scholarly journals Leptin Receptor Long-form Splice-variant Protein Expression in Neuron Cell Bodies of the Brain and Co-localization with Neuropeptide Y mRNA in the Arcuate Nucleus

1999 ◽  
Vol 47 (3) ◽  
pp. 353-362 ◽  
Author(s):  
Denis G. Baskin ◽  
Michael W. Schwartz ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Daniel Porte ◽  
...  
Keyword(s):  
Protein Expression ◽  
Neuropeptide Y ◽  
Splice Variant ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Long Form ◽  
The Brain ◽  
Variant Protein

Dexamethasone rapidly increases hypothalamic neuropeptide Y secretion in adrenalectomized ob/ob mice

1996 ◽  
Vol 271 (1) ◽  
pp. E151-E158 ◽  
Author(s):  
H. L. Chen ◽  
D. R. Romsos
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Rapid Onset ◽  
Brown Adipose ◽  
Specific Enhancement ◽  
Brown Adipose Tissue Thermogenesis ◽  
The Central Nervous System ◽  
Rapid Transport ◽  
The Brain

A single intracerebroventricular injection of dexamethasone (DEX) rapidly (within 30 min) suppresses brown adipose tissue thermogenesis and increases plasma insulin concentrations in adrenal-ectomized (ADX) ob/ob mice but not in ADX lean mice. Intracerebroventricular neuropeptide Y (NPY) administered intracerebroventricularly causes these same metabolic changes within 30 min in both ob/ob and lean ADX mice. We therefore hypothesized that DEX exerts these rapid-onset metabolic actions in ob/ob mice via a phenotype-specific enhancement of NPY secretion within the central nervous system. In support of this hypothesis, DEX (a type II glucocorticoid receptor agonist) administered intracerebroventricularly selectively lowered NPY concentrations in the whole hypothalamus of ADX ob/ob mice by 35% and in the arcuate nucleus region by approximately 70% within 30 min but not in the brain stem or hippocampus or in any of these regions of lean mice. DEX also functioned in vitro to enhance depolarization-dependent release of NPY from hypothalamic blocks of ADX ob/ob mice but not of ADX lean mice. Thus DEX acts in the hypothalamus of ob/ob mice in a phenotype-specific manner to evoke rapid transport of NPY from cell bodies within the arcuate nucleus to terminal regions including the dorsomedial and ventromedial hypothalamic regions for release.

Expression of leptin receptor mRNA (long form splice variant) in the human cerebellum

Neuroreport ◽  
1997 ◽  
Vol 8 (14) ◽  
pp. 3123-3126 ◽  
Author(s):  
Armand Savioz ◽  
Yves Charnay ◽  
Claude Huguenin ◽  
Christelle Graviou ◽  
Brigitte Greggio ◽  
...  
Keyword(s):  
Splice Variant ◽  
Leptin Receptor ◽  
Receptor Mrna ◽  
Long Form ◽  
Human Cerebellum

scholarly journals Nutritional Influences on Reproductive Neuroendocrine Output: Insulin, Leptin, and Orexigenic Neuropeptide Signaling in the Ovine Hypothalamus

Endocrinology ◽  
2007 ◽  
Vol 148 (11) ◽  
pp. 5313-5322 ◽  
Author(s):  
David W. Miller ◽  
Joanne L. Harrison ◽  
Ellen J. Bennett ◽  
Patricia A. Findlay ◽  
Clare L. Adam
Keyword(s):  
Gene Expression ◽  
Neuropeptide Y ◽  
Leptin Receptor ◽  
Nutritional Influences ◽  
Hypothalamic Arcuate Nucleus ◽  
Melanocortin Signaling ◽  
Neuroendocrine Responses ◽  
Peptide Gene ◽  
Plasma Leptin ◽  
The Brain

This study investigated how changing nutritional status may alter reproductive neuroendocrine (LH) output via circulating leptin and insulin signaling through orexigenic hypothalamic pathways. Thin sheep were given an increasing nutritional plane (INP), sheep with intermediate adiposity a static nutritional plane (SNP), and fat sheep a decreasing nutritional plane (DNP) for 6 wk. Mean group adiposities converged by wk 6, LH output increased in INP, remained unchanged in SNP, and decreased in DNP sheep. Plasma and cerebrospinal fluid (CSF) insulin and plasma leptin concentrations increased in INP but did not change in the SNP and DNP groups. In INP sheep, LH output correlated positively with adiposity and plasma and CSF insulin concentrations and negatively with orexigenic neuropeptide Y gene expression in the hypothalamic arcuate nucleus (ARC). In DNP sheep, LH output correlated positively with adiposity, CSF leptin concentrations, and ARC proopiomelanocortin gene expression and negatively with leptin receptor (OB-Rb) and agouti-related peptide gene expression in the ARC. These data are consistent with the feedback response to an increasing nutritional plane being mediated by increasing circulating insulin entering the brain and stimulating LH via inhibition of hypothalamic neuropeptide Y and the response to a decreasing nutritional plane being mediated by altered hypothalamic leptin signaling brought about by increased OB-Rb expression and decreased melanocortin signaling. Because end point adiposity was similar yet LH output was different, the hypothalamus apparently retains a nutritional memory, based on changes in orexigenic neuropeptide expression, that influences contemporary neuroendocrine responses.

Hypothyroidism Induces Hypophagia Associated with Alterations in Protein Expression of Neuropeptide Y and Proopiomelanocortin in the Arcuate Nucleus, Independently of Hypothalamic Nuclei-Specific Changes in Leptin Signaling

Thyroid ◽  
2016 ◽  
Vol 26 (1) ◽  
pp. 134-143 ◽  
Author(s):  
Camila Calvino ◽  
Güínever Eustáquio Império ◽  
Marianna Wilieman ◽  
Ricardo Henrique Costa-e-Sousa ◽  
Luana Lopes Souza ◽  
...  
Keyword(s):  
Protein Expression ◽  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Leptin Signaling ◽  
Hypothalamic Nuclei

scholarly journals Xiaoyaosan Decoction Regulates Changes in Neuropeptide Y and Leptin Receptor in the Rat Arcuate Nucleus after Chronic Immobilization Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Shao-Xian Wang ◽  
Jia-Xu Chen ◽  
Guang-Xin Yue ◽  
Ming-Hua Bai ◽  
Mei-Jing Kou ◽  
...  
Keyword(s):  
Weight Loss ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Chronic Stress ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Bodyweight Loss ◽  
Stress Group ◽  
Regulatory Effects ◽  
Neuroendocrine Mechanism

The arcuate nucleus (ARC) in the basal of hypothalamus plays an important role in appetite regulation and energy balance. We sought to investigate the central neuroendocrine mechanism of appetite decrease and weight loss under chronic stress by observing the regulatory effects of Xiaoyaosan decoction in the expression of leptin receptor (ob-R) and neuropeptide Y (NPY) in the ARC. Our results showed that bodyweight and food intake of rats in the 21-day stress group increased slower than those of the normal group. Higher contents of Leptin andob-Rwere noted in the 21-day stress group compared with control rats, while NPY expression was not statistically different. Xiaoyaosan powder can significantly downregulate the contents of leptin andob-Rin the hypothalamus of stressed rats. These findings suggest that increase ofob-Rexpression in the ARC is possibly one key central neuroendocrine change for the somatic discomfort. Weight loss and decreased food intake in rats caused by the binding of leptin toob-Rin hypothalamus do not appear to utilize the NPY pathway. This study also suggests thatob-Rin the ARC may act as the target of Xiaoyaosan in regulating the symptoms such as appetite decrease and bodyweight loss under chronic stress.

Abstract 109: Leptin Acts in POMC Neurons to Increase Sympathetic Nerve Activity

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Shannon M Harlan ◽  
Donald A Morgan ◽  
Kamal Rahmouni
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Specific Effect ◽  
Neuronal Population ◽  
Wild Type ◽  
Nerve Activity ◽  
Brown Adipose ◽  
The Brain

Leptin acts in the brain to decrease food intake and promote energy expenditure by increasing sympathetic nerve activity (SNA) to thermogenic brown adipose tissue (BAT). Leptin also increases SNA to other beds including kidney with implications for obesity-associated hypertension. We previously demonstrated the importance the arcuate nucleus (Arc) of the hypothalamus in mediating leptin-induced increases in regional SNA, but the specific neuronal population within the Arc that mediates these responses is unknown. We hypothesized that proopiomelanocortin (POMC) neurons of the Arc are critical for the increases in SNA in response to leptin. To test this, we generated mice lacking the leptin receptor (ObR) specifically in POMC neurons (ObR flox/flox / POMC Cre ). We used multifiber sympathetic nerve recording to assess the SNA effects of leptin. ObR flox/flox /POMC Cre mice exhibited a significantly (P<0.01) blunted renal SNA response to intravenous administration of 120 μg of leptin (4±18%) as compared to wild type controls (161±35%). Intracerebroventricular (ICV) injection of leptin (2 μg) also increased renal SNA in wild type mice (220±77%), but not in ObR flox/flox /POMC Cre mice (-1±13%). In contrast, the renal SNA response to ICV insulin (100 μU) was not different (P=0.27) in ObR flox/flox /POMC Cre mice (150±24%) as compared to littermate controls (195±68%) demonstrating that the loss of renal SNA response to leptin in mice lacking ObR in POMC neurons is a specific effect. Next, we investigated the requirement of ObR in POMC neurons for the sympathoexcitatory effects of leptin in other beds. Strikingly, ObR flox/flox /POMC Cre mice had a significantly (P<0.05) blunted lumbar SNA response to ICV leptin (14±22%) as compared to controls (226±38%). In addition, the BAT SNA response to ICV leptin was attenuated (P<0.01) in ObR flox/flox /POMC Cre mice (126±28%) relative to controls (309±80%). These results demonstrate the leptin receptor signaling in POMC neurons in the control of regional sympathetic nerve activity.

Association Study of Arcuate Nucleus Neuropeptide Y Neuron Receptor Gene Variation And Serum Npy Levels in Clozapine Treated Patients With Schizophrenia

2016 ◽  
Vol 40 ◽  
pp. 13-19 ◽  
Author(s):  
J.-P. Klemettilä ◽  
O. Kampman ◽  
A. Solismaa ◽  
L.-P. Lyytikäinen ◽  
N. Seppälä ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Permutation Test ◽  
Serum Insulin ◽  
Genetic Risk Score ◽  
Receptor Gene ◽  
Serum Levels ◽  
Gene Score ◽  
Insulin Receptor Gene

AbstractBackgroundAntipsychotic-induced weight gain (AIWG) leads to metabolic consequences and comorbidity, social stigmatization and nonadherence in patients with schizophrenia. Neuropeptide Y (NPY) has an important role in appetite and body weight regulation. Associations between AIWG and serum NPY levels, and genetic polymorphisms (SNPs) associated with its serum levels have been little studied in these patients.Subjects and methodsAssociations between serum NPY concentration and other metabolic and inflammatory markers, and 215 SNPs in 21 genes (NPY gene, NPY receptor genes and genes encoding arcuate nucleus NPY neuron receptors) were studied in 180 patients with schizophrenia on clozapine treatment.ResultsThe serum levels of NPY correlated with levels of resistin (r = 0.31, P < 0.001) and age (r = 0.22, P = 0.003). In the general linear univariate model the best-fitting model with explanatory factors age, serum resistin level, serum insulin level, BMI and gender explained 18.0% (P < 0.001) of the variance of serum NPY. Genetic risk score (GRSNPY) analysis found twelve significant (P < 0.05) serum NPY concentration related SNPs among α7 nicotinic acetylcholine receptor gene CHRNA7, insulin receptor gene INSR, leptin receptor gene LEPR, glucocorticoid receptor (GR) gene NR3C1, and NPY gene. However, after permutation test of gene score the predictive value of GRSNPY remained non-significant (P = 0.078).ConclusionsSerum NPY level does not seem to be a feasible biomarker of AIWG. Serum NPY level alterations are not significantly associated with the candidate gene polymorphisms studied.

scholarly journals Recent advances in understanding leptin signaling and leptin resistance

2009 ◽  
Vol 297 (6) ◽  
pp. E1247-E1259 ◽  
Author(s):  
David L. Morris ◽  
Liangyou Rui
Keyword(s):  
Endoplasmic Reticulum ◽  
Body Weight ◽  
Risk Factor ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Leptin Resistance ◽  
Leptin Signaling ◽  
Long Form ◽  
The Brain ◽  
Primary Risk Factor

The brain controls energy homeostasis and body weight by integrating various metabolic signals. Leptin, an adipose-derived hormone, conveys critical information about peripheral energy storage and availability to the brain. Leptin decreases body weight by both suppressing appetite and promoting energy expenditure. Leptin directly targets hypothalamic neurons, including AgRP and POMC neurons. These leptin-responsive neurons widely connect to other neurons in the brain, forming a sophisticated neurocircuitry that controls energy intake and expenditure. The anorexigenic actions of leptin are mediated by LEPRb, the long form of the leptin receptor, in the hypothalamus. LEPRb activates both JAK2-dependent and -independent pathways, including the STAT3, PI 3-kinase, MAPK, AMPK, and mTOR pathways. These pathways act coordinately to form a network that fully mediates leptin response. LEPRb signaling is regulated by both positive (e.g., SH2B1) and negative (e.g., SOCS3 and PTP1B) regulators and by endoplasmic reticulum stress. Leptin resistance, a primary risk factor for obesity, likely results from impairment in leptin transport, LEPRb signaling, and/or the neurocircuitry of energy balance.

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