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Insulin Stimulates Both Leptin Secretion and Production by Rat White Adipose Tissue
Abstract
Leptin, the peptide encoded by the obese gene, is secreted by adipose cells and plays a role in regulating food intake, energy expenditure, and adiposity. Because earlier studies suggested that insulin increases the expression of leptin, we investigated the effect of insulin on leptin secretion by adipose tissue. Epididymal fat pads were incubated in vitro in the presence or absence of insulin over a 4-h time course. Insulin increased leptin secretion by about 80% at all time points studied. After 10 min of insulin treatment, the amount of tissue-associated leptin was lower in insulin-stimulated tissue, presumably due to the increased secretion. At later times, both tissue-associated leptin and total leptin production were higher in insulin-treated tissue. In untreated, isolated adipose cells, immunostaining of leptin was detected in the endoplasmic reticulum by confocal microscopy. After insulin treatment, there were two populations of cells. In many cells, leptin staining became fainter and was restricted to a narrow band near the plasma membrane. However, in other cells the leptin-staining pattern was unchanged. Leptin did not colocalize with GLUT4, the glucose transporter isoform found primarily in insulin-responsive cells, in either basal or insulin-stimulated adipose cells. In this study, insulin increased both secretion and production of leptin by adipose tissue fragments. Interestingly, insulin appeared to stimulate the transport of leptin from the endoplasmic reticulum rather than acting on a pool of regulated secretory vesicles. (Endocrinology 138: 4463-4472, 1997)
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“therefore, some of the positive effects of insulin on the reproductive system might derive from its ability to stimulate leptin secretion.106”
From Pubertal development and regulation (2016) · cites this paper as [106]
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“Insulin is a major regulator of leptin production; therefore, some of the positive effects of insulin on the reproductive system might derive from its ability to stimulate leptin secretion.106”
From Pubertal development and regulation (2016) · cites this paper as [106]
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Metadata
- Authors
- Barr, V. A., Malide, D., Zarnowski, M. J., Taylor, S. I., & Cushman, S. W.
- Affiliations
- National Institutes of Health (US)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1997-10-01
- Volume
- 138
- Issue
- 10
- Pages
- 4463-4472
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2126095470
- Cited by
- 297
- References
- 36
- Citations by year
- 2025: 2 · 2024: 8 · 2023: 6 · 2022: 9 · 2021: 5 · 2020: 8 · 2019: 9 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 11 · 2014: 9 · 2013: 4 · 2012: 11
- FWCI
- 5.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- insulin, leptin, leptin secretion, white adipose tissue, epididymal adipose tissue, adipocytes, endoplasmic reticulum, GLUT4, obese gene, energy homeostasis
- MeSH terms
- Adipose Tissue, Animals, Endoplasmic Reticulum, Immunohistochemistry, Insulin, Male, Monosaccharide Transport Proteins, Muscle Proteins, Precipitin Tests, Proteins, Rats, Inbred Strains, Time Factors, Protein Biosynthesis, Microscopy, Confocal, Fluorescent Antibody Technique, Indirect, Leptin, Glucose Transporter Type 4, Rats
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