robinson, S. M., Moinuddin, A., Shultz, J. M., Nakaoke, R., & Morley, J. E. (2004) · Diabetes · doi:10.2337/diabetes.53.5.1253 · Cited by 512
Self-citationImpairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents
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Self-citationEffects of leptin on memory processing
Farr, S. A., Banks, W. A., & Morley, J. E. (2005) · Peptides · doi:10.1016/j.peptides.2005.10.006 · Cited by 324
Self-citationRole of reactive oxygen species in hippocampal long‐term potentiation: Contributory or inhibitory?
Knapp, L. T., & Klann, E. (2002) · Journal of Neuroscience Research · doi:10.1002/jnr.10371 · Cited by 225
Orexin-A (Hypocretin-1) and leptin enhance LTP in the dentate gyrus of rats in vivo
Wayner, M. J., Armstrong, D. L., Phelix, C. F., & Oomura, Y. (2004) · Peptides · doi:10.1016/j.peptides.2004.03.018 · Cited by 190
Research works printed but not linked: 1
- Shang, Biochem Biophys Res Commun, 267, 208
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Stranahan, A. M., Norman, E. D., Lee, K. M., Cutler, R. G., Telljohann, R. S., Egan, J. M., & Mattson, M. P. (2008) · Hippocampus · doi:10.1002/hipo.20470 · Cited by 766
Smith, E., Hay, P., Campbell, L. V., & Trollor, J. N. (2011) · Obesity Reviews · doi:10.1111/j.1467-789x.2011.00920.x · Cited by 706
“Obese rats have been shown to perform worse on learning and memory tasks compared with rats of normal weight (7,8).”
BackgroundWestern diet consumption and cognitive impairment: Links to hippocampal dysfunction and obesity
Kanoski, S. E., & Davidson, T. L. (2010) · Physiology & Behavior · doi:10.1016/j.physbeh.2010.12.003 · Cited by 710
“Rodents receiving several months of ad libitum exposure to diets with high levels of both SFA and sucrose [42–45], diets that contain high levels of SFA with more complex carbohydrates [46,47], as well as diets that contain high levels of sucrose without elevated levels of fat [18] are impaired in learning the locatio…”
BackgroundCognitive impairment following high fat diet consumption is associated with brain inflammation
Pistell, P. J., Morrison, C. D., Gupta, S., Knight, A. G., Keller, J. N., Ingram, D. K., & Bruce‐Keller, A. J. (2009) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2009.11.010 · Cited by 623
“For example, it has been shown that direct administration of triglycerides can impair hippocampal longterm potentiation, and lowering triglycerides pharmacologically with gemfibrozil can reduce the expression ofmarkers of oxidative stress in the brains of obese mice (Farr et al., 2008).”
Neurological consequences of obesity
O’Brien, P. D., Hinder, L. M., Callaghan, B. C., & Feldman, E. L. (2017) · The Lancet Neurology · doi:10.1016/s1474-4422(17)30084-4 · Cited by 561
Metadata
- Authors
- Farr, S. A., Yamada, K. A., Butterfield, D. A., Abdul, H. M., Xu, L., Miller, N. E., Banks, W. A., & Morley, J. E.
- Affiliations
- St. Louis VA Medical Center (US)
- Washington University in St. Louis (US)
- University of Kentucky (US)
- Department of Chemistry and Center of Membrane Sciences (D.A.B., H.M.A.), University of Kentucky, Lexington, Kentucky 40536
- Division of Geriatric Medicine (S.A.F., N.E.M., W.A.B., J.E.M.), Saint Louis University School of Medicine, St. Louis, Missouri 63104
- Corresponding author
- Banks, William A.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2008-02-14
- Volume
- 149
- Issue
- 5
- Pages
- 2628-2636
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC2329289
- OpenAlex
- W2146978742
- Cited by
- 382
- References
- 37
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 13 · 2023: 17 · 2022: 23 · 2021: 23 · 2020: 21 · 2019: 20 · 2018: 26 · 2017: 26 · 2016: 34 · 2015: 27 · 2014: 29 · 2013: 24 · 2012: 20
- FWCI
- 9.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- U.S. Public Health Service (051334, 42774)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity, hypertriglyceridemia, cognitive impairment, triglycerides, metabolic syndrome X, leptin resistance, dyslipidemia, gemfibrozil, triolein, palmitate, NMDA receptor, hippocampal long-term potentiation, oxidative stress, avoidance learning, Morris water maze, food reward
- MeSH terms
- Animals, Hypolipidemic Agents, Avoidance Learning, Cognition Disorders, Diet, Atherogenic, Male, Memory, Mice, Inbred Strains, Obesity, Swimming, Triolein, Lipid Peroxidation, Hypertriglyceridemia, Gemfibrozil, Maze Learning, Excitatory Postsynaptic Potentials, Mice
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