scholarly journals The Body Weight-related Differences of Leptin and Neuropeptide Y (NPY) Gene Expression in Pigs

2008 ◽  
Vol 21 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Tizhong Shan ◽  
Yizhen Wang ◽  
Jia Guo ◽  
Xiaona Chu ◽  
Jianxin Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Neuropeptide Y ◽  
The Body

scholarly journals Maternal low-protein diet programmes offspring growth in association with alterations in yolk leptin deposition and gene expression in yolk-sac membrane, hypothalamus and muscle of developing Langshan chicken embryos

2009 ◽  
Vol 102 (6) ◽  
pp. 848-857 ◽  
Author(s):  
Kaiqing Rao ◽  
Jingjing Xie ◽  
Xiaojing Yang ◽  
Lei Chen ◽  
Roland Grossmann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Leptin Receptor ◽  
Pectoralis Major Muscle ◽  
Yolk Sac ◽  
Pectoralis Major ◽  
The Body ◽  
Low Protein ◽  
Igf I ◽  
Offspring Growth

The present study was aimed to investigate the mechanism underlying the influence of maternal low-protein (LP) diet on offspring growth in the chicken. One hundred and twenty Chinese inbred Langshan breeder hens were allocated randomly into two groups fed diets containing low (10 %, LP) or normal (15 %) crude protein levels. Low dietary protein did not affect the body weight of hens, but significantly decreased the laying rate and egg weight. The yolk leptin content was significantly lower in eggs laid by LP hens, while no differences were detected for yolk contents of corticosterone, tri-iodothyronine (T3) or thyroxine. Despite significantly lower hatch weight, the LP offspring demonstrated obviously higher serum T3 concentration, which is in accordance with the faster post-hatch growth rate achieving significantly heavier body weight and pectoralis major muscle weight 4 weeks post-hatching. Expression of 20-hydroxysteroid dehydrogenase (20-HSD) mRNA in the yolk-sac membrane was significantly down-regulated at embryonic day 14, whereas that of transthyretin and leptin receptor (LepR) was not altered. Moreover, hypothalamic expression of 20-HSD, glucocorticoid receptors, thyrotropin-releasing hormone and LepR mRNA was significantly up-regulated in the LP group compared with their control counterparts. In the pectoralis major muscle, significantly higher expression of insulin-like growth factor (IGF)-I and IGF-I receptor mRNA was observed in LP embryos. The present study provides evidence that maternal LP diet programmes post-hatch growth of the offspring. The associated alterations in yolk leptin deposition as well as in yolk-sac membrane, fetal hypothalamus and muscle gene expression may be involved in mediating such programming effect in the chicken.

scholarly journals Early Weaning Affects Liver Antioxidant Function in Piglets

Animals ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 2679
Author(s):  
Lihuai Yu ◽  
Hongmin Li ◽  
Zhong Peng ◽  
Yuzhu Ge ◽  
Jun Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Liver Weight ◽  
The Body ◽  
Early Weaning ◽  
Large White ◽  
Enzymes Activity ◽  
Antioxidant Function ◽  
The Impact

This study examined the impact of early weaning on antioxidant function in piglets. A total of 40 Duroc × Landrace × Large White, 21-day-old piglets (half male and half female) were divided into suckling groups (SG) and weaning groups (WG). Piglets in WG were weaned at the 21st day, while the piglets in SG continued to get breastfed. Eight piglets from each group were randomly selected and slaughtered at 24th-day (SG3, WG3) and 28th-day old (SG7, WG7). The body weight, liver index, hepatocyte morphology, antioxidant enzymes activity, gene expression of antioxidant enzymes, and Nrf2 signaling in the liver of piglets were measured. The results showed that weaning caused decreased body weight (p < 0.01), lower liver weight (p < 0.01), and decreased the liver organ index (p < 0.05) of piglets. The area and size of hepatocytes in the WG group was smaller than that in the SG group (p < 0.05). We also observed that weaning reduced the activity of superoxide dismutase (SOD) and catalase (CAT) (p < 0.05) in the liver of piglets. Relative to the SG3 group, the gene expression of GSH-Px in liver of WG3 was significantly reduced (p < 0.05). The gene expression of Nrf2 in the SG3 group was higher than that in the WG3 group (p < 0.01). The gene expression of NQO1 in the SG7 group was higher than that in the WG7 group (p < 0.05). In conclusion, weaning resulted in lower weight, slowed liver development, and reduced antioxidant enzymes activity, thereby impairing liver antioxidant function and suppressing piglet growth.

scholarly journals Liraglutide, a GLP-1 Receptor Agonist, Which Decreases Hypothalamic 5-HT2A Receptor Expression, Reduces Appetite and Body Weight Independently of Serotonin Synthesis in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Katsunori Nonogaki ◽  
Takao Kaji
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Body Weight ◽  
Receptor Agonist ◽  
Tryptophan Hydroxylase ◽  
Intraperitoneal Administration ◽  
Body Weight Loss ◽  
Receptor Activation ◽  
The Body ◽  
Receptor Expression

A recent report suggested that brain-derived serotonin (5-HT) is critical for maintaining weight loss induced by glucagon-like peptide-1 (GLP-1) receptor activation in rats and that 5-HT2A receptors mediate the feeding suppression and weight loss induced by GLP-1 receptor activation. Here, we show that changes in daily food intake and body weight induced by intraperitoneal administration of liraglutide, a GLP-1 receptor agonist, over 4 days did not differ between mice treated with the tryptophan hydroxylase (Tph) inhibitor p-chlorophenylalanine (PCPA) for 3 days and mice without PCPA treatment. Treatment with PCPA did not affect hypothalamic 5-HT2A receptor expression. Despite the anorexic effect of liraglutide disappearing after the first day of treatment, the body weight loss induced by liraglutide persisted for 4 days in mice treated with or without PCPA. Intraperitoneal administration of liraglutide significantly decreased the gene expression of hypothalamic 5-HT2A receptors 1 h after injection. Moreover, the acute anorexic effects of liraglutide were blunted in mice treated with the high-affinity 5-HT2A agonist (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine hydrobromide 14 h or 24 h before liraglutide injection. These findings suggest that liraglutide reduces appetite and body weight independently of 5-HT synthesis in mice, whereas GLP-1 receptor activation downregulates the gene expression of hypothalamic 5-HT2A receptors.

Role of hypothalamic neuropeptide Y gene expression in body weight regulation

1994 ◽  
Vol 266 (5) ◽  
pp. R1687-R1691 ◽  
Author(s):  
L. Davies ◽  
J. L. Marks
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Neuropeptide Y ◽  
Food Deprivation ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Insulin Levels ◽  
Male Wistar Rats

Hypothalamic neuropeptide Y (NPY) may be involved in the hyperphagia that follows food deprivation associated with significant weight loss. However, it is unclear whether NPY is involved in body weight regulation under more physiological circumstances. Consequently, we measured body weight, food intake, arcuate nucleus (ARC) NPY mRNA, serum glucose, and insulin in male Wistar rats after 48 h of food deprivation and various refeeding protocols. Food deprivation produced a twofold increase in NPY mRNA, whereas 3 days of ad libitum refeeding returned body weight and NPY mRNA to control. If hyperphagia was prevented for 5 days during refeeding, then neither body weight nor NPY mRNA normalized. There were strong negative correlations between ARC NPY mRNA and both loss of body weight and serum insulin levels. These data suggest that hypothalamic NPY gene expression plays a role in control of body weight under physiological conditions. The data further suggest that NPY mRNA may be decreased by peripheral insulin levels.

scholarly journals Anorectic Effects of the Cytokine, Ciliary Neurotropic Factor, Are Mediated by Hypothalamic Neuropeptide Y: Comparison with Leptin*

Endocrinology ◽  
1998 ◽  
Vol 139 (2) ◽  
pp. 466-473 ◽  
Author(s):  
B. Xu ◽  
M. G. Dube ◽  
P. S. Kalra ◽  
W. G. Farmerie ◽  
A. Kaibara ◽  
...  
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Messenger Rna ◽  
Nervous System Development ◽  
Ribonuclease Protection Assay ◽  
Dependent Manner ◽  
Neurotropic Factor

Abstract Although ciliary neurotropic factor (CNTF) is a tropic factor in nervous system development and maintenance, peripheral administration of this cytokine also causes severe anorexia and weight loss. The neural mechanism(s) mediating the loss of appetite is not known. As hypothalamic neuropeptide Y (NPY) is a potent orexigenic signal, we tested the hypothesis that CNTF may adversely affect NPYergic signaling in the hypothalamus. Intraperitoneal administration of CNTF (250μ g/kg) daily for 4 days significantly suppressed 24-h food intake in a time-dependent manner and decreased body weight. The loss in body weight was similar to that which occurred in pair-fed (PF) rats. As expected, hypothalamic NPY gene expression, determined by measurement of steady state prepro-NPY messenger RNA by ribonuclease protection assay, significantly increased in PF rats in response to energy imbalance. However, despite a similar loss in body weight, there was no increase in NPY gene expression in CNTF-treated rats. Daily administration of CNTF intracerebroventricularly (0.5 or 5.0 μg/rat) also produced anorexia and body weight loss. In this experiment, negative energy balance produced by both PF and food deprivation augmented hypothalamic NPY gene expression. However, despite reduced intake and loss of body weight, no similar increment in hypothalamic NPY gene expression was observed in CNTF-treated rats. In fact, in rats treated with higher doses of CNTF (5.0 μg/rat), NPY gene expression was reduced below the levels seen in control, freely fed rats. Furthermore, CNTF treatment also markedly decreased NPY-induced feeding. These results suggested that anorexia in CNTF-treated rats may be due to a deficit in NPY supply and possibly in the release and suppression of NPY-induced feeding. The possibility that CNTF-induced anorexia may be caused by increased leptin was next examined. Daily intracerebroventricular injections of leptin (7 μg/rat) decreased food intake, body weight, and hypothalamic NPY gene expression in a manner similar to that seen after CNTF treatment. Leptin administration also suppressed NPY-induced feeding. However, peripheral and central CNTF injections markedly decreased leptin messenger RNA in lipocytes, indicating a deficiency of leptin in these rats; thus, leptin was unlikely to be involved in appetite suppression. Thus, these results show that a two-pronged central action of CNTF, causing diminution in both NPY availability and the NPY-induced feeding response, may underlie the severe anorexia. Further, unlike other members of the cytokine family, suppression of NPYergic signaling in the hypothalamus by CNTF does not involve up-regulation of leptin, but may involve a direct action on hypothalamic NPY neurons or on neural circuits that regulate NPY signaling in the hypothalamus.

scholarly journals GH improves spatial memory and reverses certain anabolic androgenic steroid-induced effects in intact rats

2012 ◽  
Vol 216 (1) ◽  
pp. 31-41 ◽  
Author(s):  
Alfhild Grönbladh ◽  
Jenny Johansson ◽  
Anatole Nöstl ◽  
Fred Nyberg ◽  
Mathias Hallberg
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Spatial Memory ◽  
Learning And Memory ◽  
Body Weight Gain ◽  
The Body ◽  
Spatial Learning And Memory ◽  
Anabolic Androgenic Steroid ◽  
Androgenic Steroid ◽  
Intact Rats

GH has previously been shown to promote cognitive functions in GH-deficient rodents. In this study we report the effects of GH on learning and memory in intact rats pretreated with the anabolic androgenic steroid nandrolone. Male Wistar rats received nandrolone decanoate (15 mg/kg) or peanut oil every third day for 3 weeks and were subsequently treated with recombinant human GH (1.0 IU/kg) or saline for 10 consecutive days. During the GH/saline treatment spatial learning and memory were tested in the Morris water maze (MWM). Also, plasma levels of IGF1 were assessed and the gene expression of the GH receptors (Ghr), Igf1 and Igf2, in hippocampus and frontal cortex was analyzed. The results demonstrated a significant positive effect of GH on memory functions and increased gene expression of Igf1 in the hippocampus was found in the animals treated with GH. In addition, GH was demonstrated to increase the body weight gain and was able to attenuate the reduced body weight seen in nandrolone-treated animals. In general, the rats treated with nandrolone alone did not exhibit any pronounced alteration in memory compared with controls in the MWM, and in many cases GH did not induce any alteration. Regarding target zone crossings, considered to be associated with spatial memory, the difference between GH- and steroid-treated animals was significant and administration of GH improved this parameter in the latter group. In conclusion, GH improves spatial memory in intact rats and can reverse certain effects induced by anabolic androgenic steroid.

scholarly journals Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity

2016 ◽  
Vol 5 (10) ◽  
pp. 869-881 ◽  
Author(s):  
Kavaljit H. Chhabra ◽  
Jessica M. Adams ◽  
Graham L. Jones ◽  
Miho Yamashita ◽  
Martin Schlapschy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
The Body ◽  
Extreme Obesity ◽  
Reciprocal Interaction ◽  
Set Point ◽  
Leptin Sensitivity ◽  
Pomc Gene

scholarly journals The Ciji-Hua’ai-Baosheng II Formula Attenuates Chemotherapy-Induced Anorexia in Mice With H22 Hepatocellular Carcinoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Shengyan Xi ◽  
Xiangyang Zhai ◽  
Yanan Wang ◽  
Yuewen Gong ◽  
Biqian Fu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Body Weight ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Inhibitory Effect ◽  
The Body ◽  
Untreated Group ◽  
Orexin A ◽  
Regulatory Factors ◽  
Group 5

Background: Ciji-Hua’ai-Baosheng II Formula (CHB-II-F) is a traditional Chinese medicine formula, which specifically targets different aspects of chemotherapy-induced adverse effects in patients with cancer. In our clinical application, CHB-II-F significantly alleviated chemotherapy-induced anorexia (loss of appetite) and improved the quality of life for patients with tumor during and after chemotherapy. However, the mechanism of CHB-II-F in alleviation of chemotherapy-induced anorexia remains to be further investigated.Aim of Study: To explore the therapeutic effect and mechanism of CHB-II-F on chemotherapy-induced anorexia in the mice model of H22 hepatoma.Materials and Methods: A total of 72 Kunming mice of SPF grade were inoculated subcutaneously with H22 hepatoma cells into the right anterior armpit of the mice. After 1 week of seeding, mice were injected intraperitoneally with a high dose of 5-fluorouracil (200 mg/kg 5-FU) to establish the model of chemotherapy. The mice were randomly divided into six groups: untreated group, 5-FU group, 5-FU plus Yangzheng Xiaoji capsule (YZXJC) group, and three groups of 5-FU plus different concentrations of CHB-II-F. All the mice in each group were treated for 14 days. The body weight, food intake, tumor volume, and tumor weight of mice were measured, and pathological examinations of tumor tissue, stomach, and duodenum were carried out. Expressions of serum Leptin, Neuropeptide Y (NPY), epidermal cell growth factor (EGF), Motilin (MTL), Orexin A (OXA), Gastrin (GAS), Ghrelin, Prostaglandin E2 (PGE2), and jejunum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were examined. The protein and mRNA levels of proopiomelanocortin (POMC), Orexin receptor 1 (OX1R), neuropeptide Y (NPY), cocaine and amphetamine regulated transcript peptide (CART), Agouti gene-related protein (AgRP), Leptin receptor (Ob-R), and Ghrelin receptor (GHSR) were examined in hypothalamus, and the protein levels of substance P (SP) and 5-hydroxytryptamine (5-HT) in duodenum were measured.Results: The combination of CHB-II-F and 5-FU could enhance the inhibitory effect of 5-FU on tumor. The tumor inhibition rates of 5-FU group, YZXJC group, CHB-II-F(H) group, CHB-II-F(M) group, and CHB-II-F(L) group were 58.88, 28.08, 54.96, 37.69, and 28.61%, respectively. Compared with untreated group and 5-FU group, CHB-II-F significantly increased the body weight and food intake of tumor-bearing mice; increased the content of NPY, Orexin A, Ghrelin, GAS, MTL, EGF, and PGE2 in serum and the activity of SOD in jejunum; and decreased the content of Leptin in serum and the content of MDA in jejunum. Compared with untreated group and 5-FU group, CHB-II-F also enhanced the expression of OX1R, GHSR, NPY, and AgRP protein and gene and decreased the expression of Ob-R, POMC, and CART protein and gene in hypothalamus of mice, and the gene expression was consistent with the protein expression. In addition, CHB-II-F decreased the expression of 5-HT and SP protein in duodenum.Conclusion: In the murine model of H22 hepatocellular carcinoma (HCC) receiving chemotherapy, CHB-II-F enhances the inhibitory effect of 5-FU on tumor, significantly improves the pathological injury of gastrointestinal tract caused by chemotherapy, and regulates the secretion of gastrointestinal hormones. It may alleviate chemotherapy-induced anorexia by affecting appetite regulatory factors in the feeding area of hypothalamus central nervous system and peripheral appetite regulatory factors.

scholarly journals Metformin-Mg2+ adjunct therapy synergistically modulates insulin and PDX-1 gene signatures in STZ-NAD induced diabetic model

2020 ◽  
Vol 8 (3) ◽  
pp. 66-71
Author(s):  
Oluwaseun FAPOHUNDA ◽  
Femi Abiola OGUNLEYE ◽  
Tomisin Happy OGUNWA ◽  
Idowu Olaposi OMOTUY ◽  
Titilola Titilayoaderonke SAMUEL ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Treated Group ◽  
Diabetic Rats ◽  
The Body ◽  
Distilled Water ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Magnesium Supplementation ◽  
Adjunct Therapy

Diabetes mellitus (DM) is a multi-factorial debilitating disorder of metabolism, usually due to a combination of hereditary and environmental causes, resulting in abnormally high blood sugar levels (hyperglycemia) as a result of defects in either insulin secretion or insulin action in the body. DM is usually accompanied by hypomagnesemia. This study was aimed at investigating the effect of oral magnesium supplementation on pancreatic gene expression of insulin and PDX-1 in type-2 streptozotocin-nicotinamide induced Sprague dawley diabetic rats. A total of 24Sprague dawleyrats (Four groups of six rats each), were used for this study; Group 1: Normal rats (CONTROL) given distilled water for 4weeks; Group 2: Metformin + Magnesium treated rats (DMM) orally given 100mg/kg and 1000mg/kg body weight respectively for 4weeks; Group 3: Metformin treated diabetic rats (DM), orally given 100mg/kg body weight for 4weeks; Group 4: Diabetic untreated control rats (DU) given distilled water for 4weeks. Measured data were analyzed statistically. The result revealed that there was significant (p<0.05) increase in the feed and water intake of the treated rats but the metformin-magnesium supplement treated group showed more increase when compared with only metformin treated group. PDX-1 and insulin gene expression levels were significantly (p<0.05) higher in the control when compared with all the diabetic groups. However, PDX-1 and insulin mRNA levels were significantly (p<0.05) higher in DMM, when compared with DM. DMM showed improvements when compared with DM which suggests magnesium supplementation as an adjunct therapy with metformin may help inthe regeneration of the beta cells of the pancreas.

scholarly journals Changes in Hypothalamic Corticotropin-Releasing Hormone, Neuropeptide Y, and Proopiomelanocortin Gene Expression during Chronic Rapid Eye Movement Sleep Deprivation of Rats

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 421-431 ◽  
Author(s):  
Michael Koban ◽  
Wei Wei Le ◽  
Gloria E. Hoffman
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Food Intake ◽  
Sleep Deprivation ◽  
Neuropeptide Y ◽  
Eye Movement ◽  
Paradoxical Sleep ◽  
Body Weight Loss ◽  
Male Rats ◽  
Rapid Eye Movement

Chronic rapid eye movement (paradoxical) sleep deprivation (REM-SD) of rats leads to two conspicuous pathologies: hyperphagia coincident with body weight loss, prompted by elevated metabolism. Our goals were to test the hypotheses that 1) as a stressor, REM-SD would increase CRH gene expression in the hypothalamus and that 2) to account for hyperphagia, hypothalamic gene expression of the orexigen neuropeptide Y (NPY) would increase, but expression of the anorexigen proopiomelanocortin (POMC) would decrease. Enforcement of REM-SD of adult male rats for 20 d with the platform (flowerpot) method led to progressive hyperphagia, increasing to approximately 300% of baseline; body weight steadily declined by approximately 25%. Consistent with changes in food intake patterns, NPY expression rapidly increased in the hypothalamic arcuate nucleus by d 5 of REM-SD, peaking at d 20; by contrast, POMC expression decreased progressively during REM-SD. CRH expression was increased by d 5, both in mRNA and ability to detect neuronal perikaryal staining in paraventricular nucleus with immunocytochemistry, and it remained elevated thereafter with modest declines. Taken together, these data indicate that changes in hypothalamic neuropeptides regulating food intake are altered in a manner consistent with the hyperphagia seen with REM-SD. Changes in CRH, although indicative of REM-SD as a stressor, suggest that the anorexigenic actions of CRH are ineffective (or disabled). Furthermore, changes in NPY and POMC agree with current models of food intake behavior, but they are opposite to their acute effects on peripheral energy metabolism and thermogenesis.

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