The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Severely Impaired Adipsin Expression in Genetic and Acquired Obesity
Abstract
Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (> 100-fold) in two strains of genetically obese mice ( db / db and ob / ob ), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.
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Cites
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Cited by
Adipose Expression of Tumor Necrosis Factor-α: Direct Role in Obesity-Linked Insulin Resistance
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Self-citationAdipose Tissue as an Endocrine Organ
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Adipokines in health and disease
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Metadata
- Authors
- Flier, J. S., Cook, K. S., Usher, P., & Spiegelman, B. M.
- Venue
- Science
- Published
- 1987-07-24
- Volume
- 237
- Issue
- 4813
- Pages
- 405-408
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2010886780
- Cited by
- 329
- References
- 29
- FWCI
- 11.00
- Type
- journal article
- Language
- en
- Open access
- closed
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