A5056004624- Metabolism, Diabetes, and Cancer
- Pancreatic function and diabetes
- Estrogen and related hormone effects
- Cytokine Signaling Pathways and Interactions
- FOXO transcription factor regulation
- Mitochondrial Function and Pathology
- Liver Disease Diagnosis and Treatment
- Bioactive Compounds and Antitumor Agents
- Adipose Tissue and Metabolism
- Problem and Project Based Learning
- Metabolism and Genetic Disorders
- Muscle metabolism and nutrition
- Cancer, Hypoxia, and Metabolism
- Diabetes and associated disorders
- Innovative Teaching Methods
- Peroxisome Proliferator-Activated Receptors
- Protein Kinase Regulation and GTPase Signaling
- Experimental Learning in Engineering
- Muscle Physiology and Disorders
- Adipokines, Inflammation, and Metabolic Diseases
University of Pennsylvania
2021-2024
National Cancer Institute
2021-2022
Center for Cancer Research
2021-2022
National Institutes of Health
2017-2022
National Institute of Environmental Health Sciences
2017-2022
Rochester Institute of Technology
2018
University of Wisconsin–Madison
2018
Glucagon-like peptide 1 (GLP-1) receptor agonists reduce food intake, producing remarkable weight loss in overweight and obese individuals. While much of this is fat mass, there also a lean similar to other approaches that induce calorie deficit. Targeting signaling pathways regulate skeletal muscle hypertrophy promising avenue preserve mass modulate body composition. Myostatin Activin A are TGFβ-like ligands signal via the activin type II receptors (ActRII) antagonize growth. Pre-clinical...
The capacity to generate new adipocytes from precursor cells is critical for maintaining metabolic health. Adipocyte (APCs) constitute a heterogenous collection of cell types; however, the contribution these various types adipose tissue expansion in vivo remains unknown. aim current study investigate Dpp4+ progenitors de novo adipogenesis. Single analysis has identified several transcriptionally distinct subpopulations APCs, including progenitor concentrated connective surrounding many...
The essence of molecular biology education lies in understanding gene expression, with subtopics including the central dogma processes, such as transcription and translation. While these concepts are core to discipline, they also notoriously difficult for students learn, probably because cannot be directly observed. nearly all active learning strategies have been shown improve compared passive lectures, little has done compare different types learning. We hypothesized that physical models...
In response to a meal, insulin drives hepatic glycogen synthesis help regulate systemic glucose homeostasis. The mechanistic target of rapamycin complex 1 (mTORC1) is well-established and contributes the postprandial control liver lipid metabolism, autophagy, protein synthesis. However, its role in metabolism less understood. Here, we used metabolomics, isotope tracing, mouse genetics define for mTORC1 signaling glycolytic intermediates deposition. We show that required synthase activity...
Abstract The liver is central in maintaining glucose homeostasis. Indeed, impaired hepatic uptake has been implicated the development of hyperglycemia type II diabetes (T2D) and non‐alcoholic fatty disease (NAFLD). However, current approaches to evaluate mobilization rely on indirect measurements that do not provide spatial temporal information. Here, we describe confocal‐based intravital microscopy (IVM) allows identification hepatocyte organization transport. Specifically, a method...
Abstract As important as the fasting response is for survival, an inability to shut it down once nutrients become available can lead exacerbated disease and severe wasting. The liver central transitions between feeding states, with glucagon being a key initiator of hepatic response. However, precise mechanisms controlling are not well defined. One potential mediator these kinase B1 (LKB1), given its role in nutrient sensing. Here, we show LKB1 knockout mice have wasting prolonged phenotype...
Abstract As important as the fasting response is for survival, an inability to shut it down once nutrients become available can lead exacerbated disease and severe wasting. The liver central transitions between feeding states, with glucagon being a key initiator of hepatic response. However, precise mechanisms controlling are not well defined. One potential mediator these Liver Kinase B1 (LKB1) given its role in nutrient sensing. Here, we show LKB1 knockout mice have wasting prolonged...