1,721,074 research outputs found
Cocaine- and amphetamine-regulated transcript peptide-(55-102) and thyrotropin releasing hormone inhibit hypothalamic dopamine release.
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Effects of isolated GH deficiency on adipose tissue, feeding and adipokines in mice
No full textObjective: Growth hormone (GH) deficiency (GHD) leads to growth failure and changes in body composition including increased fat accumulation and reduced lean body mass in both humans and rodents. The aim of this study was to characterize the consequences of isolated GHD (IGHD) on adiposity, total body weight (TBW), and food intake in a mouse model of autosomal recessive IGHD due to targeted ablation of the GH-releasing hormone (GHRH) gene [GHRH knockout (GHRHKO)]. Animals were also analyzed with respect to leptin, adiponectin and visfatin circulating levels and gene expression in both intra-abdominal and subcutaneous fat.
Design: We studied 8 male mice homozygous for GHRHKO allele (-/-) and 8 heterozygous (+/-) animals as controls. Feeding and TBW data were collected weekly from 3 through 5 months of age. Animals were then euthanized for measurement of body length and intra-abdominal (epididymal and retroperitoneal) and subcutaneous (interscapular, axillary, gluteal and inguinal) fat weights, and for blood collection for leptin, adiponectin and visfatin measurement. Gene expression of leptin, adiponectin and visfatin in adipose tissue was evaluated by real-time reverse transcription polymerase chain reaction.
Results: GHRHKO mice had significantly increased relative intra-abdominal (P<0.01) and subcutaneous (P<0.0001) fat, accompanied by significantly increased food intake per TBW (P<0.01), whereas - despite 40% higher food consumption - TBW change was not different from controls over the 2 month period. Adiponectin and visfatin mRNA levels were decreased in both intra-abdominal (P<0.001) and subcutaneous fat (P<0.0001), while leptin mRNA levels were not different from controls. Conversely, serum adiponectin levels were higher in GHRHKO mice (P<0.0001), whereas serum visfatin and leptin did not significantly differ from controls.
Conclusions: IGHD due to targeted ablation of the GHRH gene in mice is associated with increased relative subcutaneous and intra-abdominal fat mass and higher food consumption which is not related to changes in circulating leptin
Resistin, but not adiponectin, inhibits dopamine and norepinephrine release in the hypothalamus
No full textAdiponectin (Adipocyte Complement-Related Protein of 30 kDa, ACRP30) and resistin are adipocyte-derived polypeptide hormones playing a role in metabolic homeostasis. Their plasma levels are inversely (adiponectin) or directly (resistin) correlated to obesity and they have opposite effects on insulin sensitivity. Adipose tissue hormones such as leptin have been shown to modulate neurotransmitters which control feeding in the hypothalamus. We have studied the effects of adiponectin and resistin on dopamine, norepinephrine and serotonin release from hypothalamic neuronal endings (synaptosomes) in vitro. We have found that adiponectin does not modify either basal or depolarization-induced amine release, while resistin inhibits the stimulated release of dopamine and norepinephrine, leaving unaffected serotonin release. We can conclude that, similarly to leptin, but differently from adiponectin, the adipose tissue hormone resistin could affect the central mechanisms of feeding by inhibiting catecholamine release in the hypothalamus. (C) 2004 Elsevier B.V. All rights reserved
Glucagon-like-peptide 1 (7-36) amide (GLP-1) and exendin-4 stimulate serotonin release in rat hypothalamus.
No full textGlucagon-like peptide 1 (7–36) amide (GLP-1) and exendin-4 are gastrointestinal hormones
as well as neuropeptides involved in glucose homeostasis and feeding regulation, both
peripherally and at the central nervous system (CNS), acting through the same GLP-1
receptor. Aminergic neurotransmitters play a role in the modulation of feeding in the
hypothalamus and we have previously found that peripheral hormones and neuropeptides,
which are known to modulate feeding in the central nervous system, are able to modify
catecholamine and serotonin release in the hypothalamus. In the present paper we have
evaluated the effects of GLP-1 and exendin-4 on dopamine, norepinephrine, and serotonin
release fromrat hypothalamic synaptosomes, in vitro.We found that glucagon-like peptide
1 (7–36) amide and exendin-4 did not modify either basal or depolarization-induced dopa-
mine and norepinephrine release; on the other hand glucagon-like peptide 1 (7–36) amide
and exendin-4 stimulated serotonin release, in a dose dependentmanner.We can conclude
that the central anorectic effects of GLP-1 agonists could be partiallymediated by increased
serotonin release in the hypothalamus, leaving the catecholamine release unaffected
Chromatin-derived acidic peptide stimulates prolactin secretion: role of N-CAM signaling.
No full textAbst P3-15
Aging increases amyloid beta-peptide-induced 8-iso-prostaglandin F2alpha release from rat brain.
No full textIn order to investigate whether amyloid beta-peptide-induced oxidative damage in the brain could be related to aging, we studied the release of 8-iso-prostaglandin (PG)F-2alpha, a stable marker of cellular oxidative stress, in brain synaptosomes from Wistar rats of different ages (3, 6, 12, 18 months old), both basally and after amyloid beta-peptide (1-40) perfusion.
We found that basal release of 8-iso-PGF(2alpha) was not significantly different among all age groups of rats. Either phospholipase A(2) activation induced by calcium ionophore A23187 (10 nM) or amyloid beta-peptide (5 muM) did not modify isoprostane release, when these substances were used alone. In contrast, amyloid beta-peptide (1-5 muM) preincubation caused a dose-dependent increase of A23187-stimulated 8-iso-PGF(2alpha) release in each age group, which was also strikingly correlated to aging of rats. Furthermore, ferric ammonium sulfate stimulates isoprostane production to levels comparable to those induced by amyloid beta-peptide.
In conclusion, although 8-iso-PGF(2alpha) production from rat brain synaptosomes is independent from aging in the basal state, aging renders neurons more vulnerable to amyloid beta-peptide-induced oxidative toxicity. (C) 2003 Elsevier Science Inc. All rights reserved
Different effects of peptides YY (1-36) and YY (3-36) on hypothalamic dopamine and norepinephrine release.
No full textA natural formulation (imoviral) increases macrophage resistance to LPS-induced oxidative and inflammatory stress in vitro.
No full textImoviral is a natural product formulation containing a mixture of uncaria, shiitake and ribes extracts. All ingredients are recognized as antioxidant, anti-inflammatory agent and immunomodulant. In order to evaluate the rational basis of extract mixture as immunomodulatory agent, we tested the effect of Imoviral formulation on macrophage response to lipopolysaccharide (LPS)-induced stress. The effect was evaluated as variation of reactive oxygen species (ROS) and prostaglandin E2 (PGE2) production and as cytokine gene expression. The extract did not affect cell viability up to 250μg/ml. Treatment with extract (10-150 μg/ml) reduced ROS and PGE2 production as well as IL-8 and TNF-α gene expression. A pre-treatment with extract blunted LPS-induced production of ROS and PGE2, markers of oxidative and inflammatory stress, as well as the gene expression of all cytokines tested, indicators, in vitro, of immune response activation. In conclusion, we demonstrated that Imoviral formulation could be a useful tool to modulate the immune function, reducing the oxidative and inflammatory markers related to bacterial attack. Experimental data suggest that Imoviral extract mixture could also represent a preventive pharmacological strategy to enhance cell resistance to bacterial infections
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