Increased obese mRNA expression in omental fat cells from massively obese humans
Abstract
Obesity presents a significant challenge to the general health of affluent nations in terms of the number of people affected, the serious associated maladies and the lack of effective treatments. While common wisdom has held that obesity results from 'gluttony and sloth', a number of studies have indicated physiological causes of underlying the pathogenesis of obesity, with the degree of adiposity having a strong genetic component. Recently, the obese gene in the ob/ob mouse was cloned, along with its human homologue. The specific production of the obese protein by adipose tissue suggested that it may function in a feedback loop from fat tissue to the hypothalamus to control energy intake and/or energy expenditure, and that it may play a role in the pathogenesis of human obesity. In this study we report that obese mRNA expression is elevated in ex vivo omental adipocytes isolated from massively obese humans in the absence of an identifiable mutation. Therefore, we speculate that this increased expression may suggest that the massively obese are insensitive to the putative regulatory function(s) of the obese gene product.
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Plasma leptin concentrations are generally proportional to the degree of adiposity.
“Therefore, obesity is associated with excessive plasma leptin concentration (hyperleptinemia) as a result of leptin resistance, and plasma leptin concentrations are generally proportional to the degree of adiposity [96].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [96]
Obesity is associated with excessive plasma leptin concentration (hyperleptinemia) as a result of leptin resistance.
“Therefore, obesity is associated with excessive plasma leptin concentration (hyperleptinemia) as a result of leptin resistance, and plasma leptin concentrations are generally proportional to the degree of adiposity [96].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [96]
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- Authors
- Hamilton, B. S., Paglia, D., Kwan, A. Y. M., & Deitel, M.
- Affiliations
- University of Toronto (CA)
- Sunnybrook Health Science Centre (CA)
- Venue
- Nature Medicine
- Published
- 1995-09
- Volume
- 1
- Issue
- 9
- Pages
- 953-956
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2056352776
- Cited by
- 526
- References
- 3
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 9 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 4 · 2019: 7 · 2018: 6 · 2017: 13 · 2016: 4 · 2015: 11 · 2014: 11 · 2013: 14 · 2012: 17
- FWCI
- 51.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- obese gene, omental adipocytes, massive obesity, leptin, energy expenditure, leptin resistance, adipose tissue
- MeSH terms
- Adipose Tissue, Adolescent, Adult, Aged, Aged, 80 and over, Animals, Energy Metabolism, Female, Gene Expression Regulation, Humans, Male, Mice, Inbred C57BL, Middle Aged, Obesity, Omentum, Proteins, RNA, Messenger, Protein Biosynthesis, Body Mass Index, Leptin, Cell Size, Mice
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