Publications by authors named "Hayley B Burm"
Article Synopsis
- - The study highlights the potential of activating the neurokinin 2 receptor (NK2R) as a dual approach to combat obesity and type 2 diabetes by suppressing appetite and increasing energy expenditure, representing a significant advancement over current multi-drug strategies.
- - Researchers developed long-acting NK2R agonists that can be administered weekly, which showed promising results in mice, leading to weight loss and improved insulin sensitivity without relying on traditional leptin signaling.
- - In tests with diabetic, obese macaques, NK2R activation resulted in substantial reductions in body weight, blood glucose, and cholesterol levels, suggesting a single-target therapeutic option that enhances energy balance and addresses cardiometabolic issues across different species.
Midbrain dopaminergic neurons (DANs) are subject to extensive metabotropic regulation, but the repertoire of G protein-coupled receptors (GPCRs) present in these neurons has not been mapped. Here, we isolate DANs from Dat-eGFP mice to generate a GPCR atlas by unbiased qPCR array expression analysis of 377 GPCRs. Combined with data mining of scRNA-seq databases, we identify multiple receptors in DAN subpopulations with 38 of these receptors representing the majority of transcripts.
View Article and Find Full Text PDFObjective: The goal of this study was to investigate the importance of central hormone-sensitive lipase (HSL) expression in the regulation of food intake and body weight in mice to clarify whether intracellular lipolysis in the mammalian hypothalamus plays a role in regulating appetite.
Methods: Using pharmacological and genetic approaches, we investigated the role of HSL in the rodent brain in the regulation of feeding and energy homeostasis under basal conditions during acute stress and high-fat diet feeding.
Results: We found that HSL, a key enzyme in the catabolism of cellular lipid stores, is expressed in the appetite-regulating centers in the hypothalamus and is activated by acute stress through a mechanism similar to that observed in adipose tissue and skeletal muscle.
The causal contribution of glial pathology to Huntington disease (HD) has not been heavily explored. To define the contribution of glia to HD, we established human HD glial chimeras by neonatally engrafting immunodeficient mice with mutant huntingtin (mHTT)-expressing human glial progenitor cells (hGPCs), derived from either human embryonic stem cells or mHTT-transduced fetal hGPCs. Here we show that mHTT glia can impart disease phenotype to normal mice, since mice engrafted intrastriatally with mHTT hGPCs exhibit worse motor performance than controls, and striatal neurons in mHTT glial chimeras are hyperexcitable.
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