The objective of Core B (Mouse Aging Analysis Core ) is to provide a centralized core facility for the PPG at the Yale School of Medicine that will generate and analyze transgenic mouse models to determine the roles of FGF21 on lifespan extension and age-related functional decline across multiple systems. The Core B will allow the PPG to gain mechanistic insights into the pro-longevity effects of FGF21 across multiple organ systems (adipose tissue, liver, bone, CNS and the immune system) using measures of functional decline in aging, longevity and burden of disease as primary endpoints.
The Aim 1 of Core B is be work closely with the leader of the Administrative Core and leaders of the research projects, to assist in the experimental design and execution of the animal research phase of the individual projects, and to assure efficiency and standardization of procedures.
The Aim2 is To perform an omnibus study with male and female mice examining the effect of inducible overexpression of FGF21 on lifespan and the contribution of adiponectin to FGF21's pro-longevity effect.
Aim 3 : To determine the cause of death by detailed pathologic examination of inducible FGF21Tg mice and inducible FGF21Tg mice lacking adiponectin. These studies will involve gross necropsies and histological analyses to quantify pathology and disease burden in our mouse models. Dr. Caroline Zeiss (ACVP and ACLAM boarded) will direct these studies as part of the PPG team.
The aim4 will perform an omnibus study with male and female mice examining the role of the FGF21-adiponectin endocrine axis on healthspan and age-related functional decline across organ systems.
The analysis of lifespan and healthspan in mice require specialized and centralized facility to conduct metabolic testing, behavior tests like age-related changes in memory and cognition. The mice where FGF21 levels are elevated are predicted to live long. This Core will conduct detailed analyses of disease burden and pathology to determine the cause of lifespan extension and to understand the aging process.
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| Ravussin, Anthony; Youm, Yun-Hee; Sander, Jil et al. (2018) Loss of Nucleobindin-2 Causes Insulin Resistance in Obesity without Impacting Satiety or Adiposity. Cell Rep 24:1085-1092.e6 |
| Crewe, Clair; Joffin, Nolwenn; Rutkowski, Joseph M et al. (2018) An Endothelial-to-Adipocyte Extracellular Vesicle Axis Governed by Metabolic State. Cell 175:695-708.e13 |
| Song, Parkyong; Zechner, Christoph; Hernandez, Genaro et al. (2018) The Hormone FGF21 Stimulates Water Drinking in Response to Ketogenic Diet and Alcohol. Cell Metab 27:1338-1347.e4 |
| Scherer, Philipp E (2018) The many secret lives of adipocytes: implications for diabetes. Diabetologia : |
| Katafuchi, Takeshi; Holland, William L; Kollipara, Rahul K et al. (2018) PPAR?-K107 SUMOylation regulates insulin sensitivity but not adiposity in mice. Proc Natl Acad Sci U S A 115:12102-12111 |
| Kruglikov, Ilja L; Zhang, Zhuzhen; Scherer, Philipp E (2018) The Role of Immature and Mature Adipocytes in Hair Cycling. Trends Endocrinol Metab : |
| Stoiljkovic, Milan; Kelley, Craig; Horvath, Tamas L et al. (2018) Neurophysiological signals as predictive translational biomarkers for Alzheimer's disease treatment: effects of donepezil on neuronal network oscillations in TgF344-AD rats. Alzheimers Res Ther 10:105 |
| Xia, Jonathan Y; Sun, Kai; Hepler, Chelsea et al. (2018) Acute loss of adipose tissue-derived adiponectin triggers immediate metabolic deterioration in mice. Diabetologia 61:932-941 |
| Kusminski, Christine M; Scherer, Philipp E (2018) New zoning laws enforced by glucagon. Proc Natl Acad Sci U S A 115:4308-4310 |
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