1. NPY signalling in early osteoblasts controls glucose homeostasis.

    Molecular Metabolism 4(3):164 (2015) PMID 25737952 PMCID PMC4338316

    The skeleton has recently emerged as an additional player in the control of whole-body glucose metabolism; however, the mechanism behind this is not clear. Here we employ mice lacking neuropeptide Y, Y1 receptors solely in cells of the early osteoblastic lineage (Y1f3.6Cre), to examine the role ...
  2. Double deletion of orexigenic neuropeptide Y and dynorphin results in paradoxical obesity in mice.

    Neuropeptides 48(3):143 (2014) PMID 24680736

    Orexigenic neuropeptide Y (NPY) and dynorphin (DYN) regulate energy homeostasis. Single NPY or dynorphin deletion reduces food intake or increases fat loss. Future developments of obesity therapeutics involve targeting multiple pathways. We hypothesised that NPY and dynorphin regulate energy hom...
  3. Double deletion of orexigenic neuropeptide Y and dynorphin results in paradoxical obesity in mice

    Neuropeptides 48(3):143 (2014)

    Objective Orexigenic neuropeptide Y (NPY) and dynorphin (DYN) regulate energy homeostasis. Single NPY or dynorphin deletion reduces food intake or increases fat loss. Future developments of obesity therapeutics involve targeting multiple pathways. We hypothesised that NPY and...
  4. Double deletion of orexigenic neuropeptide Y and dynorphin results in paradoxical obesity in mice.

    Neuropeptides 48(3):143 (2014) PMID 24680736

    Orexigenic neuropeptide Y (NPY) and dynorphin (DYN) regulate energy homeostasis. Single NPY or dynorphin deletion reduces food intake or increases fat loss. Future developments of obesity therapeutics involve targeting multiple pathways. We hypothesised that NPY and dynorphin regulate energy hom...
  5. Intermittent energy restriction improves fat loss efficiency in diet-induced obese mice

    Obesity Research & Clinical Practice 7:e25 (2013)

  6. Neuropeptide Y is a critical modulator of leptin's regulation of cortical bone.

    Journal of Bone and Mineral Research 28(4):886 (2013) PMID 23044938

    Leptin signaling is required for normal bone homeostasis; however, loss of leptin results in differing effects on cortical and cancellous bone, as well as altered responses between the axial and appendicular regions. Local β-adrenergic actions are responsible for the greater cancellous bone volu...
  7. Neuropeptide Y is a critical modulator of leptin's regulation of cortical bone.

    Journal of Bone and Mineral Research 28(4):886 (2013) PMID 23044938

    Leptin signaling is required for normal bone homeostasis; however, loss of leptin results in differing effects on cortical and cancellous bone, as well as altered responses between the axial and appendicular regions. Local β-adrenergic actions are responsible for the greater cancellous bone volu...
  8. Arcuate NPY controls sympathetic output and BAT function via a relay of tyrosine hydroxylase neurons in the PVN.

    Cell Metabolism 17(2):236 (2013) PMID 23395170

    Neuropepetide Y (NPY) is best known for its powerful stimulation of food intake and its effects on reducing energy expenditure. However, the pathways involved and the regulatory mechanisms behind this are not well understood. Here we demonstrate that NPY derived from the arcuate nucleus (Arc) is...
  9. Arcuate NPY controls sympathetic output and BAT function via a relay of tyrosine hydroxylase neurons in the PVN.

    Cell Metabolism 17(2):236 (2013) PMID 23395170

    Neuropepetide Y (NPY) is best known for its powerful stimulation of food intake and its effects on reducing energy expenditure. However, the pathways involved and the regulatory mechanisms behind this are not well understood. Here we demonstrate that NPY derived from the arcuate nucleus (Arc) is...
  10. Arcuate NPY Controls Sympathetic Output and BAT Function via a Relay of Tyrosine Hydroxylase Neurons in the PVN

    Cell Metabolism 17(2):236 (2013)

    Neuropepetide Y (NPY) is best known for its powerful stimulation of food intake and its effects on reducing energy expenditure. However, the pathways involved and the regulatory mechanisms behind this are not well understood. Here we demonstrate that NPY derived from the arcuate nucleu...
  11. The endogenous opioid dynorphin is required for normal bone homeostasis in mice

    Neuropeptides 46(6):383 (2012)

    Chronic opiate usage, whether prescribed or illicit, has been associated with changes in bone mass and is a recognized risk factor for the development of osteoporosis; however, the mechanism behind this effect is unknown. Here we show that lack of dynorphin, an endogenous opioid, in mi...
  12. The endogenous opioid dynorphin is required for normal bone homeostasis in mice.

    Neuropeptides 46(6):383 (2012) PMID 23062312

    Chronic opiate usage, whether prescribed or illicit, has been associated with changes in bone mass and is a recognized risk factor for the development of osteoporosis; however, the mechanism behind this effect is unknown. Here we show that lack of dynorphin, an endogenous opioid, in mice (Dyn-/-...
  13. Neuropeptide Y Y1 receptor antagonism increases bone mass in mice.

    Bone 51(1):8 (2012) PMID 22484690

    The neuropeptide Y system has emerged as one of the major neural signalling pathways regulating bone homeostasis. Absence of Y1 receptor signalling from bone forming osteoblasts is responsible for an enhancement on bone mass in mice, suggesting that pharmacological blockade of Y1 receptors may o...
  14. Neuropeptide Y Y1 receptor antagonism increases bone mass in mice.

    Bone 51(1):8 (2012) PMID 22484690

    The neuropeptide Y system has emerged as one of the major neural signalling pathways regulating bone homeostasis. Absence of Y1 receptor signalling from bone forming osteoblasts is responsible for an enhancement on bone mass in mice, suggesting that pharmacological blockade of Y1 receptors may o...
  15. Neuropeptide Y Y1 receptor antagonism increases bone mass in mice

    Bone 51(1):8 (2012)

    The neuropeptide Y system has emerged as one of the major neural signalling pathways regulating bone homeostasis. Absence of Y1 receptor signalling from bone forming osteoblasts is responsible for an enhancement on bone mass in mice, suggesting that pharmacological blockade of Y1 recep...
  16. Y1 and Y5 receptors are both required for the regulation of food intake and energy homeostasis in mice.

    PLoS ONE 7(6):e40191 (2012) PMID 22768253 PMCID PMC3387009

    Neuropeptide Y (NPY) acting in the hypothalamus is one of the most powerful orexigenic agents known. Of the five known Y receptors, hypothalamic Y1 and Y5 have been most strongly implicated in mediating hyperphagic effects. However, knockout of individual Y1 or Y5 receptors induces late-onset ob...
  17. Peptide YY regulates bone remodeling in mice: a link between gut and skeletal biology.

    PLoS ONE 7(7):e40038 (2012) PMID 22792209 PMCID PMC3391226

    Gastrointestinal peptides are increasingly being linked to processes controlling the maintenance of bone mass. Peptide YY (PYY), a gut-derived satiety peptide of the neuropeptide Y family, is upregulated in some states that also display low bone mass. Importantly, PYY has high affinity for Y-rec...
  18. Y1 and Y5 receptors are both required for the regulation of food intake and energy homeostasis in mice.

    PLoS ONE 7(6):e40191 (2012) PMID 22768253 PMCID PMC3387009

    Neuropeptide Y (NPY) acting in the hypothalamus is one of the most powerful orexigenic agents known. Of the five known Y receptors, hypothalamic Y1 and Y5 have been most strongly implicated in mediating hyperphagic effects. However, knockout of individual Y1 or Y5 receptors induces late-onset ob...
  19. Peptide YY regulates bone remodeling in mice: a link between gut and skeletal biology.

    PLoS ONE 7(7):e40038 (2012) PMID 22792209 PMCID PMC3391226

    Gastrointestinal peptides are increasingly being linked to processes controlling the maintenance of bone mass. Peptide YY (PYY), a gut-derived satiety peptide of the neuropeptide Y family, is upregulated in some states that also display low bone mass. Importantly, PYY has high affinity for Y-rec...
  20. Peripheral-specific y2 receptor knockdown protects mice from high-fat diet-induced obesity.

    Obesity 19(11):2137 (2011) PMID 21546930

    Y2 receptors, particularly those in the brain, have been implicated in neuropeptide Y (NPY)-mediated effects on energy homeostasis and bone mass. Recent evidence also indicates a role for Y2 receptors in peripheral tissues in this process by promoting adipose tissue accretion; however their effe...