NPY and cohorts in regulating appetite, obesity and metabolic syndrome: beneficial effects of gene therapy

  title={NPY and cohorts in regulating appetite, obesity and metabolic syndrome: beneficial effects of gene therapy},
  author={Satya P. Kalra and Pushpa S. Kalra},
Subjugation of hypothalamic NPY and cohorts with central leptin gene therapy alleviates dyslipidemia, insulin resistance, and obesity for life-time.
Sustained repression of NPY signaling with increased leptin selectively in the hypothalamus can avert environmental obesity and the risks of metabolic diseases.
Hypothalamic regulation of appetite
This review highlights the key areas of research in the hypothalamic control of appetite, including the anorexigenic pro-opiomelanocortin/cocaine- and amphetamine-related transcript neurons in the arcuate nucleus of the hypothalamus.
Role of neuropeptides in appetite regulation and obesity – A review
Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome
It is reported that stress exaggerates diet-induced obesity through a peripheral mechanism in the abdominal white adipose tissue that is mediated by neuropeptide Y (NPY), and manipulations of NPY2R activity within fat tissue offer new ways to remodel fat and treat obesity and metabolic syndrome.
Assays of Obesity-Regulating Peptide Hormones
Food intake and fat deposition are regulated by peptide neurotransmitters, most of them located in the brain, particularly in the hypothalamus, and in the gut, and this includes peptides that are orexigenic and anorectic.


Interacting appetite-regulating pathways in the hypothalamic regulation of body weight.
Multiple orexigenic and anorexigenic pathways in the hypothalamic ARN appear to represent redundancy, a characteristic of regulated biological systems to provide a "fail-safe" neural mechanism to meet an organism's constant energy needs for growth and maintenance.
NPY: A Novel On/Off Switch for Control of Appetite and Reproduction
The information collated here supports the concept that neuropeptide Y (NPY) is an essential messenger molecule in integration of the innate appetitive drive and the urge to reproduce. There is a
A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa.
  • U. Bailer, W. Kaye
  • Biology, Psychology
    Current drug targets. CNS and neurological disorders
  • 2003
Most of the neuroendocrine and neuropeptide alterations apparent during symptomatic episodes of AN and BN tend to normalize after recovery, suggesting that most of the disturbances are consequences rather than causes of malnutrition, weight loss and/or altered meal patterns.
Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus
An integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus is proposed and it is shown that melanocortin peptides have an autoinhibitory effect on this circuit.
Daily changes in hypothalamic gene expression of neuropeptide Y, galanin, proopiomelanocortin, and adipocyte leptin gene expression and secretion: effects of food restriction.
In FF rats, gene expression of hypothalamic appetite stimulating peptides first rise and then fall to nadir during the lights-on phase when leptin levels are in low range; adipocyte leptin mRNA rises before impending ingestive behavior and increased leptin secretion reaching peak manifests itself during nocturnal feeding.
The arcuate nucleus as a conduit for diverse signals relevant to energy homeostasis
The arcuate melanocortin system is best described as a conduit of many diverse signals involved in energy homeostasis, with leptin acting tonically to regulate the responsiveness of the circuit to a wide variety of hormones and nutrients.
Role of the Y5 neuropeptide Y receptor in feeding and obesity
It is demonstrated that the Y5R contributes to feeding induced by centrally administered NPY and its analogs, but is not a critical physiological feeding receptor in mice.