scholarly journals Neuropeptide Y gene expression in lines of mice subjected to long-term divergent selection on fat content

1999 ◽  
Vol 23 (1) ◽  
pp. 77-83 ◽  
Author(s):  
T Boswell ◽  
MA Nicholson ◽  
L Bunger
Keyword(s):  
Gene Expression ◽  
Neuropeptide Y ◽  
Fat Content ◽  
Sensitivity Threshold ◽  
Mrna Levels ◽  
Fat Percentage ◽  
Fed State ◽  
Ad Libitum ◽  
Plasma Leptin

Lines of mice have been developed in our laboratory by divergent long-term selection for body fat content. This has resulted in a fivefold (23% vs 4%) higher fat percentage in the Fat line at 14 weeks of age, with little difference between the Fat and Lean lines in fat-free body weight. As part of an approach to characterize the physiological mechanisms underlying these different phenotypes, neuropeptide Y (NPY) mRNA levels in the hypothalamus and cerebral cortex of ad libitum-fed and fasted mice of the Fat and Lean selected lines were measured. Significant differences in NPY gene expression were confined to the hypothalamus. Under ad libitum-fed conditions, hypothalamic NPY mRNA levels did not differ significantly between the Fat and Lean lines. After an overnight fast of 18-20 h, hypothalamic NPY mRNA levels were increased significantly (P<0.05) by 31% in Lean animals relative to fed mice from the same line. However, fasting did not significantly stimulate NPY gene expression in the Fat line. Most plasma leptin measurements in the Lean line fell below the sensitivity threshold of the assay (0.1 ng/ml), but levels in the Fat line were at least 30 to 50 times higher under fasted and fed conditions respectively. After fasting, plasma leptin levels in the Fat line decreased significantly (P<0. 05) by 48%. Thus, unlike the situation in other rodent models, obesity in the Fat line is not associated with increased hypothalamic NPY mRNA levels in the ad libitum-fed state. The decreased sensitivity of hypothalamic NPY gene expression to fasting in the Fat line is consistent with an inhibitory effect of higher circulating leptin levels.

Parasite-induced anorexia: leptin, insulin and corticosterone responses to infection with the nematode, Nippostrongylus brasiliensis

Parasitology ◽  
1999 ◽  
Vol 118 (1) ◽  
pp. 117-123 ◽  
Author(s):  
H. C. ROBERTS ◽  
L. J. HARDIE ◽  
L. H. CHAPPELL ◽  
J. G. MERCER
Keyword(s):  
Gene Expression ◽  
Energy Balance ◽  
Neuropeptide Y ◽  
Post Infection ◽  
Plasma Insulin ◽  
Negative Energy ◽  
Nippostrongylus Brasiliensis ◽  
Corticotrophin Releasing Factor ◽  
Ad Libitum ◽  
Plasma Leptin

The nematode parasite, Nippostrongylus brasiliensis, induces a biphasic anorexia in its rat host. The mechanisms, underlying this anorexia and its possible advantages to the host or parasite are unknown. We have investigated the effect of acute (12–24 h) and chronic (2–17 days) infections on plasma concentrations of leptin, insulin and corticosterone, and on hypothalamic expression of neuropeptide Y, galanin and corticotrophin-releasing factor genes. Plasma leptin was elevated in infected rats relative to uninfected ad libitum-fed controls and pair-fed controls in 12 h infections initiated at dark onset and in infections of 2 days' duration. At other times prior to parasite expulsion, plasma leptin in infected and pair-fed rats was lower than that of uninfected ad libitum-fed controls, reflecting the existing state of negative energy balance. Elevated plasma leptin concentrations in infected rats at day 2 post-infection were accompanied by reduced neuropeptide Y gene expression in the hypothalamic arcuate nucleus compared with both ad libitum control and pair-fed animals, and by lowered corticotrophin-releasing factor gene expression in the paraventricular nucleus relative to pair-feds. Twelve hour infections were characterized by a substantial increase in plasma corticosterone that was independent of reduced food intake, and in 12 h infections initiated at dark onset, where plasma leptin was elevated, there was also increased plasma insulin concentration in infected rats. In longer infections, differences between the groups in plasma insulin and corticosterone concentration were only observed at day 4 post-infection. In summary, perturbations to leptin, insulin and corticosterone signals early in infection may have a causative role and might feed back onto hypothalamic gene expression, whereas subsequent changes in these parameters are more likely to be secondary to negative energy balance.

Neuropeptide Y in hypothalamic paraventricular nucleus: a center coordinating energy metabolism

1994 ◽  
Vol 266 (6) ◽  
pp. R1765-R1770 ◽  
Author(s):  
C. J. Billington ◽  
J. E. Briggs ◽  
S. Harker ◽  
M. Grace ◽  
A. S. Levine
Keyword(s):  
Gene Expression ◽  
Energy Metabolism ◽  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Neural Circuit ◽  
Uncoupling Protein ◽  
Brown Fat ◽  
Mrna Levels ◽  
Ad Libitum ◽  
White Fat

Intracerebroventricular injection of neuropeptide Y (NPY) has two effects on energy metabolism in addition to increased feeding: decreased brown fat thermogenesis and increased white fat lipoprotein lipase (LPL) enzymatic activity. We hypothesized that the paraventricular nucleus (PVN) of the hypothalamus is the controlling neural site for these responses. We further hypothesized that NPY stimulation at PVN would reduce gene expression for the critical brown fat thermogenic protein, uncoupling protein (UCP), and increase gene expression for the key white fat storage enzyme, LPL. In the first experiment, three groups of rats received injections every 6 h for 24 h (5 injections total) into the PVN:1) NPY (1 micrograms/1 microliters injection) and ad libitum food; 2) NPY (1 micrograms/1 microliters injection) and food restricted to control intake; 3) saline injection (1 microliter) and ad libitum food. Both NPY-treated groups showed significant reductions (P < 0.05) in brown fat UCP mRNA levels and marked stimulation of LPL mRNA levels relative to controls. In the second experiment, four groups of seven rats had NPY injected into the PVN:0 (vehicle control); 0.1 microgram; 0.5 microgram; and 1 microgram. Injections were made every 6 h for 24 h. There was a dose-related reduction in UCP mRNA produced by the NPY treatment. NPY treatment increased LPL mRNA, but a smooth dosing effect was not evident. The observation that NPY in the PVN can coordinate more than one component of energy metabolism is significant when considered with many reports of responsiveness of NPY activity in the arcuate nucleus-PVN neural circuit to perturbations of energy balance such as fasting and feeding, diabetes, and genetic obesity.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

scholarly journals Western-diet consumption induces alteration of barrier function mechanisms in the ileum that correlates with metabolic endotoxemia in rats

2017 ◽  
Vol 313 (2) ◽  
pp. E107-E120 ◽  
Author(s):  
Mathilde Guerville ◽  
Anaïs Leroy ◽  
Annaëlle Sinquin ◽  
Fabienne Laugerette ◽  
Marie-Caroline Michalski ◽  
...  
Keyword(s):  
Gene Expression ◽  
Elevated Serum ◽  
Caloric Intake ◽  
Western Diet ◽  
Chow Diet ◽  
Low Grade ◽  
Mrna Levels ◽  
Intestinal Alkaline Phosphatase ◽  
Ad Libitum ◽  
Metabolic Endotoxemia

Obesity and its related disorders have been associated with the presence in the blood of gut bacteria-derived lipopolysaccharides (LPS). However, the factors underlying this low-grade elevation in plasma LPS, so-called metabolic endotoxemia, are not fully elucidated. We aimed to investigate the effects of Western diet (WD) feeding on intestinal and hepatic LPS handling mechanisms in a rat model of diet-induced obesity (DIO). Rats were fed either a standard chow diet (C) or a Western Diet (WD, 45% fat) for 6 wk. They were either fed ad libitum or pair-fed to match the caloric intake of C rats for the first week, then fed ad libitum for the remaining 5 wk. Six-week WD feeding led to a mild obese phenotype with increased adiposity and elevated serum LPS-binding protein (LBP) levels relative to C rats, irrespective of initial energy intake. Serum LPS was not different between dietary groups but exhibited strong variability. Disrupted ileal mucus secretion and decreased ileal Reg3-γ and -β gene expression along with high ileal permeability to LPS were observed in WD compared with C-fed rats. Ileal and cecal intestinal alkaline phosphatase (IAP) activity as well as Verrucomicrobia and Bifidobacterium cecal levels were increased in WD-fed rats compared with C-fed rats. WD consumption did not impact mRNA levels of LPS-handling hepatic enzymes. Correlation analysis revealed that ileal passage of LPS, IAP activity, Proteobacteria levels and hepatic aoah gene expression correlated with serum LPS and LBP, suggesting that ileal mucosal defense impairment induced by WD feeding contribute to metabolic endotoxemia.

Dietary fish oil positively regulates plasma leptin and adiponectin levels in sucrose-fed, insulin-resistant rats

2005 ◽  
Vol 289 (2) ◽  
pp. R486-R494 ◽  
Author(s):  
Andrea S. Rossi ◽  
Yolanda B. Lombardo ◽  
Jean-Marc Lacorte ◽  
Adriana G. Chicco ◽  
Christine Rouault ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Fish Oil ◽  
Essential Role ◽  
Control Diet ◽  
Insulin Resistant ◽  
Dietary Fish ◽  
Plasma Leptin

Insulin resistance and adiposity induced by a long-term sucrose-rich diet (SRD) in rats could be reversed by fish oil (FO). Regulation of plasma leptin and adiponectin levels, as well as their gene expression, by FO might be implicated in these findings. This study was designed to evaluate the long-term regulation of leptin and adiponectin by dietary FO in a dietary model of insulin resistance induced by long-term SRD in rats and to determine their impact on adiposity and insulin sensitivity. Rats were randomized to consume a control diet (CD; n = 25) or an SRD ( n = 50) for 7 mo. Subsequently, the SRD-fed rats were randomized to consume SRD+FO or to continue on SRD for an additional 2 mo. Long-term SRD induced overweight and decreased both plasma leptin and adiponectin levels without change in gene expression. Dyslipidemia, adiposity, and insulin resistance accompanied these modifications. Shifting the source of fat to FO for 2 mo increased plasma levels of both adipokines, reversed insulin resistance and dyslipidemia, and improved adiposity. These results were not associated with modifications in gene expression. These results suggest that increasing both adipokines by dietary FO might play an essential role in the normalization of insulin resistance and adiposity in dietary-induced, insulin-resistant models.

scholarly journals Regulation of pituitary inhibin/activin subunits and follistatin gene expression by GnRH in female rats

2011 ◽  
Vol 210 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Petra Popovics ◽  
Zoltan Rekasi ◽  
Alan J Stewart ◽  
Magdolna Kovacs
Keyword(s):  
Gene Expression ◽  
Mrna Level ◽  
Inhibin B ◽  
Female Rats ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Short Term ◽  
Α Subunit ◽  
Long Term Treatment

Pituitary inhibin B, activin B, and follistatin are local regulators of FSH. Activin B is a homodimeric molecule (βB–βB), while inhibin B contains an α and a βB subunit. The regulation of gene expression of α, βB, and follistatin by local and endocrine hormones was examined in pituitaries from female rats and in perifused pituitary cells by RT-PCR. Ovariectomy (OVX) induced an elevation in the mRNA level of α and βB subunits and follistatin. Short-term (4 h) treatment of pituitary cells with GnRH decreased both the inhibin α and the inhibin/activin βB subunit mRNA levels, while long-term treatment (20 h) with 100 nM GnRH stimulated the expression of both subunits. In contrast, the mRNA level of follistatin was elevated after the short-term GnRH treatment. Long-term exposure of pituitary cells to estradiol and inhibin B suppressed the mRNA expression of βB and had no effect on the expression of α subunit and follistatin. Our results demonstrate that the increased expressions of inhibin/activin subunits and follistatin in the post-OVX period can be induced by the lack of gonadal negative feedback, resulting in a high GnRH environment in the pituitary. This study reports for the first time that GnRH administered in high doses and for a long period stimulates the gene expression of inhibin/activin subunits and thereby may contribute to the stimulatory effect of OVX on the expression of these genes.

scholarly journals The lack of specificity of neuropeptide Y (NPY) antisense oligodeoxynucleotides administered intracerebroventricularly in inhibiting food intake and NPY gene expression in the rat hypothalamus

1998 ◽  
Vol 157 (1) ◽  
pp. 169-175 ◽  
Author(s):  
S Dryden ◽  
L Pickavance ◽  
D Tidd ◽  
G Williams
Keyword(s):  
Gene Expression ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Third Ventricle ◽  
Antisense Oligodeoxynucleotides ◽  
Mrna Levels ◽  
Inhibit Gene Expression ◽  
Negative Findings ◽  
Antisense Odns

To evaluate the role of neuropeptide Y (NPY), a potent appetite stimulant, in controlling food intake and body weight, we investigated the use of antisense oligodeoxynucleotides (ODNs) to inhibit NPY gene expression in the hypothalamus. We compared the hypothalamic distribution of fluorescein-labelled ODNs administered intracerebroventricularly, and effects on food intake and NPY gene expression, of three different structural modifications of an antisense ODN sequence against NPY. Rats had either the antisense or missense ODNs (24 micrograms/day) or saline infused into the third ventricle by osmotic minipumps for 7 days. The unmodified phosphodiester ODN was not detectable in the hypothalamus after 7 days and had no effects on food intake. The phosphorothioate ODN was widely distributed throughout the hypothalamus but had nonselective effects, with similar changes in food intake and NPY mRNA levels in the antisense and missense groups, and was severely toxic. The propyl-protected ODN appeared to penetrate the hypothalamus well but had no antisense-selective effects on NPY mRNA levels or food intake. Antisense ODNs are increasingly used to inhibit gene expression in vitro and in intact animals. These negative findings underline the need for rigorous evaluation of any effects of antisense ODNs administered into the central nervous system, and raise doubts about the validity of this approach in physiological or pharmacological studies.

scholarly journals Comparison of leptin gene expression in different adipose tissues in children and adults

2004 ◽  
pp. 579-584 ◽  
Author(s):  
E Schoof ◽  
A Stuppy ◽  
F Harig ◽  
R Carbon ◽  
T Horbach ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Subcutaneous Tissue ◽  
Mrna Levels ◽  
Adipose Tissues ◽  
Metabolic Properties ◽  
Tissue Specimens ◽  
Plasma Leptin ◽  
Design And Methods

OBJECTIVE: Adipose tissue displays depot-specific metabolic properties and a predominant gene expression of leptin in subcutaneous tissue. The aim of the study was to evaluate leptin mRNA expression in various adipose tissues and to relate it to plasma leptin concentrations. Furthermore, developmental changes in leptin gene expression from childhood to adulthood were examined. DESIGN AND METHODS: Thoracic subcutaneous and intrathoracic adipose tissue specimens were obtained in 22 adults (51-81 years) and 23 children (0.1-17 years) undergoing cardiac surgery, and abdominal subcutaneous, omental and mesenterial fat specimens were collected from 21 adults (38-79 years) and 22 children (0.2-17 years) before abdominal surgery. Preoperative plasma leptin concentrations were measured by RIA. Leptin mRNA expression was quantified by TaqMan real-time PCR. RESULTS: In adults, there was no difference between leptin gene expression in subcutaneous and intrathoracic fat, whereas in children leptin mRNA expression was significantly higher in subcutaneous adipose tissue. In omental fat, leptin mRNA levels were significantly lower compared with subcutaneous and mesenterial sites in both children and adults. Adults revealed a significantly higher leptin gene expression in subcutaneous, omental and mesenterial adipose tissues than children. Subcutaneous and omental leptin gene expression are independent factors for plasma leptin concentrations in children and adults. CONCLUSION: Leptin is differentially expressed at different adipose tissue sites, a situation which is even more pronounced in children. There is a developmental increase in leptin mRNA expression in adipose tissue during childhood, reaching maximal capacity in adulthood.

Transcript of protein kinase A knock-down modulates feeding behavior and neuropeptide Y gene expression in phenylpropanolamine-treated rats

2007 ◽  
Vol 31 (2) ◽  
pp. 306-314 ◽  
Author(s):  
Yih-Shou Hsieh ◽  
Shun-Fa Yang ◽  
Shu-Chen Chu ◽  
Dong-Yih Kuo
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Neuropeptide Y ◽  
Protein Kinase A ◽  
Mrna Level ◽  
Camp Response Element Binding ◽  
Antisense Oligodeoxynucleotide ◽  
Mrna Levels ◽  
Knock Down ◽  
Kinase A

Neuropeptide Y (NPY) is an appetite-controlling neuromodulator that contributes to the appetite-suppressing effect of phenylpropanolamine (PPA). Aims of this study were to investigate whether protein kinase A (PKA) signaling is involved in regulating NPY gene expression and PPA-induced anorexia. Rats were given daily with PPA for 5 days. Changes in daily food intake and hypothalamic NPY, PKA, cAMP response element binding protein (CREB), and pro-opiomelanocortin (POMC) gene expression were measured and compared. To further determine if PKA was involved, intracerebroventricular infusions of antisense oligodeoxynucleotide were performed at 60 min before daily PPA treatment in freely moving rats. Results showed that daily PKA, CREB, and POMC expression were increased following PPA treatment, which showed a closely reverse relationship with alterations of decreased feeding behaviors and NPY mRNA levels. Results also showed that PKA knock-down could block PPA-induced anorexia as well as restore NPY mRNA level, indicating the involvement of PKA signaling in the regulation of NPY gene expression. It is suggested that hypothalamic PKA signaling may participate in the central regulation of PPA-mediated appetite suppression via the modulation of hypothalamic NPY gene expression. The present findings reveal that manipulations at the molecular level of PKA or cAMP may allow the development of therapeutic agents to improve the undesirable properties of PPA or other amphetamine-like anorectic drugs.

scholarly journals Feeding state and age dependent changes in melanin-concentrating hormone expression in the hypothalamus of broiler chickens

2018 ◽  
Vol 65 (2) ◽  
pp. 251-258
Author(s):  
Ádám Simon ◽  
József Németh ◽  
András Jávor ◽  
István Komlósi ◽  
Péter Bai ◽  
...  
Keyword(s):  
Gene Expression ◽  
Feed Intake ◽  
Broiler Chickens ◽  
Mrna Levels ◽  
Experimental Conditions ◽  
Peptide Concentration ◽  
Melanin Concentrating Hormone ◽  
Ad Libitum ◽  
Weak Expression ◽  
Intake Regulation

We aimed to quantify the gene expression changes of the potent orexigenic melanin concentrating hormone (MCH) in chicken (Gallus gallus) hypothalamus with quantitative real-time polymerase chain reaction (qPCR), and for the first time determine peptide concentrations with a novel radioimmunoassay (RIA) under different feeding status. Three different experimental conditions, namely ad libitum fed, fasting for 24h, fasting for 24h then refed for 2h were applied to study the changes of the aforementioned target and its receptor (MCHR4) gene expression to different nutritional states. The relative changes of MCH and MCHR4 were also studied from 7 to 35 days of age. Expression of PMCH and MCHR4 along the gastrointestinal tract (GIT) was also investigated. We found that both targets expression are restricted to the hypothalamus, only weak expression was detected along the GIT. Different nutritional states did not affect the PMCH and MCHR4 mRNA levels. However, fasting for 24h significantly increased MCH-like immunoreactivity with 25.65%. Fasting for 24h then refed for 2h further significantly increased MCH peptide concentration by 32.51% compared to ad libitum state. Decreasing trend with age was observable both for PMCH and MCHR4 mRNA levels and also for MCH-like immunoreactivity. Correlation analysis did not result significant correlation between MCH peptide concentration and abdominal fat mass in ad libitum fed birds. In conclusion, MCH peptide concentration altered with different feeding states, which indicated that this peptide takes part in feed intake regulation (short-term signalization of feed intake) of broiler chickens in a same manner as in mammals.

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