scholarly journals Hypothalamic Expression of Neuropeptide Y (NPY) and Pro-OpioMelanoCortin (POMC) in Adult Male Mice Is Affected by Chronic Exposure to Endocrine Disruptors

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 368
Author(s):  
Marilena Marraudino ◽  
Elisabetta Bo ◽  
Elisabetta Carlini ◽  
Alice Farinetti ◽  
Giovanna Ponti ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Neuropeptide Y ◽  
Adult Male ◽  
Endocrine Disrupting Chemicals ◽  
Endocrine System ◽  
Male Mice ◽  
Hypothalamic Nuclei ◽  
Short Term Exposure ◽  
Control Food Intake

In the arcuate nucleus, neuropeptide Y (NPY) neurons, increase food intake and decrease energy expenditure, and control the activity of pro-opiomelanocortin (POMC) neurons, that decrease food intake and increase energy expenditure. Both systems project to other hypothalamic nuclei such as the paraventricular and dorsomedial hypothalamic nuclei. Endocrine disrupting chemicals (EDCs) are environmental contaminants that alter the endocrine system causing adverse health effects in an intact organism or its progeny. We investigated the effects of long-term exposure to some EDCs on the hypothalamic NPY and POMC systems of adult male mice that had been previously demonstrated to be a target of some of these EDCs after short-term exposure. Animals were chronically fed for four months with a phytoestrogen-free diet containing two different concentrations of bisphenol A, diethylstilbestrol, tributyltin, or E2. At the end, brains were processed for NPY and POMC immunohistochemistry and quantitatively analyzed. In the arcuate and dorsomedial nuclei, both NPY and POMC immunoreactivity showed a statistically significant decrease. In the paraventricular nucleus, only the NPY system was affected, while the POMC system was not affected. Finally, in the VMH the NPY system was affected whereas no POMC immunoreactive material was observed. These results indicate that adult exposure to different EDCs may alter the hypothalamic circuits that control food intake and energy metabolism.

scholarly journals Specific transgenerational imprinting effects of the endocrine disruptor methoxychlor on male gametes

Reproduction ◽  
2011 ◽  
Vol 141 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Christelle Stouder ◽  
Ariane Paoloni-Giacobino
Keyword(s):  
Adult Male ◽  
Endocrine Disrupting Chemicals ◽  
Methylation Pattern ◽  
Imprinted Genes ◽  
Male Mice ◽  
Systematic Analysis ◽  
Adult Mice ◽  
Male Gametes ◽  
Pregnant Mice ◽  
Methylation Defects

Endocrine-disrupting chemicals (EDCs), among which methoxychlor (MXC), have been reported to affect the male reproductive system. This study evaluates the possible deleterious effects of MXC on imprinted genes. After administration of the chemical in adult male mice or in pregnant mice we analyzed by pyrosequencing possible methylation defects in two paternally imprinted (H19 and Meg3 (Gtl2)) and three maternally imprinted (Mest (Peg1), Snrpn, and Peg3) genes in the sperm and in the tail, liver, and skeletal muscle DNAs of the adult male mice and of the male offspring. MXC treatment of adult mice decreased the percentages of methylated CpGs of Meg3 and increased those of Mest, Snrpn, and Peg3 in the sperm DNA. MXC treatment of pregnant mice decreased the mean sperm concentrations by 30% and altered the methylation pattern of all the imprinted genes tested in the F1 offspring. In the latter case, MXC effects were transgenerational but disappeared gradually from F1 to F3. MXC did not affect imprinting in the somatic cells, suggesting that it exerts its damaging effects via the process of reprogramming that is unique to gamete development. A systematic analysis at the CpG level showed a heterogeneity in the CpG sensitivity to MXC. This observation suggests that not only DNA methylation but also other epigenetic modifications can explain the transgenerational effects of MXC. The reported effects of EDCs on human male spermatogenesis might be mediated by complex imprinting alterations analogous to those described in this study.

scholarly journals Mechanism of Action of Acupuncture in Obesity: A Perspective From the Hypothalamus

2021 ◽  
Vol 12 ◽  
Author(s):  
Li Wang ◽  
Chao-Chao Yu ◽  
Jia Li ◽  
Qing Tian ◽  
Yan-Jun Du
Keyword(s):  
Metabolic Disease ◽  
Food Intake ◽  
Energy Expenditure ◽  
Mechanism Of Action ◽  
Energy Homeostasis ◽  
Current Evidence ◽  
Appetite Regulation ◽  
Hypothalamic Nuclei ◽  
Treatment Of Obesity ◽  
The Relationship

Obesity is a prevalent metabolic disease caused by an imbalance in food intake and energy expenditure. Although acupuncture is widely used in the treatment of obesity in a clinical setting, its mechanism has not been adequately elucidated. As the key pivot of appetite signals, the hypothalamus receives afferent and efferent signals from the brainstem and peripheral tissue, leading to the formation of a complex appetite regulation circuit, thereby effectively regulating food intake and energy homeostasis. This review mainly discusses the relationship between the hypothalamic nuclei, related neuropeptides, brainstem, peripheral signals, and obesity, as well as mechanisms of acupuncture on obesity from the perspective of the hypothalamus, exploring the current evidence and therapeutic targets for mechanism of action of acupuncture in obesity.

scholarly journals Central and peripheral control of food intake

2017 ◽  
Vol 51 (1) ◽  
pp. 52-70 ◽  
Author(s):  
M. M. I. Abdalla
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Current Knowledge ◽  
The Body ◽  
Therapeutic Implications ◽  
New Therapeutic Approaches ◽  
Control Food ◽  
Adiposity Signals ◽  
Control Food Intake

Abstract The maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. The obesity has an evil effect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity.

Increased adiposity in DNA binding-dependent androgen receptor knockout male mice associated with decreased voluntary activity and not insulin resistance

2011 ◽  
Vol 301 (5) ◽  
pp. E767-E778 ◽  
Author(s):  
Kesha Rana ◽  
Barbara C. Fam ◽  
Michele V. Clarke ◽  
Tammy P. S. Pang ◽  
Jeffrey D. Zajac ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Androgen Receptor ◽  
Food Intake ◽  
Dna Binding ◽  
Energy Expenditure ◽  
Body Mass ◽  
Fat Mass ◽  
Resting Energy Expenditure ◽  
Male Mice ◽  
Voluntary Activity

In men, as testosterone levels decrease, fat mass increases and muscle mass decreases. Increased fat mass in men, in particular central obesity, is a major risk factor for type 2 diabetes, cardiovascular disease, and all-cause mortality. Testosterone treatment has been shown to decrease fat mass and increase fat-free mass. We hypothesize that androgens act directly via the DNA binding-dependent actions of the androgen receptor (AR) to regulate genes controlling fat mass and metabolism. The aim of this study was to determine the effect of a global DNA binding-dependent (DBD) AR knockout (DBD-ARKO) on the metabolic phenotype in male mice by measuring body mass, fat mass, food intake, voluntary physical activity, resting energy expenditure, substrate oxidation rates, serum glucose, insulin, lipid, and hormone levels, and metabolic gene expression levels and second messenger protein levels. DBD-ARKO males have increased adiposity despite a decreased total body mass compared with wild-type (WT) males. DBD-ARKO males showed reduced voluntary activity, decreased food intake, increased serum leptin and adiponectin levels, an altered lipid metabolism gene profile, and increased phosphorylated CREB levels compared with WT males. This study demonstrates that androgens acting via the DNA binding-dependent actions of the AR regulate fat mass and metabolism in males and that the increased adiposity in DBD-ARKO male mice is associated with decreased voluntary activity, hyperleptinemia and hyperadiponectinemia and not with insulin resistance, increased food intake, or decreased resting energy expenditure.

Phosphorylation of STAT3 in hypothalamic nuclei is stimulated by lower doses of leptin than are needed to inhibit food intake

2021 ◽  
Author(s):  
Ruth B.S. Harris
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Random Order ◽  
Progressive Increase ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Hypothalamic Nuclei ◽  
Brown Adipose ◽  
Integrated Response

This experiment investigated which hypothalamic nuclei were activated by a dose of leptin that inhibited food intake. Food intake, energy expenditure, respiratory exchange ratio (RER) and intrascapular brown adipose tissue (IBAT) temperature were measured in male and female Sprague Dawley rats for 36 hours following an intraperitoneal injection of 0, 50, 200, 500 or 1000 mg leptin/kg with each rat tested with each dose of leptin in random order. In both males and females RER and 12 hour food intake and were inhibited only by 1000 mg leptin/kg, but there was no effect on energy expenditure or IBAT temperature. At the end of the experiment pSTAT3 immunoreactivity was measured one hour after injection of 0, 50, 500 or 1000 mg leptin/kg. In male rats the lowest dose of leptin produced a maximal activation of STAT3 in the Arc and nucleus of the solitary tract (NTS). There was no response in the dorsomedial hypothalamus but there was a progressive increase in VMH pSTAT3 with increasing doses of leptin. In female rats there was no significant change in Arc pSTAT3, NTS activation was maximal with 500 mg leptin/kg, but only the highest dose of leptin increased VMH pSTAT3. These results suggest that the VMH plays an important role in the energetic response to elevations of circulating leptin, but do not exclude the possibility that multiple nuclei provide the appropriate integrated response to hyperleptinemia.

scholarly journals Orectic And Anorectic Peptides And Their Implication In Obesity And The Metabolic Syndrome

2015 ◽  
Vol 22 (2) ◽  
pp. 187-191
Author(s):  
Alina Bodea ◽  
Amorin Remus Popa
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Energy Expenditure ◽  
Neuropeptide Y ◽  
Related Protein ◽  
The Metabolic Syndrome ◽  
Hypothalamic Neuropeptides ◽  
Clinical Conditions ◽  
Agouti Related Protein ◽  
Adipose Cells

AbstractBackground and aims: Cardiovascular diseases, diabetes mellitus, the metabolic syndrome and obesity are now globally widespread clinical conditions, addressing different ages, lately extending to young and children. The causes are multiple, involving an interaction between individual genetic risk factors and environmental factors. Many studies showed the importance of the hypothalamic neuropeptides and other neuropeptides in the regulation of the balance between food intake and energy consumption. We reviewed 25 recent research studies describing the physiological and physiopathological mechanisms of the orectic and anorectic peptides and their interaction to adjust the balance between food intake and energy expenditure.Conclusions: The hypothalamus, through its nuclei (arcuate and paraventricular) controls the balance between food intake and energy expenditure. The proopiomelanocortin (POMC) / Cocaine and amphetamine-related transcript (CART) neurons represent the anorectic centre. The neurons that release neuropeptide Y (NPY) and agouti-related protein (AgRP) by stimulation form the orectic centre. The neuropeptide Y (NPY) is the main hypothalamic orectic neuropeptide. Its action, besides stimulating the orectic effect, is to modulate the release of other hypothalamic orectic and anorectic neuropeptides. In addition, the energy balance is regulated by adipokines released by the adipose cells, hormones and neurotransmitters, blood glucose level and other metabolites.

Neuropeptide Y is associated with changes in appetite-associated hypothalamic nuclei but not food intake in a hypophagic avian model

2013 ◽  
Vol 236 ◽  
pp. 327-331 ◽  
Author(s):  
Brandon A. Newmyer ◽  
Wint Nandar ◽  
Rebekah I. Webster ◽  
Elizabeth Gilbert ◽  
Paul B. Siegel ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuropeptide Y ◽  
Hypothalamic Nuclei

scholarly journals Central Injection of the Stable Somatostatin Analog ODT8-SST Induces a Somatostatin2 Receptor-Mediated Orexigenic Effect: Role of Neuropeptide Y and Opioid Signaling Pathways in Rats

Endocrinology ◽  
2010 ◽  
Vol 151 (9) ◽  
pp. 4224-4235 ◽  
Author(s):  
Andreas Stengel ◽  
Tamer Coskun ◽  
Miriam Goebel ◽  
Lixin Wang ◽  
Libbey Craft ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Neuropeptide Y ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Somatostatin Receptors ◽  
Opiate Receptors ◽  
Dark Phase ◽  
Solid Meal ◽  
Μ Opioid Receptor

Somatostatin and octreotide injected into the brain have been reported to modulate food intake. However, little is known regarding the underlying mechanisms. The stable oligosomatostatin analog, des-AA1,2,4,5,12,13-[DTrp8]-somatostatin (ODT8-SST), like somatostatin, binds to all five somatostatin receptors (sst1–5). We characterized the effects of ODT8-SST injected intracerebroventricularly (icv) on food consumption and related mechanisms of action in freely fed rats. ODT8-SST (0.3 and 1 μg per rat, icv) injected during the light or dark phase induced an early onset (within 1 h) and long-lasting (4 h) increase in food intake in nonfasted rats. By contrast, ip injection (0.3–3 mg/kg) or icv injection of selective sst1 or sst4 agonists (1 μg per rat) had no effect. The 2 h food intake response during the light phase was blocked by icv injection of a sst2 antagonist, the neuropeptide Y (NPY) Y1 receptor antagonist, BIBP-3226, and ip injection of the μ-opioid receptor antagonist, naloxone, and not associated with changes in plasma ghrelin levels. ODT8-SST (1 μg per rat, icv) stimulated gastric emptying of a solid meal which was also blocked by naloxone. The increased food intake was accompanied by a sustained increase in respiratory quotient, energy expenditure, and drinking as well as μ-opioid receptor-independent grooming behavior and hyperthermia, while ambulatory movements were not altered after ODT8-SST (1 μg per rat, icv). These data show that ODT8-SST acts primarily through brain sst2 receptors to induce a long-lasting orexigenic effect that involves the activation of Y1 and opiate-receptors, accompanied by enhanced gastric transit and energy expenditure suggesting a modulation of NPYergic and opioidergic orexigenic systems by brain sst2 receptors.

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