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Results: 1 to 10 of 46

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The Pdx1-Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet β-Cell Function.
Spaeth JM, Liu JH, Peters D, Guo M, Osipovich AB, Mohammadi F, Roy N, Bhushan A, Magnuson MA, Hebrok M, Wright CVE, Stein R
(2019) Diabetes 68: 1806-1818
MeSH Terms: Animals, Cell Proliferation, Chromatin Assembly and Disassembly, DNA Helicases, Gene Expression Regulation, Glucose Intolerance, Homeodomain Proteins, Insulin, Insulin-Secreting Cells, Mice, Mice, Transgenic, Nuclear Proteins, Pancreas, Trans-Activators, Transcription Factors
Added June 28, 2019
1 Communities
3 Members
0 Resources
15 MeSH Terms
Impaired insulin signaling in the B10.D2--/oSnJ mouse model of complement factor 5 deficiency.
Peterson KR, Gutierrez DA, Kikuchi T, Anderson-Baucum EK, Winn NC, Shuey MM, Bolus WR, McGuinness OP, Hasty AH
(2019) Am J Physiol Endocrinol Metab 317: E200-E211
MeSH Terms: Adenoviridae, Animals, Complement C5, Disease Models, Animal, Energy Metabolism, Glucose Intolerance, Hereditary Complement Deficiency Diseases, Insulin Resistance, Mice, Mice, Inbred AKR, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Inbred DBA, Mice, Inbred NOD, Mice, Transgenic, Signal Transduction, Transduction, Genetic
Added March 3, 2020
0 Communities
1 Members
0 Resources
MeSH Terms
Metformin reduces liver glucose production by inhibition of fructose-1-6-bisphosphatase.
Hunter RW, Hughey CC, Lantier L, Sundelin EI, Peggie M, Zeqiraj E, Sicheri F, Jessen N, Wasserman DH, Sakamoto K
(2018) Nat Med 24: 1395-1406
MeSH Terms: Adenosine Monophosphate, Aminoimidazole Carboxamide, Animals, Base Sequence, Chickens, Disease Models, Animal, Fructose-Bisphosphatase, Glucose, Glucose Intolerance, Homeostasis, Humans, Hypoglycemia, Liver, Metformin, Mice, Inbred C57BL, Mutation, Obesity, Prodrugs, Ribonucleotides
Added March 26, 2019
1 Communities
1 Members
0 Resources
19 MeSH Terms
GRP94 Is an Essential Regulator of Pancreatic β-Cell Development, Mass, and Function in Male Mice.
Kim DS, Song L, Wang J, Wu H, Gu G, Sugi Y, Li Z, Wang H
(2018) Endocrinology 159: 1062-1073
MeSH Terms: Animals, Cell Count, Cell Differentiation, Cell Proliferation, Cells, Cultured, Embryo, Nonmammalian, Glucose Intolerance, HEK293 Cells, Humans, Insulin-Secreting Cells, Male, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Organ Size, Pancreas
Added December 4, 2020
1 Communities
1 Members
0 Resources
MeSH Terms
Synergistic Modulation of Inflammatory but not Metabolic Effects of High-Fat Feeding by CCR2 and CX3CR1.
Zhang H, Hinkle CC, O'Neill SM, Shi J, Caughey J, Lynch E, Lynch G, Gerelus M, Tsai ASD, Shah R, Ferguson JF, Ahima RS, Reilly MP
(2017) Obesity (Silver Spring) 25: 1410-1420
MeSH Terms: Animals, Body Composition, CX3C Chemokine Receptor 1, Diet, High-Fat, Female, Glucose Intolerance, Inflammation, Insulin, Insulin Resistance, Insulin Secretion, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity, Receptors, CCR2, Weight Gain
Added April 2, 2019
0 Communities
1 Members
0 Resources
MeSH Terms
Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion.
Syring KE, Boortz KA, Oeser JK, Ustione A, Platt KA, Shadoan MK, McGuinness OP, Piston DW, Powell DR, O'Brien RM
(2016) Endocrinology 157: 4534-4541
MeSH Terms: Animals, Body Weight, Cation Transport Proteins, Female, Glucagon-Secreting Cells, Glucose, Glucose Intolerance, Insulin, Insulin Secretion, Insulin-Secreting Cells, Islets of Langerhans, Male, Mice, Mice, Knockout, Sex Factors, Zinc Transporter 8
Added March 14, 2018
0 Communities
1 Members
0 Resources
16 MeSH Terms
Connective tissue growth factor is critical for proper β-cell function and pregnancy-induced β-cell hyperplasia in adult mice.
Pasek RC, Dunn JC, Elsakr JM, Aramandla M, Matta AR, Gannon M
(2016) Am J Physiol Endocrinol Metab 311: E564-74
MeSH Terms: Aging, Alleles, Animals, Cell Size, Connective Tissue Growth Factor, Diabetes, Gestational, Disease Models, Animal, Embryonic Development, Endocrine Cells, Female, Glucose, Glucose Intolerance, Glucose Tolerance Test, Insulin, Insulin-Secreting Cells, Islets of Langerhans, Mice, Mice, Knockout, Pregnancy
Added August 24, 2016
0 Communities
2 Members
0 Resources
19 MeSH Terms
Decreased Consumption of Branched-Chain Amino Acids Improves Metabolic Health.
Fontana L, Cummings NE, Arriola Apelo SI, Neuman JC, Kasza I, Schmidt BA, Cava E, Spelta F, Tosti V, Syed FA, Baar EL, Veronese N, Cottrell SE, Fenske RJ, Bertozzi B, Brar HK, Pietka T, Bullock AD, Figenshau RS, Andriole GL, Merrins MJ, Alexander CM, Kimple ME, Lamming DW
(2016) Cell Rep 16: 520-530
MeSH Terms: Adipose Tissue, White, Amino Acids, Branched-Chain, Animals, Blood Glucose, Dietary Proteins, Fibroblast Growth Factors, Gluconeogenesis, Glucose Intolerance, Humans, Insulin-Secreting Cells, Male, Mice, Inbred C57BL, Middle Aged, Obesity, Organ Size, Stress, Physiological
Added August 2, 2016
0 Communities
1 Members
0 Resources
16 MeSH Terms
Extranuclear Actions of the Androgen Receptor Enhance Glucose-Stimulated Insulin Secretion in the Male.
Navarro G, Xu W, Jacobson DA, Wicksteed B, Allard C, Zhang G, De Gendt K, Kim SH, Wu H, Zhang H, Verhoeven G, Katzenellenbogen JA, Mauvais-Jarvis F
(2016) Cell Metab 23: 837-51
MeSH Terms: Animals, Cell Line, Tumor, Cell Nucleus, Cyclic AMP, Glucose, Glucose Intolerance, Humans, Insulin, Insulin-Secreting Cells, Male, Mice, Knockout, Models, Biological, Receptors, Androgen, Signal Transduction, Testosterone
Added November 13, 2017
0 Communities
1 Members
0 Resources
15 MeSH Terms
Alternative rapamycin treatment regimens mitigate the impact of rapamycin on glucose homeostasis and the immune system.
Arriola Apelo SI, Neuman JC, Baar EL, Syed FA, Cummings NE, Brar HK, Pumper CP, Kimple ME, Lamming DW
(2016) Aging Cell 15: 28-38
MeSH Terms: Animals, Blood Glucose, Cell Proliferation, Glucose Intolerance, Homeostasis, Immune System, Insulin-Secreting Cells, Mice, Inbred C57BL, Signal Transduction, Sirolimus
Show Abstract · Added August 2, 2016
Inhibition of the mechanistic target of rapamycin (mTOR) signaling pathway by the FDA-approved drug rapamycin has been shown to promote lifespan and delay age-related diseases in model organisms including mice. Unfortunately, rapamycin has potentially serious side effects in humans, including glucose intolerance and immunosuppression, which may preclude the long-term prophylactic use of rapamycin as a therapy for age-related diseases. While the beneficial effects of rapamycin are largely mediated by the inhibition of mTOR complex 1 (mTORC1), which is acutely sensitive to rapamycin, many of the negative side effects are mediated by the inhibition of a second mTOR-containing complex, mTORC2, which is much less sensitive to rapamycin. We hypothesized that different rapamycin dosing schedules or the use of FDA-approved rapamycin analogs with different pharmacokinetics might expand the therapeutic window of rapamycin by more specifically targeting mTORC1. Here, we identified an intermittent rapamycin dosing schedule with minimal effects on glucose tolerance, and we find that this schedule has a reduced impact on pyruvate tolerance, fasting glucose and insulin levels, beta cell function, and the immune system compared to daily rapamycin treatment. Further, we find that the FDA-approved rapamycin analogs everolimus and temsirolimus efficiently inhibit mTORC1 while having a reduced impact on glucose and pyruvate tolerance. Our results suggest that many of the negative side effects of rapamycin treatment can be mitigated through intermittent dosing or the use of rapamycin analogs.
© 2015 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
0 Communities
1 Members
0 Resources
10 MeSH Terms