Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice
Open accessAbstract
In lipoatrophic diabetes, a lack of fat is associated with insulin resistance and hyperglycemia. This is in striking contrast to the usual association of diabetes with obesity. To understand the underlying mechanisms, we transplanted adipose tissue into A-ZIP/F-1 mice, which have a severe form of lipoatrophic diabetes. Transplantation of wild-type fat reversed the hyperglycemia, dramatically lowered insulin levels, and improved muscle insulin sensitivity, demonstrating that the diabetes in A-ZIP/F-1 mice is caused by the lack of adipose tissue. All aspects of the A-ZIP/F-1 phenotype including hyperphagia, hepatic steatosis, and somatomegaly were either partially or completely reversed. However, the improvement in triglyceride and FFA levels was modest. Donor fat taken from parametrial and subcutaneous sites was equally effective in reversing the phenotype. The beneficial effects of transplantation were dose dependent and required near-physiological amounts of transplanted fat. Transplantation of genetically modified fat into A-ZIP/F-1 mice is a new and powerful technique for studying adipose physiology and the metabolic and endocrine communication between adipose tissue and the rest of the body.
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Transplantation of body fat from wild-type animals improves insulin sensitivity in a mouse model of lipodystrophy, whereas transplantation of fat from ob/ob mice has no effect.
“transplantation of body fat from wild-type animals improves insulin sensitivity in a mouse model of lipodystrophy, whereas transplantation of fat from ob/ob mice has no effect (38, 63).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [63]
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“For one, transplantation of body fat from wild-type animals improves insulin sensitivity in a mouse model of lipodystrophy, whereas transplantation of fat from ob/ob mice has no effect (38, 63).”
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- Authors
- Gavrilova, O., Marcus-Samuels, B., Graham, D., Kim, J. K., Shulman, G. I., Castle, A. L., Vinson, C., Eckhaus, M., & Reitman, M. L.
- Affiliations
- National Institutes of Health (US)
- Howard Hughes Medical Institute (US)
- National Cancer Institute (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2000-02-01
- Volume
- 105
- Issue
- 3
- Pages
- 271-278
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC377444
- OpenAlex
- W1986131332
- Cited by
- 676
- References
- 33
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 11 · 2023: 25 · 2022: 15 · 2021: 13 · 2020: 19 · 2019: 12 · 2018: 21 · 2017: 25 · 2016: 15 · 2015: 20 · 2014: 22 · 2013: 23 · 2012: 24
- FWCI
- 28.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK080756, R01DK040936)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- lipoatrophic diabetes, adipose tissue transplantation, insulin resistance, hyperglycemia, skeletal muscle insulin sensitivity, hyperphagia, hepatic steatosis, adipose tissue physiology, triglycerides, free fatty acids
- MeSH terms
- Adipose Tissue, Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Lipoatrophic, Fatty Acids, Gene Expression Regulation, Insulin Resistance, Triglycerides, Gene Transfer Techniques, Mice
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