Search

Your search keyword '"Bartke, Andrzej"' showing total 22 results
Start Over Author "Bartke, Andrzej" Journal aging cell
22 results on '"Bartke, Andrzej"'

1. Early life interventions metformin and trodusquemine metabolically reprogram the developing mouse liver through transcriptomic alterations

Author

Ashiqueali, Sarah A., primary, Schneider, Augusto, additional, Zhu, Xiang, additional, Juszczyk, Ewelina, additional, Mansoor, Mishfak A. M., additional, Zhu, Yun, additional, Fang, Yimin, additional, Zanini, Bianka M., additional, Garcia, Driele N., additional, Hayslip, Natalie, additional, Medina, David, additional, McFadden, Samuel, additional, Stockwell, Robert, additional, Yuan, Rong, additional, Bartke, Andrzej, additional, Zasloff, Michael, additional, Siddiqi, Shadab, additional, and Masternak, Michal M., additional

Published
2024
Full Text
View/download PDF

3. Circulating microRNA profile in humans and mice with congenital GH deficiency

Author

Saccon, Tatiana D., primary, Schneider, Augusto, additional, Marinho, Cindi G., additional, Nunes, Allancer D. C., additional, Noureddine, Sarah, additional, Dhahbi, Joseph, additional, Nunez Lopez, Yury O., additional, LeMunyan, Gage, additional, Salvatori, Roberto, additional, Oliveira, Carla R. P., additional, Oliveira‐Santos, Alécia A., additional, Musi, Nicolas, additional, Bartke, Andrzej, additional, Aguiar‐Oliveira, Manuel H., additional, and Masternak, Michal M., additional

Published
2021
Full Text
View/download PDF

9. Interventions to Slow Aging in Humans: Are We Ready?

Author

Longo, Valter D., primary, Antebi, Adam, additional, Bartke, Andrzej, additional, Barzilai, Nir, additional, Brown‐Borg, Holly M., additional, Caruso, Calogero, additional, Curiel, Tyler J., additional, Cabo, Rafael, additional, Franceschi, Claudio, additional, Gems, David, additional, Ingram, Donald K., additional, Johnson, Thomas E., additional, Kennedy, Brian K., additional, Kenyon, Cynthia, additional, Klein, Samuel, additional, Kopchick, John J., additional, Lepperdinger, Guenter, additional, Madeo, Frank, additional, Mirisola, Mario G., additional, Mitchell, James R., additional, Passarino, Giuseppe, additional, Rudolph, Karl L., additional, Sedivy, John M., additional, Shadel, Gerald S., additional, Sinclair, David A., additional, Spindler, Stephen R., additional, Suh, Yousin, additional, Vijg, Jan, additional, Vinciguerra, Manlio, additional, and Fontana, Luigi, additional

Published
2015
Full Text
View/download PDF

14. Metabolic effects of intra‐abdominal fat in GHRKO mice

Author

Masternak, Michal M., primary, Bartke, Andrzej, additional, Wang, Feiya, additional, Spong, Adam, additional, Gesing, Adam, additional, Fang, Yimin, additional, Salmon, Adam B., additional, Hughes, Larry F., additional, Liberati, Teresa, additional, Boparai, Ravneet, additional, Kopchick, John J., additional, and Westbrook, Reyhan, additional

Published
2011
Full Text
View/download PDF

21. Specific suppression of insulin sensitivity in growth hormone receptor gene-disrupted ( GHR- KO) mice attenuates phenotypic features of slow aging.

Author

Arum, Oge, Boparai, Ravneet K., Saleh, Jamal K., Wang, Feiya, Dirks, Angela L., Turner, Jeremy G., Kopchick, John J., Liu, Jun‐Li, Khardori, Romesh K., and Bartke, Andrzej

Subjects
INSULIN resistance, SOMATOTROPIN receptors, PHENOTYPES, LIFE spans, CELLULAR aging, GENE knockout, LABORATORY mice
Abstract

In addition to their extended lifespans, slow-aging growth hormone receptor/binding protein gene-disrupted (knockout) ( GHR- KO) mice are hypoinsulinemic and highly sensitive to the action of insulin. It has been proposed that this insulin sensitivity is important for their longevity and increased healthspan. We tested whether this insulin sensitivity of the GHR- KO mouse is necessary for its retarded aging by abrogating that sensitivity with a transgenic alteration that improves development and secretory function of pancreatic β-cells by expressing Igf-1 under the rat insulin promoter 1 ( RIP:: IGF-1). The RIP:: IGF-1 transgene increased circulating insulin content in GHR- KO mice, and thusly fully normalized their insulin sensitivity, without affecting the proliferation of any non-β-cell cell types. Multiple (nonsurvivorship) longevity-associated physiological and endocrinological characteristics of these mice (namely beneficial blood glucose regulatory control, altered metabolism, and preservation of memory capabilities) were partially or completely normalized, thus supporting the causal role of insulin sensitivity for the decelerated senescence of GHR- KO mice. We conclude that a delayed onset and/or decreased pace of aging can be hormonally regulated. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

22. Metabolic effects of intra-abdominal fat in GHRKO mice.

Author

Masternak, Michal M., Bartke, Andrzej, Wang, Feiya, Spong, Adam, Gesing, Adam, Fang, Yimin, Salmon, Adam B., Hughes, Larry F., Liberati, Teresa, Boparai, Ravneet, Kopchick, John J., and Westbrook, Reyhan

Subjects
*SOMATOTROPIN receptors, *OBESITY, *INSULIN, *METABOLISM, *ADIPONECTIN, *BODY temperature, *LABORATORY mice
Abstract

Summary Mice with targeted deletion of the growth hormone receptor (GHRKO mice) are growth hormone (GH) resistant, small, obese, hypoinsulinemic, highly insulin sensitive and remarkably long-lived. To elucidate the unexpected coexistence of adiposity with improved insulin sensitivity and extended longevity, we examined effects of surgical removal of visceral (epididymal and perinephric) fat on metabolic traits related to insulin signaling and longevity. Comparison of results obtained in GHRKO mice and in normal animals from the same strain revealed disparate effects of visceral fat removal (VFR) on insulin and glucose tolerance, adiponectin levels, accumulation of ectopic fat, phosphorylation of insulin signaling intermediates, body temperature, and respiratory quotient (RQ). Overall, VFR produced the expected improvements in insulin sensitivity and reduced body temperature and RQ in normal mice and had opposite effects in GHRKO mice. Some of the examined parameters were altered by VFR in opposite directions in GHRKO and normal mice, and others were affected in only one genotype or exhibited significant genotype × treatment interactions. Functional differences between visceral fat of GHRKO and normal mice were confirmed by measurements of adipokine secretion, lipolysis, and expression of genes related to fat metabolism. We conclude that in the absence of GH signaling, the secretory activity of visceral fat is profoundly altered and unexpectedly promotes enhanced insulin sensitivity. The apparent beneficial effects of visceral fat in GHRKO mice may also explain why reducing adiposity by calorie restriction fails to improve insulin signaling or further extend longevity in these animals. [ABSTRACT FROM AUTHOR]

Published
2012
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results