Research Topics
Genomes and Genes
| Oksana GavrilovaSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
|
Detail Information
Publications
Recombinant human insulin-like growth factor-I treatment inhibits gluconeogenesis in a transgenic mouse model of type 2 diabetes mellitusPatricia Pennisi
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Betheda, MD 20892, USA
Endocrinology 147:2619-30. 2006..Also, these results suggest that a functional IGF-I receptor in skeletal muscle is required for IGF-I to improve insulin sensitivity in this mouse model of type 2 DM...
The alternative stimulatory G protein alpha-subunit XLalphas is a critical regulator of energy and glucose metabolism and sympathetic nerve activity in adult miceTao Xie
Metabolic Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 281:18989-99. 2006..XLalphas (or XLN1) is a negative regulator of sympathetic nervous system activity in mice...- Lack of responses to a beta3-adrenergic agonist in lipoatrophic A-ZIP/F-1 miceO 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... - Liver peroxisome proliferator-activated receptor gamma contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat massOksana Gavrilova
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 278:34268-76. 2003..Thus, liver PPAR gamma regulates triglyceride homeostasis, contributing to hepatic steatosis, but protecting other tissues from triglyceride accumulation and insulin resistance... - Leptin improves insulin resistance and hyperglycemia in a mouse model of type 2 diabetesYuka Toyoshima
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Room 8D12, Building 10, MSC 1758, National Institutes of Health, Bethesda, Maryland 20892-1758, USA
Endocrinology 146:4024-35. 2005..Our data suggest that leptin could be a potent antidiabetic drug in cases of type 2 diabetes that are not leptin resistant... - Hepatic muscarinic acetylcholine receptors are not critically involved in maintaining glucose homeostasis in miceJian H Li
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 58:2776-87. 2009..Since acetylcholine (ACh) is the major neurotransmitter of the vagus nerve and exerts its parasympathetic actions via activation of muscarinic ACh receptors (mAChRs), we examined the potential metabolic relevance of hepatocyte mAChRs... - Increased glucose tolerance and reduced adiposity in the absence of fasting hypoglycemia in mice with liver-specific Gs alpha deficiencyMin Chen
Metabolic Diseases Branch, NIDDK, NIH, Bethesda, Maryland 20892 1752, USA
J Clin Invest 115:3217-27. 2005..Our results define novel roles for hepatic G(s)-signaling pathways in glucose and lipid regulation, which may prove useful in designing new therapeutic targets for diabetes and obesity... - G(s)alpha deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiencyMin Chen
Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
Am J Physiol Cell Physiol 296:C930-40. 2009..MGsKO mice are a valuable model for future studies of the role of G(s)alpha signaling pathways in skeletal muscle adaptation and their effects on whole body metabolism... - Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob miceMartin Haluzik
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Endocrinology 145:3258-64. 2004.... - G(s)alpha deficiency in adipose tissue leads to a lean phenotype with divergent effects on cold tolerance and diet-induced thermogenesisMin Chen
Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Cell Metab 11:320-30. 2010..In normal mice, high-fat diet raised sympathetic nerve activity in muscle, but not in BAT. Our results show that cold- and diet-induced thermogenesis may occur in separate tissues, especially when BAT function is impaired... - Severe obesity and insulin resistance due to deletion of the maternal Gsalpha allele is reversed by paternal deletion of the Gsalpha imprint control regionTao Xie
Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Building 10, Room 8C101, Bethesda, Maryland 20892 1752, USA
Endocrinology 149:2443-50. 2008.... - Beneficial metabolic effects caused by persistent activation of beta-cell M3 muscarinic acetylcholine receptors in transgenic miceDinesh Gautam
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 8 Center Drive MSC 0810, Bethesda, MD 20892 0810, USA
Endocrinology 151:5185-94. 2010..These results suggest that chronic activation of β-cell M3Rs may represent a useful approach to boost insulin output in the long-term treatment of type 2 diabetes... - Liver-specific disruption of PPARgamma in leptin-deficient mice improves fatty liver but aggravates diabetic phenotypesKimihiko Matsusue
Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Frederick, Maryland 20892, USA
J Clin Invest 111:737-47. 2003..These data indicate that hepatic PPARgamma plays a critical role in the regulation of TG content and in the homeostasis of blood glucose and insulin resistance in steatotic diabetic mice... - Effect of adipocyte beta3-adrenergic receptor activation on the type 2 diabetic MKR miceHyunsook Kim
Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA
Am J Physiol Endocrinol Metab 290:E1227-36. 2006.... - Central nervous system imprinting of the G protein G(s)alpha and its role in metabolic regulationMin Chen
Signal Transduction Section, Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Cell Metab 9:548-55. 2009.... - Metabolic roles of the M3 muscarinic acetylcholine receptor studied with M3 receptor mutant mice: a reviewDinesh Gautam
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892 0810, USA
J Recept Signal Transduct Res 28:93-108. 2008..These findings are of potential interest for the development of novel therapeutic approaches for the treatment of obesity and associated metabolic disorders... - Alterations in regulation of energy homeostasis in cyclic nucleotide phosphodiesterase 3B-null miceYoung Hun Choi
Pulmonary Critical Care Medicine Branch, NIH, Bethesda, MD 20892, USA
J Clin Invest 116:3240-51. 2006..Altered expression and/or regulation of PDE3B may contribute to metabolic dysregulation, including systemic insulin resistance... - Hepatic CCAAT/enhancer binding protein alpha mediates induction of lipogenesis and regulation of glucose homeostasis in leptin-deficient miceKimihiko Matsusue
Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Endocrinol 18:2751-64. 2004..Taken together, these results indicate that hepatic C/EBP alpha plays a critical role in the acceleration of lipogenesis in ob/ob mice and in glucose homeostasis by the indirect regulation of insulin secretion... - Adrenalectomy improves diabetes in A-ZIP/F-1 lipoatrophic mice by increasing both liver and muscle insulin sensitivityMartin Haluzik
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases NIH, Building 10, Room 8N 250, 10 Center Drive, Bethesda, MD 20892 1770, USA
Diabetes 51:2113-8. 2002..These results suggest that the chronically increased serum corticosterone levels contribute to the diabetes of the A-ZIP/F-1 mice and that removal of the glucocorticoid excess improves the insulin sensitivity in both muscle and liver... - Absence of the glucagon-like peptide-1 receptor does not affect the metabolic phenotype of mice with liver-specific G(s)α deficiencyMin Chen
Metabolic Diseases Branch, Building 10 Room 8C101, National Institute for Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1752, USA
Endocrinology 152:3343-50. 2011.... - Phloridzin improves hyperglycemia but not hepatic insulin resistance in a transgenic mouse model of type 2 diabetesHong Zhao
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-1758, USA
Diabetes 53:2901-9. 2004..These results suggest that glucotoxicity plays little or no role in the worsening of insulin resistance that occurs in the MKR mouse model of type 2 diabetes... - Disruption of hypoxia-inducible factor 1 in adipocytes improves insulin sensitivity and decreases adiposity in high-fat diet-fed miceChangtao Jiang
Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
Diabetes 60:2484-95. 2011..The role of hypoxia and hypoxia-inducible factor 1 (HIF1) in the development of high-fat diet (HFD)-induced obesity and insulin resistance was investigated using animal models... - Myostatin inhibition prevents diabetes and hyperphagia in a mouse model of lipodystrophyTingqing Guo
Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 61:2414-23. 2012..These results further suggest that muscle may play a heretofore unappreciated role in regulating food intake... - Hepatic Sirt1 deficiency in mice impairs mTorc2/Akt signaling and results in hyperglycemia, oxidative damage, and insulin resistanceRui Hong Wang
Genetics of Development and Disease Branch, NIH, 10 9N105, 10 Center Drive, Bethesda, Maryland 20892, USA
J Clin Invest 121:4477-90. 2011..These data delineate a pathway through which Sirt1 maintains insulin sensitivity and suggest that treatment with antioxidants might provide protection against progressive insulin resistance in older human populations... - Opposite effects of background genotype on muscle and liver insulin sensitivity of lipoatrophic mice. Role of triglyceride clearanceCarlo Colombo
Diabetes Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 278:3992-9. 2003..Thus, it is likely that increased triglyceride clearance in B6, as compared with FVB, mice contributes to the strain differences in insulin resistance and lipid metabolism... - Neuronal M3 muscarinic acetylcholine receptors are essential for somatotroph proliferation and normal somatic growthDinesh Gautam
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 106:6398-403. 2009..Our data reveal an unexpected and critical role for central M(3) receptors in regulating longitudinal growth by promoting the proliferation of pituitary somatotroph cells... - Muscle-specific overexpression of CD36 reverses the insulin resistance and diabetes of MKR miceLisa Heron-Milhavet
Diabetes Branch, NIDDK, Room 8D12, Building 10, National Institutes of Health, Bethesda, Maryland 20892 1758, USA
Endocrinology 145:4667-76. 2004.... - WY14,643, a peroxisome proliferator-activated receptor alpha (PPARalpha ) agonist, improves hepatic and muscle steatosis and reverses insulin resistance in lipoatrophic A-ZIP/F-1 miceChieh J Chou
Diabetes Branch, NIDDK and the Metabolism Branch, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 277:24484-9. 2002.... - Myostatin inhibition in muscle, but not adipose tissue, decreases fat mass and improves insulin sensitivityTingqing Guo
Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
PLoS ONE 4:e4937. 2009..These data suggest that increasing muscle mass by administration of myostatin antagonists may be a promising therapeutic target for treating patients with obesity or diabetes... - Persistent diet-induced obesity in male C57BL/6 mice resulting from temporary obesigenic dietsJuen Guo
Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
PLoS ONE 4:e5370. 2009.... - Suppression of the C/EBP family of transcription factors in adipose tissue causes lipodystrophyRaghunath Chatterjee
Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Building 37, Room 3128, Bethesda, Maryland 20892, USA
J Mol Endocrinol 46:175-92. 2011..These results demonstrate that the C/EBP family is essential for adipose tissue development during the early postnatal period, the regulation of glucose and lipid homeostasis in adults, and the suppression of the muscle lineage... - Alternative Gnas gene products have opposite effects on glucose and lipid metabolismMin Chen
Metabolic Diseases 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 102:7386-91. 2005..Differences between E1m-/+ and E1+/p- mice presumably result from differential effects on G(s)alpha expression in tissues where G(s)alpha is normally imprinted... - RGS4 is a negative regulator of insulin release from pancreatic beta-cells in vitro and in vivoInigo Ruiz de Azua
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 107:7999-8004. 2010..These findings indicate that RGS4 is a potent negative regulator of M3R function in pancreatic beta-cells, suggesting that RGS4 may represent a potential target to promote insulin release for therapeutic purposes... - Gsα deficiency in the paraventricular nucleus of the hypothalamus partially contributes to obesity associated with Gsα mutationsMin Chen
Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health, Bethesda, Maryland 20892 1752, USA
Endocrinology 153:4256-65. 2012.... - Impaired glucose tolerance in the absence of adenosine A1 receptor signalingRobert Faulhaber-Walter
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 60:2578-87. 2011..The role of adenosine (ADO) in the regulation of glucose homeostasis is not clear. In the current study, we used A1-ADO receptor (A1AR)-deficient mice to investigate the role of ADO/A1AR signaling for glucose homeostasis... - SIRT6 deficiency results in severe hypoglycemia by enhancing both basal and insulin-stimulated glucose uptake in miceCuiying Xiao
Genetics of Development and Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 285:36776-84. 2010..The absence of SIRT6, consequently, enhances insulin signaling and activation of AKT, leading to hypoglycemia. These data uncover an essential role of SIRT6 in modulating glucose metabolism through mediating insulin sensitivity... - The transcription factors Stat5a/b are not required for islet development but modulate pancreatic beta-cell physiology upon agingJi Yeon Lee
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 8 Center Drive, Room 101, Bethesda, MD 20892 0822, USA
Biochim Biophys Acta 1773:1455-61. 2007..Mild glucose intolerance occurred with age. We conclude that Stat5 is not essential for islet development but may modulate beta-cell function... - Loss of cytokine-STAT5 signaling in the CNS and pituitary gland alters energy balance and leads to obesityJi Yeon Lee
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
PLoS ONE 3:e1639. 2008..These results demonstrate that STAT5 mediates energy homeostasis in response to endogenous cytokines such as GM-CSF... - Mouse models created to study the pathophysiology of Type 2 diabetesDerek LeRoith
Diabetes Branch, National Institutes of Health, Room 8D12, Building 10, Bethesda, MD 20892 1758, USA
Int J Biochem Cell Biol 38:904-12. 2006..This review will summarize many of the more appropriate models that study insulin resistance and Type 2 diabetes... - Hypertrophy and/or Hyperplasia: Dynamics of Adipose Tissue GrowthJunghyo Jo
Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethedsa, Maryland, USA
PLoS Comput Biol 5:e1000324. 2009..Additionally, high-fat diet leads to a dramatic spreading of the size distribution of adipose cells in both strains; this implies an increase in size fluctuations of adipose cells through lipid turnover... - Loss of signal transducer and activator of transcription 5 leads to hepatosteatosis and impaired liver regenerationYongzhi Cui
Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892 0822, USA
Hepatology 46:504-13. 2007..CONCLUSION: Aberrant cytokine-Stat5 signaling in hepatocytes alters their physiology through increased activity of Stat1 and Stat3. Such cross-talk between different pathways could add to the complexity of syndromes observed in disease... - Beneficial metabolic effects of M3 muscarinic acetylcholine receptor deficiencyDinesh Gautam
Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA
Cell Metab 4:363-75. 2006..These findings suggest that the M3 receptor may represent a potential pharmacologic target for the treatment of obesity and associated metabolic disorders... - Insulin resistance in the liver-specific IGF-1 gene-deleted mouse is abrogated by deletion of the acid-labile subunit of the IGF-binding protein-3 complex: relative roles of growth hormone and IGF-1 in insulin resistanceMartin Haluzik
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892 1758, USA
Diabetes 52:2483-9. 2003..The present study suggests that whereas GH plays a major role in inducing insulin resistance, IGF-1 may have a direct modulatory role... - A model for obesity and gigantism due to disruption of the Ankrd26 geneTapan K Bera
Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 4264, USA
Proc Natl Acad Sci U S A 105:270-5. 2008..These results show that alterations in an unidentified gene can lead to obesity and identify a molecular target for the treatment of obesity... - Protection from obesity and diabetes by blockade of TGF-β/Smad3 signalingHariom Yadav
Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Clinical Research Center, South Drive and Old Georgetown Road, Bethesda, MD 20892, USA
Cell Metab 14:67-79. 2011..Together, these results demonstrate that TGF-β signaling regulates glucose tolerance and energy homeostasis and suggest that modulation of TGF-β activity might be an effective treatment strategy for obesity and diabetes... - Wnt signaling regulates hepatic metabolismHongjun Liu
Center for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Sci Signal 4:ra6. 2011..These observations implicate Wnt signaling in the modulation of hepatic metabolism and raise the possibility that Wnt signaling may play a similar role in the metabolic regulation of other tissues... - Dynamic changes in pancreatic endocrine cell abundance, distribution, and function in antigen-induced and spontaneous autoimmune diabetesKlaus Pechhold
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 58:1175-84. 2009..Less is known about beta-cell numbers and phenotype remaining at diabetes onset and the fate of other pancreatic endocrine cellular constituents... - p53 regulates mitochondrial respirationSatoaki Matoba
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
Science 312:1650-3. 2006..That SCO2 couples p53 to mitochondrial respiration provides a possible explanation for the Warburg effect and offers new clues as to how p53 might affect aging and metabolism... - The growth hormone-insulin like growth factor axis revisited: lessons from IGF-1 and IGF-1 receptor gene targetingShoshana Yakar
Diabetes Branch, National Institutes of Health, MSC 1758, Bethesda, MD 20892-1758, USA
Pediatr Nephrol 20:251-4. 2005..These models are therefore very useful in studying human physiology and disease states... - Disruption of the Arnt gene in endothelial cells causes hepatic vascular defects and partial embryonic lethality in miceSun Hee Yim
Laboratory of Metabolism, National Cancer Institute, Bethesda, MD 20892, USA
Hepatology 44:550-60. 2006..Adult ArntDeltaEC mice carrying embryonic hepatic defects developed what was possibly an early stage of cirrhosis with consequences of limited oxygen availability and altered lipid metabolism... - A selective EP4 PGE2 receptor agonist alleviates disease in a new mouse model of X-linked nephrogenic diabetes insipidusJian Hua Li
Molecular Signaling Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA
J Clin Invest 119:3115-26. 2009..These findings illustrate the usefulness of the newly generated V2R mutant mice for elucidating and testing new strategies for the potential treatment of humans with XNDI... - Disrupted erythropoietin signalling promotes obesity and alters hypothalamus proopiomelanocortin productionRuifeng Teng
Molecular Cell Biology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892, USA
Nat Commun 2:520. 2011..This study provides the first evidence that mice lacking EpoR in non-haematopoietic tissue become obese and insulin resistant with loss of Epo regulation of energy homeostasis... - Transplantation of adipose tissue lacking leptin is unable to reverse the metabolic abnormalities associated with lipoatrophyCarlo Colombo
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 51:2727-33. 2002..Taken together, these results suggest that sequestration of triglycerides into fat may not be enough to restore a nondiabetic phenotype and that leptin deficiency plays a major role in causing the metabolic complications of lipoatrophy... - Transduction of rat pancreatic islets with pseudotyped adeno-associated virus vectorsAnthony T Craig
Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
Virol J 6:61. 2009..We are therefore investigating the use of adeno-associated viruses (AAVs) as gene therapy vectors to transduce rat islets with immunosuppressive genes prior to transplantation into diabetic mice... - Histone methylation regulator PTIP is required for PPARgamma and C/EBPalpha expression and adipogenesisYoung Wook Cho
Nuclear Receptor Biology Section, CEB, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Cell Metab 10:27-39. 2009..Finally, deletion of PTIP in brown adipose tissue significantly reduces tissue weight. Thus, by regulating PPARgamma and C/EBPalpha expression, PTIP plays a critical role in adipogenesis... - Insulin stimulates fusion, but not tethering, of GLUT4 vesicles in skeletal muscle of HA-GLUT4-GFP transgenic miceVladimir A Lizunov
Program in Physical Biology, National Institute of Child Health and Human Development National Institutes of Health, Bethesda, MD, USA
Am J Physiol Endocrinol Metab 302:E950-60. 2012..Most likely, pretethered GLUT4 structures are responsible for the initial phase of insulin-stimulated exocytosis... - The clinical uses of leptinPhillip Gorden
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Building 10, Room 8S 235S, Bethesda, MD 20892 1770, USA
Curr Opin Pharmacol 3:655-9. 2003..In both these leptin-deficient states, leptin therapy restores gonadotrophin secretion, as well as luteinizing hormone and thyroid-stimulating hormone pulsitility... - Small-molecule agonists for the thyrotropin receptor stimulate thyroid function in human thyrocytes and miceSusanne Neumann
Clinical Endocrinology 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 106:12471-6. 2009..Thus, we discovered a small molecule that activates human TSHR in vitro, is orally active in mice, and could be a lead for development of drugs to use in place of recombinant human TSH in patients with thyroid cancer... - Resistance to thyroid hormone is modulated in vivo by the nuclear receptor corepressor (NCOR1)Laura Fozzatti
Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Proc Natl Acad Sci U S A 108:17462-7. 2011..The present study suggests that therapies aimed at the TR-NCOR1 interaction or its downstream actions could be tested as potential targets in treating RTH... - Peroxisome proliferator-activated receptor-alpha deficiency does not alter insulin sensitivity in mice maintained on regular or high-fat diet: hyperinsulinemic-euglycemic clamp studiesMartin Haluzik
Third Department of Medicine, First Faculty of Medicine, Charles University, Prague, Czech Republic
Endocrinology 145:1662-7. 2004.... - Differential effects of rosiglitazone on skeletal muscle and liver insulin resistance in A-ZIP/F-1 fatless miceJason K Kim
Department of Internal Medicine, Section of Endocrinology, Howard Hughes Medical Institute, Yale University School of Medicine, S269C CAB, PO Box 208020, New Haven, CT 06520 8020, USA
Diabetes 52:1311-8. 2003..In conclusion, these data support the hypothesis that rosiglitazone treatment enhanced insulin action in skeletal muscle mostly by its ability to repartition fat away from skeletal muscle... - Xanthine oxidoreductase is a regulator of adipogenesis and PPARgamma activityKevin J Cheung
Laboratory of Molecular Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Cell Metab 5:115-28. 2007..Our results identify XOR as a potential therapeutic target for metabolic abnormalities beyond hyperuricemia... - Resistin is expressed in pancreatic isletsAlexandra H Minn
Endocrinology Section, Department of Medicine, University of Wisconsin, Madison, WI 53792, USA
Biochem Biophys Res Commun 310:641-5. 2003..Our results demonstrate that resistin is expressed in islets and up-regulated in insulin resistance and thereby shed new light on the role of resistin in mice and humans...