The DOI matches its Crossref record; 52 of the 53 references it cites were found in a registry or an index.
Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity
Open accessAbstract
Once considered divine retribution for sins, comorbidities of obesity (metabolic syndrome) are today attributed to obesity-induced metabolic defects. Here, we propose that obesity and hyperleptinemia protect lipid-intolerant nonadipose organs against lipotoxic lipid spillover during sustained caloric surplus. Metabolic syndrome is ascribed to lipotoxicity caused by age-related resistance to antilipotoxic protection by leptin.
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“Excessive RSF and PRF may also cause lipotoxicity owing to the accumulation of intracellular triglycerides and toxic metabolites such as ceramides57,58.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [58]
Experimental — accuracy not yet measuredIn the citing paper
“However, not all AT expansion is necessarily associated with pathological changes.”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [3]
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Cites
A Novel Serum Protein Similar to C1q, Produced Exclusively in Adipocytes
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Self-citationDiabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?
Neel, J. V. (1962) · Europe PMC (PubMed Central) · Cited by 3,172
Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?
(1962) · PubMed Central · Cited by 2,182
Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase
Minokoshi, Y., Kim, Y.-B., Peroni, O. D., Fryer, L. G. D., Müller, C., Carling, D., & Kahn, B. B. (2002) · Nature · doi:10.1038/415339a · Cited by 2,053
Cohen, J., Pertsemlidis, A., Kotowski, I. K., Graham, R., Garcia, C. K., & Hobbs, H. H. (2005) · Nature Genetics · doi:10.1038/ng1509 · Cited by 1,381
Obesity-associated improvements in metabolic profile through expansion of adipose tissue
Kim, J.-Y., van de Wall, E., Laplante, M., Azzara, A., Trujillo, M. E., Hofmann, S. M., Schraw, T., Durand, J. L., Li, H., Li, G., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci31021 · Cited by 1,310
Self-citationBoden, G., & Shulman, G. I. (2002) · European Journal of Clinical Investigation · doi:10.1046/j.1365-2362.32.s3.3.x · Cited by 1,300
Leptin-Replacement Therapy for Lipodystrophy
Oral, E. A., Simha, V., Ruiz, E., Andewelt, A., Premkumar, A., Snell, P., Wagner, A. J., DePaoli, A. M., Reitman, M. L., Taylor, S. I., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa012437 · Cited by 1,247
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Metabolic Dysregulation and Adipose Tissue Fibrosis: Role of Collagen VI
Khan, T., Muise, E. S., Iyengar, P., Wang, Z. V., Chandalia, M., Abate, N., Zhang, B. B., Bonaldo, P., Chua, S., & Scherer, P. E. (2009) · Molecular and Cellular Biology · doi:10.1128/mcb.01300-08 · Cited by 1,053
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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis
Tilg, H., & Moschen, A. R. (2010) · Hepatology · doi:10.1002/hep.24001 · Cited by 2,548
Adipose tissue remodeling and obesity
Sun, K., Kusminski, C. M., & Scherer, P. E. (2011) · Journal of Clinical Investigation · doi:10.1172/jci45887 · Cited by 1,941
Self-citationType 2 diabetes across generations: from pathophysiology to prevention and management
Nolan, C. J., Damm, P., & Prentki, M. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60614-4 · Cited by 923
Obesity and cancer—mechanisms underlying tumour progression and recurrence
Park, J., Morley, T. S., Kim, M. G., Clegg, D. J., & Scherer, P. E. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.94 · Cited by 813
Self-citationLipolysis: cellular mechanisms for lipid mobilization from fat stores
Grabner, G. F., Xie, H., Schweiger, M., & Zechner, R. (2021) · Nature Metabolism · doi:10.1038/s42255-021-00493-6 · Cited by 809
Metadata
- Authors
- Unger, R. H., & Scherer, P. E.
- Affiliations
- Veterans Health Administration (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Unger, Roger H.
- ORCID
- Scherer, Philipp E.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 21
- Issue
- 6
- Pages
- 345-352
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC2880185
- OpenAlex
- W1994949025
- Cited by
- 436
- References
- 53
- Citations by year
- 2026: 20 · 2025: 17 · 2024: 30 · 2023: 18 · 2022: 17 · 2021: 15 · 2020: 21 · 2019: 28 · 2018: 18 · 2017: 24 · 2016: 28 · 2015: 31 · 2014: 50 · 2013: 30 · 2012: 40
- FWCI
- 4.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK002700)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- metabolic syndrome, lipotoxicity, obesity, leptin resistance, hyperleptinemia, gluttony, sloths
- MeSH terms
- Adipose Tissue, Energy Intake, Humans, Hyperphagia, Lipids, Obesity, Leptin, Metabolic Syndrome
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