A5064765902- Regulation of Appetite and Obesity
- Neuropeptides and Animal Physiology
- Adipose Tissue and Metabolism
- Hypothalamic control of reproductive hormones
- Biochemical Analysis and Sensing Techniques
- Adipokines, Inflammation, and Metabolic Diseases
- Pancreatic function and diabetes
- Growth Hormone and Insulin-like Growth Factors
- Genetic Syndromes and Imprinting
- Metabolism, Diabetes, and Cancer
- Stress Responses and Cortisol
- Bone Metabolism and Diseases
- Chemokine receptors and signaling
- Epigenetics and DNA Methylation
- Muscle metabolism and nutrition
- Climate Change and Health Impacts
- Pharmacological Effects and Assays
- Receptor Mechanisms and Signaling
- Retinal Imaging and Analysis
- Radiomics and Machine Learning in Medical Imaging
- Glaucoma and retinal disorders
- Hormonal and reproductive studies
- Prostate Cancer Diagnosis and Treatment
- Retinal Diseases and Treatments
- Genetics and Neurodevelopmental Disorders
Bradford Teaching Hospitals NHS Foundation Trust
2020-2023
St Vincent's Hospital
2006-2023
St Vincent's Clinic
2018-2023
Garvan Institute of Medical Research
2012-2023
UNSW Sydney
2007-2023
The University of Sydney
2023
Gartnavel General Hospital
2015-2021
University of Sheffield
2021
St Vincent's Hospital Sydney
2006-2020
Australian College of Optometry
2020
The importance of neuropeptide Y (NPY) and Y2 receptors in the regulation bone energy homeostasis has recently been demonstrated. However, contributions other are less clear. Here we show that Y1 expressed on osteoblastic cells. Moreover, adipose tissue mass elevated Y1(-/-) mice with a generalized increase formation cortical cancellous surfaces. Importantly, inhibitory effects NPY marrow stromal cells vitro absent derived from mice, indicating direct action via this receptor. Interestingly,...
Changes in whole body energy levels are closely linked to alterations weight and bone mass. Here, we show that hypothalamic signals contribute the regulation of mass a manner consistent with central perception status. Mice lacking neuropeptide Y (NPY), well-known orexigenic factor whose expression is increased fasting, have significantly association enhanced osteoblast activity elevated osteogenic transcription factors, Runx2 Osterix. In contrast, wild type NPY knockout (NPY −/−) mice which...
Abstract Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans. Recent clinical reports have suggested that micro-deletion Snord116 gene cluster can lead to PWS, however, extent contributions encoded snoRNAs unknown. Here we show mice lacking globally low birth weight, increased body weight gain, energy expenditure and hyperphagia. Consistent with this, microarray analysis hypothalamic expression revealed a significant alteration feeding related pathways was also...
Abstract Background/Objective Female mice are often excluded from diet-induced obesity studies as they more resistant to the obesifying effects of a high-fat diet (HFD). However, underlying mechanisms behind this sex disparity may actually have important implications for development and management in humans. Therefore, we systematically investigated immediate sex-specific transitioning HFD C57BL/6J well monitored whether these altered after sustained feeding affects response return chow,...
Mutations in the human ALMS1 gene are responsible for Alström syndrome, a disorder which key metabolic and endocrinological features include childhood-onset obesity, diabetes, as well infertility. localizes to basal bodies of cilia plays role intracellular trafficking, but biological functions how these relate pathogenesis infertility remain unclear. Here we describe new mouse model fat aussie, caused by spontaneous mutation Alms1 gene. Fat aussie (Alms1 foz/foz) mice normal weight when...
Germ line or hypothalamus-specific deletion of Y2 receptors in mice results a doubling trabecular bone volume. However, the specific mechanism by which increases mass has not yet been identified. Here we show that cultured adherent marrow stromal cells from <i>Y2</i><sup>-/-</sup> also demonstrate increased mineralization <i>in vitro</i>. Isolation two populations progenitor cell types, an immature mesenchymal stem population and more highly differentiated cells, revealed greater number...
Abstract The neuropeptide Y (NPY) system has been implicated in the regulation of bone homeostasis and osteoblast activity, but mechanism behind this is unclear. Here we show that Y1 receptor signaling directly involved differentiation mesenchymal progenitor cells isolated from tissue, as well activity mature osteoblasts. Importantly, mRNA levels two key osteogenic transcription factors, runx2 osterix, adipogenic factor PPAR-γ, were increased long bones Y1−/− mice compared with wild-type...
Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but mechanisms underlying stress-induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally peripherally, plays a critical role in protecting against loss. Mice lacking anxiolytic factor NPY exhibit more anxious behavior elevated corticosterone levels. Additionally, following 6-week restraint, or cold-stress protocol, Npy-null mice three-fold greater compared...
Abstract Excess caloric intake results in increased fat accumulation and an increase energy expenditure via diet-induced adaptive thermogenesis; however, the underlying mechanisms controlling these processes are unclear. Here we identify neuropeptide FF receptor-2 (NPFFR2) as a critical regulator of thermogenesis bone homoeostasis. Npffr2 −/− mice exhibit stronger phenotype when fed HFD display exacerbated obesity associated with failure activating brown adipose tissue (BAT) thermogenic...
The skeleton, which is strongly controlled by endocrine factors, has recently been shown to also play an active role itself, specifically influencing energy metabolism. However, much less known about this role. Therefore, we sought identify novel factors involved in the regulation of both bone mass and whole-body glucose homeostasis.We used transcriptomic proteomic analysis Y1 receptor deficient osteoblasts combined with generation a osteoglycin mouse model performed comprehensive vivo...
The skeleton has recently emerged as an additional player in the control of whole-body glucose metabolism; however, mechanism behind this is not clear.Here we employ mice lacking neuropeptide Y, Y1 receptors solely cells early osteoblastic lineage (Y1f3.6Cre), to examine role signalling glycaemic control.Y1f3.6Cre only have a high bone mass phenotype, but importantly also display altered homeostasis; significantly decreased pancreas weight, islet number and pancreatic insulin content leading...
Aguti-related protein (AGRP) neurons in the arcuate nucleus of hypothalamus (ARC), which co-express neuropeptide Y (NPY), are key regulators feeding and energy homeostasis. However, precise role NPY has within these specific pathways that it control still unclear. In this article, we aimed to determine what aspects behaviour homeostasis controlled by originating from AGRP Y-receptor utilised fulfil function. Novel conditional Agrpcre/+;Npylox/lox knockout mice were generated comprehensively...
Reduction in levels of sex hormones at menopause women is associated with two common, major outcomes, the accumulation white adipose tissue, and progressive loss bone because excess osteoclastic resorption exceeding osteoblastic formation. Current antiresorptive therapies can reduce activity but have only limited capacity to stimulate formation restore lost skeletal mass. Likewise, availability effective pharmacological weight treatments currently limited. Here we demonstrate that...
Neuropeptide Y (NPY) is a key regulator of energy homeostasis and implicated in the development obesity type 2 diabetes. Whereas it known that hypothalamic administration exogenous NPY peptides leads to increased body weight gain, hyperphagia, many hormonal metabolic changes characteristic an syndrome, receptor(s) mediating these effects disputed unclear. To investigate role different receptors NPY-induced we used recombinant adeno-associated viral vector overexpress mice deficient selective...