M L Reitman

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Transgenic mice lacking white fat: models for understanding human lipoatrophic diabetes
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 892:289-96. 1999
  2. ncbi request reprint Lipoatrophy revisited
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10, Room 8N 250, 10 Center Drive, Bethesda, MD 20892 1770, USA
    Trends Endocrinol Metab 11:410-6. 2000
  3. ncbi request reprint Hyperleptinemia of pregnancy associated with the appearance of a circulating form of the leptin receptor
    O Gavrilova
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    J Biol Chem 272:30546-51. 1997
  4. ncbi request reprint Identification of a placental enhancer for the human leptin gene
    S Bi
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    J Biol Chem 272:30583-8. 1997
  5. ncbi request reprint Thyroid hormone and other regulators of uncoupling proteins
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1770, USA
    Int J Obes Relat Metab Disord 23:S56-9. 1999
  6. ncbi request reprint A-ZIP/F-1 mice lacking white fat: a model for understanding lipoatrophic diabetes
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1770, USA
    Int J Obes Relat Metab Disord 24:S11-4. 2000
  7. ncbi request reprint Lack of obesity and normal response to fasting and thyroid hormone in mice lacking uncoupling protein-3
    D W Gong
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 275:16251-7. 2000
  8. ncbi request reprint Lack of responses to a beta3-adrenergic agonist in lipoatrophic A-ZIP/F-1 mice
    O Gavrilova
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    Diabetes 49:1910-6. 2000
  9. pmc Torpor in mice is induced by both leptin-dependent and -independent mechanisms
    O Gavrilova
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 96:14623-8. 1999
  10. pmc Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity
    J T Tansey
    Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:6494-9. 2001

Collaborators

Detail Information

Publications18

  1. ncbi request reprint Transgenic mice lacking white fat: models for understanding human lipoatrophic diabetes
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 892:289-96. 1999
    ..the questions: Is the lack of fat causative of the diabetes, and if so by what mechanism? How could the other clinical features be explained mechanistically? And finally, what can be gleaned about insight into treatment options?..
  2. ncbi request reprint Lipoatrophy revisited
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 10, Room 8N 250, 10 Center Drive, Bethesda, MD 20892 1770, USA
    Trends Endocrinol Metab 11:410-6. 2000
    ..Thiazolidinedione therapy improves metabolic control in lipoatrophic patients; the efficacy of leptin treatment is currently being investigated...
  3. ncbi request reprint Hyperleptinemia of pregnancy associated with the appearance of a circulating form of the leptin receptor
    O Gavrilova
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    J Biol Chem 272:30546-51. 1997
    ..Thus, the extreme hyperleptinemia of late pregnancy is attributable to binding of the leptin by a secreted form of the leptin receptor made by the placenta...
  4. ncbi request reprint Identification of a placental enhancer for the human leptin gene
    S Bi
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    J Biol Chem 272:30583-8. 1997
    ..Upon triplication, the PLE3 element was a strong enhancer in choriocarcinoma cells but not in HeLa cells. The protein binding to the PLE3 motif appears to be a novel, placenta-specific transcription factor...
  5. ncbi request reprint Thyroid hormone and other regulators of uncoupling proteins
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 1770, USA
    Int J Obes Relat Metab Disord 23:S56-9. 1999
    ..Since free fatty acids appear to regulate UCP3 expression and T3 stimulates lipolysis, further experiments are required to determine if T3 regulation of UCP3 expression is direct or not...
  6. ncbi request reprint A-ZIP/F-1 mice lacking white fat: a model for understanding lipoatrophic diabetes
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 1770, USA
    Int J Obes Relat Metab Disord 24:S11-4. 2000
    ..Leptin replacement is not very effective in reversing the diabetes of the A-ZIP/F-1 mice, which contrasts with its efficacy in the aP2-SREBP-lc mouse...
  7. ncbi request reprint Lack of obesity and normal response to fasting and thyroid hormone in mice lacking uncoupling protein-3
    D W Gong
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 275:16251-7. 2000
    ..The phenotype of Ucp1/Ucp3 double knockout mice was indistinguishable from Ucp1 single knockout mice. These data suggest that Ucp3 is not a major determinant of metabolic rate but, rather, has other functions...
  8. ncbi request reprint Lack of responses to a beta3-adrenergic agonist in lipoatrophic A-ZIP/F-1 mice
    O Gavrilova
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1770, USA
    Diabetes 49:1910-6. 2000
    ..From these results, we suggest that all of the effects of beta3 agonists are initiated at the adipocyte with the nonadipose effects being secondary events presumably mediated by signals from adipose tissue...
  9. pmc Torpor in mice is induced by both leptin-dependent and -independent mechanisms
    O Gavrilova
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 96:14623-8. 1999
    ..Studying rodent torpor provides insight into human torpor-like states such as near drowning in cold water and induced hypothermia for surgery...
  10. pmc Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity
    J T Tansey
    Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:6494-9. 2001
    ..The data reveal a major role for perilipin in adipose lipid metabolism and suggest perilipin as a potential target for attacking problems associated with obesity...
  11. pmc Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice
    O Gavrilova
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Clin Invest 105:271-8. 2000
    ..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...
  12. pmc Growth, adipose, brain, and skin alterations resulting from targeted disruption of the mouse peroxisome proliferator-activated receptor beta(delta)
    J M Peters
    Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Mol Cell Biol 20:5119-28. 2000
    ..These results are the first to provide in vivo evidence of significant roles for PPARbeta in development, myelination of the corpus callosum, lipid metabolism, and epidermal cell proliferation...
  13. ncbi request reprint Genomic organization and regulation by dietary fat of the uncoupling protein 3 and 2 genes
    D W Gong
    Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland, 20892 1770, USA
    Biochem Biophys Res Commun 256:27-32. 1999
    ..The data suggest that it is not a reduction in UCP2 or UCP3 expression that causes obesity in the susceptible mice...
  14. ncbi request reprint Efficacy and safety of troglitazone in the treatment of lipodystrophy syndromes
    E Arioglu
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann Intern Med 133:263-74. 2000
    ..Troglitazone promotes adipocyte differentiation in vitro and increases insulin sensitivity in vivo. Therefore, troglitazone may have therapeutic benefit in lipoatrophic diabetes...
  15. pmc Paternal versus maternal transmission of a stimulatory G-protein alpha subunit knockout produces opposite effects on energy metabolism
    S Yu
    Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institute of Health, Bethesda, MD 20892, USA
    J Clin Invest 105:615-23. 2000
    ..This probably results from deficiency of maternal- and paternal-specific Gnas gene products, respectively...
  16. ncbi request reprint Leptin and its role in pregnancy and fetal development--an overview
    M L Reitman
    Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Building 10, Room 8N 250, Bethesda, MD 20892 1770, U S A
    Biochem Soc Trans 29:68-72. 2001
    ..The physiology of leptin during pregnancy and fetal development differs significantly between species, and is not well understood in any...
  17. ncbi request reprint Transgenic overexpression of leptin rescues insulin resistance and diabetes in a mouse model of lipoatrophic diabetes
    K Ebihara
    Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara cho, Sakyo ku, Kyoto 606 8507, Japan
    Diabetes 50:1440-8. 2001
    ....
  18. ncbi request reprint The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity
    T Yamauchi
    Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
    Nat Med 7:941-6. 2001
    ..These data also indicate that the replenishment of adiponectin might provide a novel treatment modality for insulin resistance and type 2 diabetes...