Changes in the responsiveness of serum leptin and hypothalamic neuropeptide Y mRNA levels to food deprivation in developing rats

2011 ◽  
Vol 29 (4) ◽  
pp. 377-380 ◽  
Author(s):  
Takeshi Iwasa ◽  
Toshiya Matsuzaki ◽  
Riyo Kinouchi ◽  
Ganbat Gereltsetseg ◽  
Masahiro Murakami ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Food Deprivation ◽  
Mrna Levels ◽  
Serum Leptin

Naltrexone induces arcuate nucleus neuropeptide Y gene expression in the rat

1996 ◽  
Vol 271 (1) ◽  
pp. R289-R294 ◽  
Author(s):  
C. M. Kotz ◽  
M. K. Grace ◽  
J. E. Briggs ◽  
C. J. Billington ◽  
A. S. Levine
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Arcuate Nucleus ◽  
Uncoupling Protein ◽  
Endogenous Opioids ◽  
Brown Fat ◽  
Mrna Levels ◽  
Sprague Dawley

Neuropeptide Y (NPY) has potent effects on several components of energy metabolism, including increased feeding and decreased brown fat thermogenesis. Negative energy balance, such as food deprivation, increases NPY mRNA in hypothalamic arcuate nucleus (ARC). Naltrexone (NLTX), an opioid receptor antagonist, decreases NPY-induced feeding. We hypothesized that NLTX would alter ARC NPY mRNA and change NPY effects on brown fat. Osmotic minipumps prefilled with either saline or NLTX (70 micrograms/h) were implanted subcutaneously in 32 male Sprague-Dawley rats. One-half of the rats were food deprived and one-half were allowed food ad libitum for 48 h. Food intake was measured at 24 and 48 h. At 48 h, ARC NPY mRNA and brown fat uncoupling protein (UCP) mRNA levels were determined using cDNA probes. Forty-eight-hour food intake was significantly decreased by 24% after NLTX infusion. Food deprivation and NLTX treatment significantly and independently increased ARC NPY mRNA and decreased UCP mRNA levels in brown fat, suggesting a complex interaction between hypothalamic NPY and endogenous opioids in the regulation of energy balance.

Aging and fasting regulation of leptin and hypothalamic neuropeptide Y gene expression

1998 ◽  
Vol 275 (3) ◽  
pp. E405-E411 ◽  
Author(s):  
Hua Li ◽  
Michael Matheny ◽  
Nihal Tümer ◽  
Philip J. Scarpace
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Neuropeptide Y ◽  
Mrna Levels ◽  
Aged Rats ◽  
Serum Leptin ◽  
Epididymal White Adipose Tissue ◽  
Ad Libitum ◽  
Fasted Rats

To investigate the role of aging on the fasting-induced suppression of leptin gene expression and increase in hypothalamic neuropeptide Y (NPY) gene expression, we fasted or fed ad libitum male F-344xBN rats aged 3, 24, and 31 mo for 2 days. We examined leptin mRNA levels in retroperitoneal, inguinal, and epididymal white adipose tissue (WAT); serum leptin levels; and NPY mRNA levels in the hypothalamus. We found that leptin mRNA levels were increased from 3 to 24 mo and leveled off between 24 and 31 mo in both retroperitoneal WAT and inguinal WAT but were unchanged with age in epididymal WAT. Serum leptin levels increased with age, whereas hypothalamic NPY mRNA levels did not change with age. Fasting suppressed leptin gene expression in all three WATs and serum leptin. Moreover, this suppression of serum leptin and of leptin message in retroperitoneal WAT was less in aged rats. Conversely, fasting increased hypothalamic NPY message, again to a lesser extent in aged rats. In both fed (ad libitum) and fasted rats, there was a strong correlation between serum leptin and hypothalamic NPY mRNA levels in the young but not in either of the two aged groups. These data suggest that aged F-344xBN rats are leptin resistant and that the fasting regulation of serum leptin, leptin mRNA, and hypothalamic NPY mRNA is impaired in aged rats.

In vivo action of a new octadecaneuropeptide antagonist on neuropeptide Y and corticotropin-releasing hormone mRNA levels in rat

2005 ◽  
Vol 141 (2) ◽  
pp. 156-160 ◽  
Author(s):  
V. Compère ◽  
S. Li ◽  
J. Leprince ◽  
M.C. Tonon ◽  
H. Vaudry ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

scholarly journals Secretogranin II binds to secretogranin III and forms secretory granules with orexin, neuropeptide Y, and POMC

2009 ◽  
Vol 202 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Kikuko Hotta ◽  
Masahiro Hosaka ◽  
Atsushi Tanabe ◽  
Toshiyuki Takeuchi
Keyword(s):  
Body Weight ◽  
Neuropeptide Y ◽  
Secretory Granules ◽  
Immunohistochemical Analysis ◽  
Mrna Levels ◽  
Weight Changes ◽  
Body Weight Changes ◽  
Hypothalamic Area ◽  
Double Labeling ◽  
Secretogranin Ii

Functional variations in the secretogranin III (SCG3) gene are associated with susceptibility to obesity. SCG3 forms secretory granules with orexin, melanin-concentrating hormone (MCH), neuropeptide Y (NPY), and POMC in the hypothalamus. In this study, we screened proteins for SCG3-binding activity and identified secretogranin II (SCG2) using a yeast two-hybrid system. Immunoprecipitation revealed that SCG2 interacts with SCG3. In situ hybridization and immunohistochemistry indicated that SCG2 was highly expressed in the lateral hypothalamic area, paraventricular nucleus, and arcuate nucleus of the hypothalamus. Double-labeling immunohistochemical analysis demonstrated that SCG2 was expressed in orexin-, MCH-, NPY-, and POMC-expressing neurons. SCG2 was also coexpressed with SCG3. Upon introduction into neuroblastoma cells, SCG2 was expressed in the cytosol and formed granule-like structures with SCG3, orexin, NPY, or POMC. SCG3 bound to POMC; however, it did not bind to orexin, MCH, or NPY. By contrast, SCG2 formed aggregates with orexin, MCH, NPY, and POMC. SCG2 may act as a hormone carrier for orexin, MCH, NPY, and POMC by binding with SCG3, which targets proteins to the secretory granules. SCG2 mRNA levels increased along with those of SCG3, orexin, MCH, and NPY after a 24-h fast, suggesting that the SCG2/SCG3 system may respond in an adaptive manner to acute body weight changes. However, this SCG2/SCG3 system appears to be unresponsive to chronic body weight changes, such as diet-induced obesity or obesity in ob/ob mice. We suggest that SCG2, as well as SCG3, may be a potential regulator of food intake based on its capacity to accumulate appetite-related hormones into secretory granules.

Regulation of food intake by neuropeptide Y in goldfish

2000 ◽  
Vol 279 (3) ◽  
pp. R1025-R1034 ◽  
Author(s):  
Yuwaraj K. Narnaware ◽  
Pierre P. Peyon ◽  
Xinwei Lin ◽  
Richard E. Peter
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Mrna Levels ◽  
Food Ration ◽  
Y1 Receptor ◽  
Daily Food ◽  
Daily Food Ration ◽  
Brain Ventricle ◽  
Dose Dependent Increase ◽  
Dose Dependent

In mammals, neuropeptide Y (NPY) is a potent orexigenic factor. In the present study, third brain ventricle (intracerebroventricular) injection of goldfish NPY (gNPY) caused a dose-dependent increase in food intake in goldfish, and intracerebroventricular administration of NPY Y1-receptor antagonist BIBP-3226 decreased food intake; the actions of gNPY were blocked by simultaneous injection of BIBP-3226. Goldfish maintained on a daily scheduled feeding regimen display an increase in NPY mRNA levels in the telencephalon-preoptic area and hypothalamus shortly before feeding; however, a decrease occured in optic tectum-thalamus. In both fed and unfed fish, brain NPY mRNA levels decreased after scheduled feeding. Restriction in daily food ration intake for 1 wk or food deprivation for 72 h resulted in increased brain NPY mRNA levels. Results from these studies demonstrate that NPY is a physiological brain signal involved in feeding behavior in goldfish, mediating its effects, at least in part, through Y1-like receptors in the brain.

scholarly journals Zinc Deficiency Increases Hypothalamic Neuropeptide Y and Neuropeptide Y mRNA Levels and Does Not Block Neuropeptide Y–Induced Feeding in Rats

1998 ◽  
Vol 128 (7) ◽  
pp. 1218-1223 ◽  
Author(s):  
Rita G. Lee ◽  
Tia M. Rains ◽  
Claudia Tovar-Palacio ◽  
J. Lee Beverly ◽  
Neil F. Shay
Keyword(s):  
Neuropeptide Y ◽  
Zinc Deficiency ◽  
Mrna Levels

scholarly journals Abnormal Response of the Neuropeptide Y-Deficient Mouse Reproductive Axis to Food Deprivation But Not Lactation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 1780-1786 ◽  
Author(s):  
Jennifer W. Hill ◽  
Jon E. Levine
Keyword(s):  
Neuropeptide Y ◽  
Food Consumption ◽  
Food Deprivation ◽  
Normal Female ◽  
Estrous Cycles ◽  
Energy Deficiency ◽  
Steroid Dependent ◽  
Reproductive Axis ◽  
Estrous Cyclicity ◽  
Lh Release

Neuropeptide Y (NPY) plays a key role in both food intake and GnRH secretion. Food deprivation elevates hypothalamic NPY activity and suppresses LH and gonadal steroid secretion. Similarly, lactation up-regulates NPY expression as food consumption increases and estrous cycles cease. These observations suggest that NPY coordinates reproductive suppression in response to energy deficiency; if so, the reproductive axis of NPY knockout (KO) mice should be impervious to lactation and food deprivation. We monitored food consumption, body weight, and estrous cyclicity during lactation in NPY KO mice with large and small litters. NPY KO mice with either litter size resembled wild types (WTs) in weight regulation and food consumption. Large-litter mothers had longer anestrous periods and smaller pups at weaning, but NPY KOs and WTs did not differ in either respect. We also examined the LH response of NPY KO mice to 48 h without food. Basal levels of LH in ovariectomized NPY KO animals decreased in response to fasting, but LH levels in intact and estrogen-treated ovariectomized NPY KO animals did not. In contrast, WTs consistently showed fasting-induced suppression of LH. Our findings suggest that other systems can sustain the hyperphagia of lactation and NPY alone is not responsible for suppressing cyclicity during lactation. Nevertheless, the suppression of basal LH release that accompanies food deprivation in normal female mice appears to require the steroid-dependent actions of NPY.

Prenatal exposure to glucocorticoids affects body weight, serum leptin levels, and hypothalamic neuropeptide‐Y expression in pre‐pubertal female rat offspring

2014 ◽  
Vol 36 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Takeshi Iwasa ◽  
Toshiya Matsuzaki ◽  
Munkhsaikhan Munkhzaya ◽  
Altankhuu Tungalagsuvd ◽  
Takako Kawami ◽  
...  
Keyword(s):  
Body Weight ◽  
Neuropeptide Y ◽  
Prenatal Exposure ◽  
Female Rat ◽  
Serum Leptin ◽  
Rat Offspring

Aqueous Extract of Ma huang Suppresses Neuropeptide Y Expression in Food-Deprived Rat Hypothalamus

2004 ◽  
Vol 32 (05) ◽  
pp. 659-667 ◽  
Author(s):  
Ee-Hwa Kim ◽  
Mal-Soon Shin ◽  
Hyun-Kyung Chang ◽  
Taeck-Hyun Lee ◽  
Mi-Hyeon Jang ◽  
...  
Keyword(s):  
Weight Loss ◽  
Amino Acid ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Aqueous Extract ◽  
Rat Hypothalamus ◽  
Amino Acid Peptide ◽  
Ma Huang ◽  
Plant Stem

Ma huang, the dried plant stem of Ephedra Intermedia Schrenk et C.A., contains an ephedrine-type alkaloid and has been used for weight loss. Neuropeptide Y (NPY), a 36-amino acid peptide, is concentrated in the hypothalamus and stimulates feeding desire. In this study, the effect of Ma huang on the expressions of NPY in the hypothalamus of rats was investigated using immunohistochemistry. Food-deprivation enhanced the NPY expression in the hypothalamus. Ma huang suppressed the food-deprivation-induced enhancement of NPY expression. Present results suggest that Ma huang curbs the food desire by suppressing the NPY expression under food-deprivation conditions.

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