scholarly journals The regulation of body weight: lessons from the seasonal animal

2001 ◽  
Vol 60 (1) ◽  
pp. 127-134 ◽  
Author(s):  
Peter J. Morgan ◽  
Julian G. Mercer
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Homeostasis ◽  
Mutant Mouse ◽  
Neural Pathways ◽  
Control Mechanisms ◽  
Gene Deletions ◽  
Regulate Body Weight ◽  
Human Energy ◽  
Ingestive Behaviour

The hypothalamus is a major regulatory centre involved in the control of many important physiological axes. One of these axes is the regulation of ingestive behaviour. Recent work using a combination of genetic-mutant mouse models together with targeted gene deletions has contributed much to our understanding of how neural pathways of the hypothalamus are involved in the regulation of energy balance in animals. These pathways are also relevant to human energy homeostasis, as mutations in key genes are correlated with obesity. Many of the genes identified mediate the effects of leptin, and are therefore primarily involved in sensing and responding to peripheral signals. In seasonal animals, such as the Siberian hamster (Phodopus sungorus), there is evidence for a higher level of regulation. The systems involved regulate body weight around an apparent 'set-point' through the action of photoperiod via the neurohormone, melatonin. The ability to manipulate energy balance through photoperiod (and melatonin) in the seasonal-animal model offers novel opportunities to identify further fundamental aspects of the control mechanisms involved in the central control of energy homeostasis and body weight.

scholarly journals COMPARISON EFFECT OF CV 12, ST 36 AND ST 40 EA ON SHORT TERM ENERGY BALANCE REGULATION IN HIGH FAT DIET RAT

2017 ◽  
Vol 52 (3) ◽  
pp. 174
Author(s):  
Purwo Sri Rejeki ◽  
Harjanto Harjanto ◽  
Raden Argarini ◽  
Imam Subadi
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Energy Balance ◽  
High Fat Diet ◽  
Energy Homeostasis ◽  
Continuous Wave ◽  
Positive Control ◽  
Control Group ◽  
High Fat ◽  
Short Term

The aim of this study was to determine the comparative effects of EA (EA) on the CV12, ST36 and ST40 to weight gain prevention over the short-term regulation of energy balance. The study was conducted with a completely randomized design. Rats were divided into five groups: negative control group (no treatment, n=5), positive control (sham EA/back, n=5), EA CV 12 (n=6), EA ST 36 (n=6) and EA ST 40 (n=7). Rats were exposed to high-fat diet for two weeks and EA was simultaneously performed once daily, five days a week for two weeks with 2 Hz, for 10 minutes with continuous wave. Body weight, BMI, front limb circumference and rear were measured during study. Levels of blood glucose, cholesterol, triglycerides, LDL and HDL were measured at the end of the study; which reflects the short-term regulation of energy homeostasis. For weight loss, EA CV12, ST36 and ST40 group have lost weight significantly compared to the negative and positive control group. The ST40 group has a significant decrease than ST36 and CV12. The most significant decrease in BMI found in the ST40 group. EA did not affect blood glucose levels, but modulated blood lipid profile. In ST 40 group there was a significant decrease in cholesterol, LDL and triglycerides. EA at point ST 40 is potential in preventing increased body weight and BMI in rats exposed to high-fat diet compared to the CV 12 and ST 36. ST 40 is a point with a potential of lowering LDL and triglycerides serum so that it can play a role in the short term regulation of energy homeostasis but also in the prevention of dyslipidemia.

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

2010 ◽  
Vol 298 (3) ◽  
pp. E726-E734 ◽  
Author(s):  
Paulo José Forcina Martins ◽  
Marina Soares Marques ◽  
Sergio Tufik ◽  
Vânia D'Almeida
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Sleep Deprivation ◽  
Weight Control ◽  
Time Course ◽  
Energy Homeostasis ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Mrna Levels

Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25–35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.

Paraventricular Calcitonin Receptor Expressing Neurons Modulate Energy Homeostasis in Male Mice

Endocrinology ◽  
2021 ◽  
Author(s):  
Ian E Gonzalez ◽  
Julliana Ramirez-Matias ◽  
Chunxia Lu ◽  
Warren Pan ◽  
Allen Zhu ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Energy Homeostasis ◽  
Balance Control ◽  
Weight Maintenance ◽  
Abnormal Development ◽  
Calcitonin Receptor ◽  
Neuronal Populations ◽  
Treatment And Prevention

Abstract The paraventricular nucleus of the hypothalamus (PVH) is a heterogeneous collection of neurons that play important roles in modulating feeding and energy expenditure. Abnormal development or ablation of the PVH results in hyperphagic obesity and defects in energy expenditure whereas selective activation of defined PVH neuronal populations can suppress feeding and may promote energy expenditure. Here, we characterize the contribution of calcitonin receptor-expressing PVH neurons (CalcR PVH) to energy balance control. We used Cre-dependent viral tools delivered stereotaxically to the PVH of CalcR 2Acre mice to activate, silence and trace CalcR PVH neurons and determine their contribution to body weight regulation. Immunohistochemistry of fluorescently-labelled CalcR PVH neurons demonstrates that CalcR PVH neurons are largely distinct from several PVH neuronal populations involved in energy homeostasis; these neurons project to regions of the hindbrain that are implicated in energy balance control, including the nucleus of the solitary tract and the parabrachial nucleus. Acute activation of CalcR PVH neurons suppresses feeding without appreciably augmenting energy expenditure, whereas their silencing leads to obesity that may be due in part due to loss of PVH melanocortin-4 receptor (MC4R) signaling. These data show that CalcR PVH neurons are an essential component of energy balance neurocircuitry and their function is important for body weight maintenance. A thorough understanding of the mechanisms by which CalcR PVH neurons modulate energy balance might identify novel therapeutic targets for the treatment and prevention of obesity.

scholarly journals Effects of Naltrexone on Energy Balance and Hypothalamic Melanocortin Peptides in Male Mice Fed a High-Fat Diet

2019 ◽  
Vol 3 (3) ◽  
pp. 590-601 ◽  
Author(s):  
Sunil K Panigrahi ◽  
Kana Meece ◽  
Sharon L Wardlaw
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
High Fat ◽  
Melanocortin System ◽  
Endogenous Opioid ◽  
Processing Enzymes ◽  
Agouti Related Protein

Abstract The hypothalamic melanocortin system composed of proopiomelanocortin (POMC) and agouti-related protein (AgRP) neurons plays a key role in maintaining energy homeostasis. The POMC-derived peptides, α-MSH and β-EP, have distinct roles in this process. α-MSH inhibits food intake, whereas β-EP, an endogenous opioid, can inhibit POMC neurons and stimulate food intake. A mouse model was used to examine the effects of opioid antagonism with naltrexone (NTX) on Pomc and Agrp gene expression and POMC peptide processing in the hypothalamus in conjunction with changes in energy balance. There were clear stimulatory effects of NTX on hypothalamic Pomc in mice receiving low- and high-fat diets, yet only transient decreases in food intake and body weight gain were noted. The effects on Pomc expression were accompanied by an increase in POMC prohormone levels and a decrease in levels of the processed peptides α-MSH and β-EP. Arcuate expression of the POMC processing enzymes Pcsk1, Pcsk2, and Cpe was not altered by NTX, but expression of Prcp, an enzyme that inactivates α-MSH, increased after NTX exposure. NTX exposure also stimulated hypothalamic Agrp expression, but the effects of NTX on energy balance were not enhanced in Agrp-null mice. Despite clear stimulatory effects of NTX on Pomc expression in the hypothalamus, only modest transient decreases in food intake and body weight were seen. Effects of NTX on POMC processing, and possibly α-MSH inactivation, as well as stimulatory effects on AgRP neurons could mitigate the effects of NTX on energy balance.

Hypothalamic regulation of energy homeostasis when consuming diets of different energy concentrations: Comparison between Tibetan and Small-tailed Han sheep

2021 ◽  
pp. 1-25
Author(s):  
Xiaoping Jing ◽  
Yamin Guo ◽  
Allan Degen ◽  
Wenji Wang ◽  
Jingpeng Kang ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Energy Intake ◽  
Energy Homeostasis ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Positive Energy ◽  
Tibetan Sheep ◽  
Protein Expressions ◽  
Positive Energy Balance

Abstract Seasonal energy intake of Tibetan sheep on the harsh Qinghai-Tibetan Plateau (QTP) fluctuates greatly and is often well below maintenance requirements. The aim of this study was to gain insight into how the hypothalamus regulates energy homeostasis in Tibetan and Small-tailed Han sheep. We compared Tibetan and Small-tailed Han sheep (n=24 of each breed), which were offered one of four diets that differed in digestible energy (DE) densities: 8.21, 9.33, 10.45 and 11.57 MJ/kg dry matter. Sheep were weighed every two weeks, and it was assumed that the change in body weight reflected the change in energy balance. The arcuate nucleus of the hypothalamus in Tibetan sheep had greater protein expressions of neuropeptide Y (NPY) and agouti-related peptide (AgRP) when in negative energy balance, but lesser protein expressions of proopiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART) when in positive energy balance than Small-tailed Han sheep. As a result, Tibetan sheep had a lesser body weight (BW) loss when in negative energy balance and stored more energy and gained more BW when in positive energy balance than Small-tailed Han sheep with the same dietary intake. Moreover, in the hypothalamic AMPK regulation pathway, Tibetan sheep had greater AMPKα2 protein expression than Small-tailed Han sheep, which supported the premise of a better ability to regulate energy homeostasis and better growth performance. These differences in the hypothalamic NPY/AgRP, POMC/CART and AMPK pathways between breeds conferred an advantage to the Tibetan over Small-tailed Han sheep to cope with low energy intake on the harsh QTP.

scholarly journals SAT-LB102 Obesity Is Associated With Reduced Expression of the Anorexigenic Neuropeptide Nucleobindin-2/Nesfatin-1 in the Human Nucleus of the Solitary Tract

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Aristea Psilopanagioti ◽  
Maria Makrygianni ◽  
Sofia Nikou ◽  
Souzana Logotheti ◽  
Dionysios Chartoumpekis ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Locus Coeruleus ◽  
Energy Homeostasis ◽  
Inferior Olive ◽  
Normal Weight ◽  
Ingestive Behavior ◽  
Negative Regulator ◽  
Solitary Tract ◽  
Immunofluorescence Labeling

Abstract Introduction: Feeding is a complex behavior coordinated by interrelated forebrain, hypothalamic, and brainstem neuronal networks. Brainstem neurons constitute an important input for the neural circuitry integrating nutrient signals to control ingestive behavior. Orexigenic and anorexigenic neuropeptides act in concert to regulate energy balance. Data from animal models suggest that altered neuropeptidergic expression contributes to obesity. Nucleobindin-2/nesfatin-1, an appetite-suppressing neuropeptide and negative regulator of body weight, is reduced in the hypothalamus of mouse obesity models. In obese and overweight humans, we have recently reported decreased nucleobindin-2/nesfatin-1 immunoexpression in the lateral hypothalamic area, which is critically involved in appetite and metabolic regulation and has extensive connections with brainstem feeding circuits. Objective: The present study explored nucleobindin-2/nesfatin-1 localization pattern as well as the association between nucleobindin-2/nesfatin-1 protein expression and body weight in human brainstem nuclei. Methods: Sections of 20 human brainstems (13 males, 7 females; 8 normal weight, 6 overweight, 6 obese) were examined by means of immunohistochemistry and double immunofluorescence labeling. Results: Nucleobindin-2/nesfatin-1 widespread distribution was observed in various brainstem areas, including nuclei with well-defined roles in energy homeostasis and in autonomic and behavioral processes, such as the nucleus of the solitary tract, dorsal motor nucleus of vagus, area postrema, inferior olive, raphe nuclei, reticular formation, locus coeruleus, parabrachial nuclei, and pontine nuclei, and in Purkinje cells of the cerebellum. Interestingly, nucleobindin-2/nesfatin-1 immunofluorescence signal extensively localized in neuronal subpopulations expressing neuropeptide Y and cocaine- and amphetamine-regulated transcript (peptides known to exert potent actions on food intake and energy balance) in nucleus of the solitary tract, inferior olive, locus coeruleus, and dorsal raphe nucleus. Of note, nucleobindin-2/nesfatin-1 immunoexpression was significantly lower in obese than normal weight subjects in the nucleus of the solitary tract (p<0.05). Conclusions: These data provide for the first time neuroanatomical support for the potential role of nucleobindin-2/nesfatin-1 in human brainstem circuits controlling energy homeostasis. In nucleus of the solitary tract, a key integrator of nutrient state signals and a neural substrate of food reward-related processes, altered neurochemistry such as nucleobindin-2/nesfatin-1 deficiency may contribute to dysregulation of homeostatic and/or hedonic feeding behavior and ultimately to obesity.

scholarly journals The Role of Mediobasal Hypothalamic PACAP in the Control of Body Weight and Metabolism

Endocrinology ◽  
2021 ◽  
Vol 162 (4) ◽  
Author(s):  
Nadejda Bozadjieva-Kramer ◽  
Rachel A Ross ◽  
David Q Johnson ◽  
Henning Fenselau ◽  
David L Haggerty ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Energy Balance ◽  
Energy Homeostasis ◽  
Brain Area ◽  
Hypothalamic Nucleus ◽  
Multiple Time Scales ◽  
Multiple Time ◽  
Physiologic Mechanism ◽  
Brown Adipose

Abstract Body energy homeostasis results from balancing energy intake and energy expenditure. Central nervous system administration of pituitary adenylate cyclase activating polypeptide (PACAP) dramatically alters metabolic function, but the physiologic mechanism of this neuropeptide remains poorly defined. PACAP is expressed in the mediobasal hypothalamus (MBH), a brain area essential for energy balance. Ventromedial hypothalamic nucleus (VMN) neurons contain, by far, the largest and most dense population of PACAP in the medial hypothalamus. This region is involved in coordinating the sympathetic nervous system in response to metabolic cues in order to re-establish energy homeostasis. Additionally, the metabolic cue of leptin signaling in the VMN regulates PACAP expression. We hypothesized that PACAP may play a role in the various effector systems of energy homeostasis, and tested its role by using VMN-directed, but MBH encompassing, adeno-associated virus (AAVCre) injections to ablate Adcyap1 (gene coding for PACAP) in mice (Adcyap1MBHKO mice). Adcyap1MBHKO mice rapidly gained body weight and adiposity, becoming hyperinsulinemic and hyperglycemic. Adcyap1MBHKO mice exhibited decreased oxygen consumption (VO2), without changes in activity. These effects appear to be due at least in part to brown adipose tissue (BAT) dysfunction, and we show that PACAP-expressing cells in the MBH can stimulate BAT thermogenesis. While we observed disruption of glucose clearance during hyperinsulinemic/euglycemic clamp studies in obese Adcyap1MBHKO mice, these parameters were normal prior to the onset of obesity. Thus, MBH PACAP plays important roles in the regulation of metabolic rate and energy balance through multiple effector systems on multiple time scales, which highlight the diverse set of functions for PACAP in overall energy homeostasis.

scholarly journals Proopiomelanocortin and Energy Balance: Insights from Human and Murine Genetics

2004 ◽  
Vol 89 (6) ◽  
pp. 2557-2562 ◽  
Author(s):  
Anthony P. Coll ◽  
I. Sadaf Farooqi ◽  
Benjamin G. Challis ◽  
Giles S. H. Yeo ◽  
Stephen O’Rahilly
Keyword(s):  
Energy Balance ◽  
Energy Homeostasis ◽  
Skin Pigmentation ◽  
Biologically Active ◽  
Melanocortin System ◽  
Active Peptides ◽  
Adrenal Steroidogenesis ◽  
Human Energy ◽  
Biologically Active Peptides ◽  
Synthesis And Processing

Abstract Proopiomelanocortin (POMC) undergoes extensive and tissuespecific posttranslational processing to yield a range of biologically active peptides. Historically, the most clearly defined roles of these peptides are in the control of adrenal steroidogenesis by corticotroph-derived ACTH and skin pigmentation by αMSH. However, a rapidly expanding body of work has established that POMC-derived peptides synthesized in neurons of the hypothalamus play a central role in the control of energy homeostasis. We review how inherited abnormalities in POMC synthesis and processing and defects in the action of POMC-derived peptides in both humans and mice have helped shape our current understanding of the importance of the melanocortin system in human energy balance.

scholarly journals NKX2.1 is critical for melanocortin neuron identity, hypothalamic Pomc expression and body weight

2018 ◽  
Author(s):  
Daniela P. Orquera ◽  
M. Belén Tavella ◽  
Flavio S. J. de Souza ◽  
Sofía Nasif ◽  
Malcolm J. Low ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Body Weight ◽  
Transcription Factors ◽  
Energy Balance ◽  
Mutant Mouse ◽  
Terminal Differentiation ◽  
Mediobasal Hypothalamus ◽  
Transcriptional Enhancer ◽  
Enhancer Activity ◽  
Early Establishment

AbstractFood intake is tightly regulated by a group of neurons present in the mediobasal hypothalamus which activate satiety by releasing Pomc-encoded melanocortins. Although the relevance of hypothalamic POMC neurons in the regulation of energy balance and body weight is well appreciated, little is known about the transcription factors that establish their cellular fate, terminal differentiation and phenotypic maintenance. Here, we report that the transcription factor Nkx2.1 activates hypothalamic Pomc expression from early development to adulthood by binding to conserved canonical NKX motifs present in the neuronal Pomc enhancers nPE1 and nPE2. Transgenic and mutant mouse studies showed that the NKX motifs present in nPE1 and nPE2 are essential for their transcriptional enhancer activity. Early inactivation of Nkx2.1 in the ventral hypothalamus prevented the onset of Pomc expression and selective Nkx2.1 ablation from POMC neurons impaired Pomc expression and increased body weight and adiposity. These results demonstrate that NKX2.1 is critical in the early establishment of arcuate melanocortin neurons and the regulation of Pomc expression and body weight in adulthood.

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