Synphilin-1 is a cytoplasmic protein that has been shown to be involved in the control of energy balance. Previously, we reported on the generation of a human synphilin-1 transgenic mouse model (SP1), in which overexpression of human synphilin-1 resulted in hyperphagia and obesity. Here, behavioral measures in SP1 mice were compared with those of their age-matched controls (NTg) at two time points: when there was not yet a group body weight difference (
Humans, like all animals, have a sophisticated system of hormones and brain regions whose function is to maintain a proper energy balance. Part of the systems job is to keep fat mass at an appropriate level. With a properly functioning system, feedback loops inhibit hunger once fat mass has reached a certain level, and also increase resting metabolic rate to burn excess calories. If the system is working properly, its very difficult to gain weight. There have been a number of overfeeding studies in which subjects have consumed huge amounts of excess calories. Some people gain weight, many dont. ...
Innovative Glycation Stop Goods (AGEs) and Sugar Overconsumption of sugar is often a renowned wellness dilemma but most do not comprehend how really serious...
PubMed journal article: High circulating ghrelin: a potential cause for hyperphagia and obesity in prader-willi syndrome. Download Prime PubMed App to iPhone, iPad, or Android
In contrast to the acute and chronic anorectic responses to EAA deprivation, dietary MR produces a hyperphagic response within 6-7 days after introduction of the diet, and the 20-25% increase in consumption of the diet continues indefinitely (7,64). A compilation of the short-term responses to dietary MR and leucine deprivation are summarized in Fig. 2, with differences highlighted in yellow. The acute responses to the diets also share several similarities, including comparable transcriptional effects on lipogenic genes in the liver, increased oxidative genes in WAT, increased EE, and enhanced insulin sensitivity (7-10,30,39,48,58,76,77). A key similarity is that both diets increase SNS stimulation of adipose tissue, which induces oxidative and thermogenic gene programs, resulting in increased EE. Recent studies provide evidence that leucine deprivation activates the SNS by increasing expression of corticotropin-releasing hormone in the hypothalamic paraventricular nucleus (10) through a ...
TY - JOUR. T1 - Deficient melanocortin-4 receptor causes abnormal reproductive neuroendocrine profile in female mice. AU - Chen, Xiaolin. AU - Huang, Lili. AU - Tan, Hwee Y.. AU - Li, Hongzhuo. AU - Wan, Ying. AU - Cowley, Michael. AU - Veldhuis, Johannes D. AU - Chen, Chen. PY - 2017. Y1 - 2017. N2 - Deletion of the melanocortin-4-receptor (Mc4r) gene in mice causes hyperphagia, followed by hyperinsulinemia, obesity and progressive infertility. Evidence shows that the number of developed corpora lutea is reduced in obese MC4R-knockout (MC4R KO) female mice, but the mechanism is unclear. The effect of hyperphagia and obesity by MC4R KO on pulsatile luteinizing hormone (LH) secretion and ovulation remains unknown. In MC4R KO mice and wild-type littermates (WT LM) during the diestrus period throughout different ages, we examined and monitored their metabolic status, pulsatile LH profiles, follicular morphology and the number of corpora lutea. MC4R KO mice were hyperphagic, obese, hyperglycemic, ...
The causes of post-restriction hyperphagia (PRH) represent a target for drug-based therapies to prevent obesity. However, the factors causing PRH are poorly understood. We show that, in mice, the extent of PRH was independent of the time under restriction, but depended on its severity, suggesting that PRH was driven by signals from altered body composition. Signals related to fat mass were important drivers. Circulating levels of leptin and TNFα were significantly depleted following caloric restriction (CR). We experimentally repleted their levels to match those of controls, and found that in both treatment groups the level of PRH was significantly blunted. These data establish a role for TNFα and leptin in the non-pathological regulation of energy homeostasis. Signals from adipose tissue, including but not limited to leptin and TNFα, regulate PRH and might be targets for therapies that support people engaged in CR to reduce obesity. ...
To date, the role of endogenous CNS GLP-1 in the regulation of energy balance has remained elusive, largely because of discrepancies between genetic and pharmacological studies (Scrocchi et al., 1996; Meeran et al., 1999). In addition, the current models of GLP-1r knock-out mice and pharmacological GLP-1r blockade are limited in that they fail to directly target hindbrain-derived GLP-1. Here, for the first time, we address this limitation by using RNAi against NTS PPG in adult rats. Using this method, we aimed to downregulate the presumed sole source of ligand for GLP-1r throughout the CNS by directly targeting the majority of GLP-1-producing neurons. We compared this novel method to direct blockade of GLP-1r throughout the CNS with chronic ICV Ex9. NTS PPG knockdown resulted in hyperphagia and exacerbation of HFD-induced obesity, whereas chronic ICV Ex9 increased food intake and fat accumulation regardless of diet. Together, these data support the hypothesis that CNS GLP-1 activity modulates ...
In growing male obese Zucker rats, hyperphagia reaches a maximum or "breakpoint" and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 ...
In growing male obese Zucker rats, hyperphagia reaches a maximum or "breakpoint" and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 ...
AbstractMelanin-concentrating hormone (MCH) is an important regulator of food intake, glucose metabolism, and adiposity. However, the mechanisms mediating these
We recently identified acyl coenzyme A-binding proteins (ACBP)/diazepam binding inhibitor (DBI) being a book hunger aspect: a proteins thats upregulated in individual or murine weight problems which, if administered to mice, causes hyperphagy, obesity and adipogenesis. 13?C-glucose in liver organ and plasma (b), or entire body respirometry (c). Energy expenses (EE) and air consumption and skin tightening and creation (RQ?=?vCO2/vO2) were utilized to calculate fatty acidity oxidation. ACBP/DBI neutralization highly decreased the hyperphagic response induced by transient Rabbit Polyclonal to FPR1 hunger (24?h). As as 30 shortly?min after intraperitoneal shot of the anti-ACBP/DBI mAb, the activation of orexigenic neurons was inhibited, suggesting these results are mediated with the neutralization of peripheral (not central-nervous) ACBP/DBI because an antibody is expected should combination the brain bloodstream hurdle [8]. In given mice, ACBP/DBI neutralization triggered a transient and moderate ...
PubMed journal article Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrom were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
As an absolute number, your dog might not seem at first glance to have gained much weight. It is only when one expresses the gain as a percentage of the starting weight that this becomes apparent as a truly significant weight gain. A 1.4 pound gain for your dog is a 15% increase in bodyweight, irrespective of whether one is using American or British Imperial pounds.. Hyperphagia is not a term commonly used in the UK. Your reference to American pounds leads me to suspect you are American and it may be that the term hyperphagia is used that side of the pond for what we would call polyphagia, or increased appetite. If I am wrong, then apologies! There are several conditions characterised by polyphagia such as:. - Diabetes mellitus - often weight loss rather than weight gain; often overweight initially; also polyuria/polydipsia or increased urination and thirst (hence pp/pu/pd); characteristically glucose in the urine and a fasting raised blood glucose;. - Cushings syndrome or ...
In growing male obese Zucker rats, hyperphagia reaches a maximum or "breakpoint" and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 ...
Background: The melanocortin-4-receptor gene (MC4R) is a key regulator of energy homeostasis, food intake and body weight which has intensively been analyzed in molecular genetic obesity research. MC4R dysfunction in humans causes hyperphagia, impaired satiety and obesity.. Objective and hypotheses: To identify MC4R mutations prevelance in Turkish obese children and adolescents.. Method: Ninenty three pediatric and adolescent patients aged between 1.3 and 15 years old with early onset obesity (45 female/48 male) were enrolled. Obesity was defined as a body mass index (BMI) standart deviation score (SDS) of +2.0 according to the Turkish Population. Children with genetic syndromes associated with obesity or mental retardation, or taking drugs that promote changes in eating behavior or weight were excluded. Coding region of the MC4R gene was sequenced by Illumina MiSeq Next Generation Sequencing System.. Results: The mean age of the patients was 7.3±3.7 years and mean BMI was SDS 3.7±0.7SD. ...
To determine the potential roles for Jak2-autonomous LepRb signals in leptin action in vivo, we generated a mouse model in which LepRb is replaced by a truncation mutant (LepRbΔ65) that contains within its intracellular domain only the sequences required to associate with and activate Jak2. We found that the hyperphagia, obesity, linear growth, ARC physiology, and immune function of these Δ/Δ mice closely resembled that of entirely LepRb-deficient db/db mice. Δ/Δ and db/db animals did demonstrate some modest differences in glucose homeostasis; however, both male and female Δ/Δ mice exhibited a delayed progression to frank hyperglycemia compared with db/db mice. Taken together, these findings demonstrate that Jak2-autonomous LepRb signals may contribute modestly to the modulation of glucose homeostasis by leptin, but emphasize the necessity of signals emanating from the COOH-terminus of LepRb (beyond the Jak2-associating Box1 and Box2 motifs) for most leptin action.. The finding that ...
Over three million people died from alcohol consumption in 2016, equating to 1 in 20 deaths globally, according to a new report by theWorld Health Organization.
As free-radical-forming poisons build up in our environment and bodies, antioxidants may ward off some of their harmful health effects. But free radicals
We go on about Less is the New More- so many of our problems are the result of overconsumption, of building, driving or eating what we want, rather than what we need. Thats why we like this glass from industrial designer Inna Alesina- a small hole in
Our previous data described significant differences between N/OFQ-induced food intake in DA and WOKW male rats [4]. Our concluding hypothesis was that N/OFQ-induced hyperphagia could be regulated by the Cart peptide. In the present study, in order to further explore this phenomenon, we extended inquiry to include female as well as male DA and WOKW rats, performing N/OFQ injections and analyzing their N/OFQ-induced food intake. We also looked at the Cart gene expression of their littermates. We observed significant differences in feeding behavior between DA and WOKW males, confirming data previously observed after injecting N/OFQ in the lateral ventricle. We also observed significant differences in N/OFQ-induced food intake between WOKW males and females after 1 h at a treatment of 0.5 nmol/rat. Looking at the Cart gene expression of littermates that were not part of the N/OFQ feeding behavior experiments, we noted that WOKW females have high Cart gene expression compared to WOKW males, while DA ...
Polyphagia or hyperphagia is an abnormally strong sensation of hunger or desire to eat often leading to or accompanied by overeating.[1] In contrast to an increase in appetite following exercise, polyphagia does not subside after eating and often leads to rapid intake of excessive quantities of food. Polyphagia is not a disorder by itself, rather it is a symptom indicating an underlying medical condition. It is frequently a result of abnormal blood glucose levels (both hyperglycemia and hypoglycemia), and, along with polydipsia and polyuria, it is one of the "3 Ps" commonly associated with diabetes mellitus.[2][3] ...
Comparison of the number of hyperphagic access, over 7 consecutive days, before starting therapy with light therapy and 30 days after discontinuation of ...
Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also appears to function downstream of the leptin-melanocortin signaling pathway to control appetite. In both animals and humans, diminished BDNF function is associated with hyperphagia, obesity, and neurocognitive deficits. We propose to study BDNF in two hyperphagic disorders: Prader-Willi syndrome and MC4R function-altering mutations. We hypothesize that patients with PWS may have increased BDNF during infancy, followed by a decline in BDNF that precedes the onset of hyperphagia and persists after the onset of obesity. We hypothesize that patients with MC4R mutations will have decreased BDNF, the severity of which will be associated with the degree of MC4R functional loss caused by the specific mutation(s) in each individual. To test these hypotheses, we wish to conduct cross-sectional studies to evaluate serum BDNF concentrations, metabolism, body composition, and ...
PLoS One. 2008 Mar 5;3(3):e1709. doi: 10.1371/journal.pone.0001709. Research Support, N.I.H., Extramural; Research Support, Non-U.S. Govt
In contrast with our previous findings on laboratory mice [10,11], our data clearly demonstrate that dietary supplementation with either vitamin E or vitamin C dramatically shortened lifespan in voles. This occurred despite the fact that hepatic lipid peroxidation was significantly reduced in all but one (cold, vitamin C-supplemented) treatment group, although lymphocyte and hepatocyte DNA oxidative damage was unaffected by antioxidant supplementation. The reasons for this lifespan effect are currently unclear. Dietary restriction extends lifespan in many animals [19], and the antioxidant diets may have been more palatable, driving hyperphagia that potentially affect health and survival. While absolute daily food intake at 11 months of age was unaffected by diet, supplemented voles at both temperatures tended to be heavier than the control animals, although this reached significance, relative to controls, only in the cold exposed vitamin E group. Increased body mass is a major risk factor for ...
Administration of an anorexigenic dose of PYY3-36, whether it is intraperitoneally or by an OS, increased the number of c-Fos+ neurons in the forebrain Arc, PVN, and LHA nuclei and increased p-ERK in the Arc and PVN nuclei. Therefore, the inevitable conclusion is that supraphysiological salivary PYY3-36 can modulate satiety/feeding centers without reaching plasma. Phenotypic identification neurons in the PVN shows that both AVP+ and AVP-negative but not OXT neurons were activated, suggesting that PYY induced satiation by stimulating AVP secretion. AVP is involved in appetite suppression by opposing neuropeptide Y (NPY)-induced orexigenic effects (Olson et al., 1991a,b; Verbalis et al., 1993; Aoyagi et al., 2009).. Both intraperitoneal and OS PYY also induced p-ERK in a significant population within the parvocellular subnuclei of the PVN that are known to express CRF. CRF has been shown to act on the CNS to inhibit FI in several models of hyperphagia (Currie et al., 2001; Fekete et al., ...
Appetite is regulated by a number of hypothalamic neuropeptides including neuropeptide Y (NPY), a powerful feeding stimulator that responds to feeding status, and drugs such as nicotine and cannabis. There is debate regarding the extent of the influence of obesity on hypothalamic NPY. We measured hypothalamic NPY in male SpragueDawley rats after short or long term exposure to cafeteria-style high fat diet (32% energy as fat) or laboratory chow (12% fat). Caloric intake and body weight were increased in the high fat diet group, and brown fat and white fat masses were significantly increased after 2 weeks. Hypothalamic NPY concentration was only significantly decreased after long term consumption of the high fat diet. Nicotine decreases food intake and body weight, with conflicting effects on hypothalamic NPY reported. Body weight, plasma hormones and brain NPY were investigated in male Balb/c mice exposed to cigarette smoke for 4 days, 4 and 12 weeks. Food intake was significantly decreased by ...
Bulimia or bulimia nervosa refers to episodes of excessive and impulsive eating of a large amount of food (hyperphagia, or what people may call "overeating" or "binge eating "), followed by various harmful behaviours in response to the loss of food control and a fear of getting fat, e.g., vomiting, taking diuretics or laxatives, or exercising excessively. According to the diagnostic criteria of the DSM-V (Diagnostic and Statistical Manual of Mental Disorders), these episodes must occur at least once a week for the condition to qualify as bulimia. In general, people with bulimia will maintain a normal weight, which can allow them to hide the problem for years.. Like with anorexia, bulimia also causes great physical and psychological suffering. Vomiting can cause inflammation of the esophagus and swelling of the salivary glands. In rare cases, hyperphagia may cause the stomach to rupture. The abuse of laxatives or diuretics can cause electrolyte disorders and lead to heart or other problems. Like ...
Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 1997; 387 903-8
Surgical treatment of obesity is as effective for individuals who developed the disorder early, by the age of 20, as for those who have developed obesity later in life, a study from the University of Gothenburg shows.
Several different single-gene mutations are known to cause varying degrees of diabetes and obesity in mice. The severity of the diabetes produced depends on both the mutation itself and the interaction of the mutant gene with the inbred background. Establishing the nature of these gene-background interactions should aid us in our understanding of similar interactions that occur in human diabetes. The documentation of several different genes that produce similar, if not identical, diabetes-obesity syndromes suggests that lesions in many pathways can cause diabetes. An understanding of these defects in mice should help us to understand similar defects involved in the human disease. The developmental stages in each mutant are similar. The early symptoms include hyperphagia, hyperinsulinemia, and hypertrophy and hyperplasia of the beta cells of the islets of Langerhans. Hyperglycemia, obesity, and severe diabetes are secondary features that result from insulin resistance and the failure to
A recent study identified FAAH as a critical molecule involved in mood control in humans, showing that carriers of an FAAH gene mutation with reduced enzyme activity had both decreased threat-related brain reactivity and reduced anxiety (Hariri et al., 2009). These findings are particularly relevant because they allow generalizing to humans the results of the existing literature on the antianxiety effects of reduced FAAH activity in rodents. Both genetic and pharmacological inactivation of FAAH, in fact, exerts anxiolytic and antidepressant actions in rodents (Kathuria et al., 2003; Gobbi et al., 2005; Patel and Hillard, 2006; Bortolato et al., 2007; Hill et al., 2007; Naidu et al., 2007; Cippitelli et al., 2008; Moreira et al., 2008; Rubino et al., 2008; Scherma et al., 2008; Haller et al., 2009; Micale et al., 2009, and does not cause sedation, hypothermia, hyperphagia, or abuse potential (Fegley et al., 2005; Gobbi et al., 2005; Lichtman and Martin, 2005), which are important side effects of ...
Thanks to an ever diversifying market, our consumer choices are supposed to reveal precisely what we prefer. But is all this choice overwhelming our personal preferences and sweeping us up into futile overconsumption?
Besides genetic factors, diet components may contribute to the development of obesity, and it is known that cafeteria diet is characterized by a high caloric intake. Thus, the present study evaluated the mutagenic effects that cafeteria diet exerted on Wistar rats and its consequences on female offspring. Twelve females (generation 1) were separated in control group (CTL) and Cafeteria Diet group (CAF). At 70 days of age, females were mated with non-obese control males. Weaning at 21 days of age, female offspring (2nd generation) were separated into daughters of CTL or CAF mothers and subdivided according to previous diet. Ratio of polychromatic erythrocytes (PCE) / normochromatic erythrocytes (NCE) in a total of 1000 cells and Micronuclei (MN) 1000 PCE were evaluated. Were observed high MN frequencies, body weight, retroperitoneal and perigonadal fat; and low PCE/NCE ratio in generation 1. In generation 2, cafeteria diet caused high body weight, retroperitoneal and perigonadal fat and ...
TLR4-mediated signaling pathways also activate the MAPK pathway, which triggers p38- and JNK-dependent signaling and activation of various activator protein-1 (AP-1) subunits. JNK mediates inhibitory phosphorylation of insulin receptor substrate (IRS) proteins at serine 307, thereby impairing insulin action (54). Constitutive JNK activation in AgRP neurons of the hypothalamus induces weight gain and adiposity in mice as a consequence of hyperphagia (55). In fact, conditional JNK1 knockout specifically in the brain, but not in other tissues, leads to protection against insulin resistance, hyperinsulinemia, and glucose intolerance (56, 57). Interestingly, activation of TLR4 signaling controls apoptotic activity of cells in the hypothalamus but subsequently activates proinflammatory pathways that ultimately lead to the development of central insulin and leptin resistance (58).. Elevations of sphingolipids such as ceramides, whose synthesis depends on SFAs, and alterations in downstream ...
Oldspeak: Noting that warnings of collapse are often seen to be fringe or controversial, the study attempts to make sense of compelling historical data showing that the process of rise-and-collapse is actually a recurrent cycle found throughout history. Cases of severe civilisational disruption due to precipitous collapse - often lasting centuries - have been quite…
he is being a lazy little bugger and has dropped his daily food intake down to reduced levels. nominally he is taking 150 mls per kilo. he was 4.3 kilo this morning and those of you with an abacus or two ( like @MrsLPikon - aged but nimble with a zimmer ) will come to the same conclusion as us, he needs to take 645 mls per day. with 4 hourly feeding, thats 6 feeds, or 107 mls per feed ...
All decisions about the group and what we do are made by consensus, and we are committed to a horizontal/non-heirarchical group formation. We dont accept "alternative" fuels to be a solution to climate crisis, nor alternative to any other corporatized post-grassroots movement. We hold that bicycles, particularly, those that would otherwise fill landfills, are a real solution to the issues of overconsumption that created the environmental crises today. "Alternative," "conscious," etc. consumption will never solve consumption, only "hopenotize" those concerned OUT of action against the source of their misery ...
Industrial agribusiness and hydraulic fracturing, play an even greater role in climate change than the overconsumption of fossil fuels.
More than two in three adults in the United States are considered overweight or obese, with substantial biomedical and clinical evidence suggesting that chronic overconsumption of a
Classic lesion experiments from the 1940s have established the hypothalamus as playing an essential role in controlling energy homeostasis. Gold-thioglucose (GTG) induces lesions in the ventromedial nucleus of the hypothalamus (VMH) resulting in hyperphagia and obesity. To identify genes involved in the hypothalamic regulation of energy homeostasis, we employed a screen to search for genes that were dysregulated in GTG induced obese mice. In this screen, GPR7, the endogenous G protein-coupled receptor (GPCR) for the recently identified ligands neuropeptide B (NPB) and neuropeptide W (NPW), was found to be specifically down-regulated after GTG treatment. The physiological role of GPR7 was investigated by generating and analyzing mice with targeted disruption of GPR7. Male GPR7-/- mice developed an adult-onset obesity syndrome that progressively worsened with age and was greatly exacerbated when animals were fed a high fat diet. Male GPR7A mice were hyperphagic and had decreased energy expenditure and
PWS is frequently associated with a constant, extreme, ravenous, insatiable appetite, which persists no matter how much the patient eats, often resulting in morbid obesity. Caregivers need to strictly limit the patients access to food, usually by installing locks on refrigerators and on all closets and cabinets where food is stored.[20] It is the most common genetic cause of morbid obesity in children.[21] Currently, no consensus exists as to the cause for this symptom, although genetic abnormalities in chromosome 15 disrupt the normal functioning of the hypothalamus.[15] Given that the hypothalamic arcuate nucleus regulates many basic processes, including appetite, a link may well exist. In the hypothalamus of people with PWS, nerve cells that produce oxytocin, a hormone thought to contribute to satiety, have been found to be abnormal. People with PWS have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and obesity seen in this ...
In this study, we demonstrate that deletion of Thm1, a component of the IFT-A complex, causes hyperphagia-induced obesity in mice. These findings add a new mutant class to the list of ciliary mouse models of hyperphagia and obesity, which includes mutants of the BBS complex, of Alms1, of the IFT-B complex, and of the transition zone (Arsov et al., 2006; Collin et al., 2005; Davenport et al., 2007; Rahmouni et al., 2008; Stratigopoulos et al., 2014). The Thm1-cko obese phenotype further causes glucose intolerance and insulin resistance, which together indicate metabolic syndrome. In the human population, metabolic syndrome has become epidemic worldwide and a predictor of DM2, cardiovascular disease, and non-alcoholic fatty liver disease (Shin et al., 2013). Obese Thm1-cko mice also develop diabetes and fatty liver disease, modeling the human condition.. Prior to the increased weight gain and elevated serum metabolite levels in Thm1-cko mice, POMC mRNA levels in the ARC were reduced. This POMC ...
Public dialogue concerning metabolic adaptations that occur with weight loss has only partially addressed the scientific evidence on this topic. This is clear in the 2016 public dialogue on the research published in Obesity based on participants in the television show "The Biggest Loser".1 This paper reported that 6 years after a substantial intensive weight reduction most of the contestants on this program were hypometabolic and had regained some or all of the weight they had lost.. Persistent reduction of metabolic rate both during and after weight loss (i.e., adaptive thermogenesis) has been shown following even relatively small (10% or less) degrees of weight loss.2-4 This hypometabolic state is exacerbated by hyperphagia reflecting changes in pathways regulating appetite and energy balance (delayed satiation, increased hunger), interrupting communication between adipose (fat) cells, gastrointestinal (stomach, intestines, pancreas) cells, and the brain (increased responsiveness to food in ...
EGUCHI, Ricardo et al. Effects of the chronic exercise on the circulating concentration of leptin and ghrelin in rats With diet-induced obesity. Rev Bras Med Esporte [online]. 2008, vol.14, n.3, pp.182-187. ISSN 1517-8692. http://dx.doi.org/10.1590/S1517-86922008000300004.. Obesity is becoming one of the biggest worldwide epidemics. Therefore, knowing its etiology and mechanisms that regulate its development is of great relevance for its treatment. Thus, the aim of the present study was to evaluate the effects of obesity induced by the palatable hyperlipidic diet and of the chronic physical activity in rats, on the adiposity and the serum concentration of regulating hormones of the energy balance (leptin and ghrelin). 32 male Wistar rats were divided in four groups: Sedentary fed with chow diet (SN), sedentary fed with cafeteria diet (SC), trained fed with chow diet (TN) and trained fed with cafeteria diet (TC). The cafeteria diet led to a significant increase of central (RET) and visceral (EPI) ...
Экономические системы Латинской Америки процветают с 2003 года. Их ВВП, включая предварительный показатель за 2006 год, вырос на 17%, средний годовой темп роста составил 4,3%, а прирост ВВП на душу населения равен 12%. Несмотря на столь внушительные показатели, ситуация, когда Латинская Америка испытывает положительный экономический рост в течение четырех лет подряд, возникает лишь второй раз за 25 лет. Как долго продолжатся такие хорошие времена? Этот недавний рост произошел благодаря буму цен на сырьевые товары, который включил в себя не только ...
Prader-Willi syndrome (PWS) is characterized by neonatal hypotonia, developmental delay and hyperphagia/obesity and is caused by the absence of paternal contribution to chromosome 15q11-q13. Using induced pluripotent stem cell (iPSC) models of PWS, we previously discovered an epigenetic complex that is comprised of the zinc-finger protein ZNF274 and the SET domain bifurcated 1 (SETDB1) histone H3 lysine 9 (H3K9) methyltransferase and that silences the maternal alleles at the PWS locus. Here, we have knocked out ZNF274 and rescued the expression of silent maternal alleles in neurons derived from PWS iPSC lines, without affecting DNA methylation at the PWS-Imprinting Center (PWS-IC ...
The melanocortin-4 receptor (MC4R) is a member of the superfamily of seven transmembrane G-protein coupled receptors that are involved in multiple signal transduction pathways including the cAMP and MAPK signaling pathways. It is thought that the melanocortin system modulates energy expenditure and insulin sensitivity; activation of the MC4R results in the inhibition of c-Jun N-terminal kinase (JNK) activity and promotes insulin signaling. MC4R-null mice display maturity onset obesity characterized by hyperphagia, increased adiposity, hyperinsulinaemia and hyperleptinaemia, suggesting that like other obesity-linked genes such as FTO, PTER, and NPC1, MC4R is a potential candidate target for the treatment of obesity. ...
Todays daily food intake…. Argh today was not the best day! I woke up feeling all great and ready to face the scales, which I did. Then I wish I hadnt. I wasnt expecting a huge loss, but I was expecting a loss. I know from having done the 12WBT program before that you can still lose weight on the program even if you arent doing exercise. Not that I would encourage that kind of behaviour, because really, that is going to defeat the purpose of getting a healthy lifestyle happening and, well, you can only keep that up for so long before you wont lose weight just by eating healthy. But I had been slack and working myself up to get into the exercising.. So I got on the scales and what did I see? A little loss? No. A big loss? No.. A BIG FAT GAIN!!! Thats what I saw. 1.1kg of fat has been added to my body in only two days. I really cant explain it. I was quite devastated. Here was me coming along with my haha Ive been great for the last two days attitude and boy did I get kicked in the face. ...