scholarly journals Neurotensin neurons in the central extended amygdala control energy balance

2021 ◽  
Author(s):  
Alessandro Furlan ◽  
Alberto Corona ◽  
Sara Boyle ◽  
Radhashree Sharma ◽  
Rachel Rubino ◽  
...  
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Neuronal Population ◽  
Dependent Manner ◽  
Palatable Food ◽  
Extended Amygdala ◽  
Diet Induced Obesity ◽  
Sedentary Life Style ◽  
Metabolic Dysfunctions

Overeating and a sedentary life style are major causes of obesity and related metabolic disorders. Identification of the neurobiological processes that regulate energy balance will facilitate development of interventions for these disorders. Here we show that the Neurotensin-expressing neurons in the mouse IPAC (IPACNts), a nucleus of the central extended amygdala, bidirectionally coordinate hedonic feeding and physical activity, thereby regulating energy balance, metabolic processes and bodyweight. IPACNts are preferentially activated by consumption of highly palatable food or exposure to its taste and smell. Activating IPACNts promotes food intake in a palatability-dependent manner and decreases locomotion. Conversely, inhibiting IPACNts selectively reduces palatable food intake and dramatically enhances physical activity and energy expenditure, and in parallel stimulates physiological responses that oppose diet-induced obesity and metabolic dysfunctions. Thus, a single neuronal population, Neurotensin-expressing neurons in the IPAC, acts to control obesogenic and leptogenic processes by synergistically coordinating energy intake and expenditure with metabolism.

Central administration of metformin into the third ventricle of C57BL/6 mice decreases meal size and number and activates hypothalamic S6 kinase

2013 ◽  
Vol 305 (5) ◽  
pp. R499-R505 ◽  
Author(s):  
Hyun-Ju Kim ◽  
Eun-Young Park ◽  
Mi-Jeong Oh ◽  
Sung-Soo Park ◽  
Kyung-Ho Shin ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Third Ventricle ◽  
Meal Size ◽  
Dependent Manner ◽  
Central Administration ◽  
Mediobasal Hypothalamus ◽  
S6 Kinase ◽  
The Third

Administration of metformin is known to reduce both body weight and food intake. Although the hypothalamus is recognized as a critical regulator of energy balance and body weight, there is currently no evidence for an effect of metformin in the hypothalamus. Therefore, we sought to determine the central action of metformin on energy balance and body weight, as well as its potential involvement with key hypothalamic energy sensors, including adenosine monophosphate-activated protein kinase (AMPK) and S6 kinase (S6K). We used meal pattern analysis and a conditioned taste aversion (CTA) test and measured energy expenditure in C56BL/6 mice administered metformin (0, 7.5, 15, or 30 μg) into the third ventricle (I3V). Furthermore, we I3V-administered either control or metformin (30 μg) and compared the phosphorylation of AMPK and S6K in the mouse mediobasal hypothalamus. Compared with the control, I3V administration of metformin decreased body weight and food intake in a dose-dependent manner and did not result in CTA. Furthermore, the reduction in food intake induced by I3V administration of metformin was accomplished by decreases in both nocturnal meal size and number. Compared with the control, I3V administration of metformin significantly increased phosphorylation of S6K at Thr389 and AMPK at Ser485/491 in the mediobasal hypothalamus, while AMPK phosphorylation at Thr172 was not significantly altered. Moreover, I3V rapamycin pretreatment restored the metformin-induced anorexia and weight loss. These results suggest that the reduction in food intake induced by the central administration of metformin in the mice may be mediated by activation of S6K pathway.

scholarly journals Effects of continuous positive airway pressure on energy balance regulation: a systematic review

2016 ◽  
Vol 48 (6) ◽  
pp. 1640-1657 ◽  
Author(s):  
Ari Shechter
Keyword(s):  
Physical Activity ◽  
Systematic Review ◽  
Weight Loss ◽  
Energy Metabolism ◽  
Continuous Positive Airway Pressure ◽  
Energy Balance ◽  
Food Intake ◽  
Metabolic Rate ◽  
Airway Pressure ◽  
Positive Airway Pressure

Obesity is both a cause and a possible consequence of obstructive sleep apnoea (OSA), as OSA seems to affect parameters involved in energy balance regulation, including food intake, hormonal regulation of hunger/satiety, energy metabolism and physical activity. It is known that weight loss improves OSA, yet it remains unclear why continuous positive airway pressure (CPAP) often results in weight gain.The goal of this systematic review is to explore if and how CPAP affects the behaviour and/or metabolism involved in regulating energy balance.CPAP appears to correct for a hormonal profile characterised by abnormally high leptin and ghrelin levels in OSA, by reducing the circulating levels of each. This is expected to reduce excess food intake. However, reliable measures of food intake are lacking, and not yet sufficient to make conclusions. Although studies are limited and inconsistent, CPAP may alter energy metabolism, with reports of reductions in resting metabolic rate or sleeping metabolic rate. CPAP appears to not have an appreciable effect on altering physical activity levels. More work is needed to characterise how CPAP affects energy balance regulation.It is clear that promoting CPAP in conjunction with other weight loss approaches should be used to encourage optimal outcomes in OSA patients.

scholarly journals Developmental programming of energy balance regulation: is physical activity more ‘programmable’ than food intake?

2015 ◽  
Vol 75 (1) ◽  
pp. 73-77 ◽  
Author(s):  
Shaoyu Zhu ◽  
Jesse Eclarinal ◽  
Maria S. Baker ◽  
Ge Li ◽  
Robert A. Waterland
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Environmental Influences ◽  
Female Offspring ◽  
Developmental Programming ◽  
Critical Periods ◽  
Early Postnatal Development ◽  
Underlying Mechanisms

Extensive human and animal model data show that environmental influences during critical periods of prenatal and early postnatal development can cause persistent alterations in energy balance regulation. Although a potentially important factor in the worldwide obesity epidemic, the fundamental mechanisms underlying such developmental programming of energy balance are poorly understood, limiting our ability to intervene. Most studies of developmental programming of energy balance have focused on persistent alterations in the regulation of energy intake; energy expenditure has been relatively underemphasised. In particular, very few studies have evaluated developmental programming of physical activity. The aim of this review is to summarise recent evidence that early environment may have a profound impact on establishment of individual propensity for physical activity. Recently, we characterised two different mouse models of developmental programming of obesity; one models fetal growth restriction followed by catch-up growth, and the other models early postnatal overnutrition. In both studies, we observed alterations in body-weight regulation that persisted to adulthood, but no group differences in food intake. Rather, in both cases, programming of energy balance appeared to be due to persistent alterations in energy expenditure and spontaneous physical activity (SPA). These effects were stronger in female offspring. We are currently exploring the hypothesis that developmental programming of SPA occurs via induced sex-specific alterations in epigenetic regulation in the hypothalamus and other regions of the central nervous system. We will summarise the current progress towards testing this hypothesis. Early environmental influences on establishment of physical activity are likely an important factor in developmental programming of energy balance. Understanding the fundamental underlying mechanisms in appropriate animal models will help determine whether early life interventions may be a practical approach to promote physical activity in man.

scholarly journals A Negative Energy Balance Is Associated with Metabolic Dysfunctions in the Hypothalamus of a Humanized Preclinical Model of Alzheimer’s Disease, the 5XFAD Mouse

2021 ◽  
Vol 22 (10) ◽  
pp. 5365
Author(s):  
Antonio J. López-Gambero ◽  
Cristina Rosell-Valle ◽  
Dina Medina-Vera ◽  
Juan Antonio Navarro ◽  
Antonio Vargas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Mouse Model ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
5Xfad Mouse ◽  
5Xfad Mice ◽  
Metabolic Dysfunctions

Increasing evidence links metabolic disorders with neurodegenerative processes including Alzheimer’s disease (AD). Late AD is associated with amyloid (Aβ) plaque accumulation, neuroinflammation, and central insulin resistance. Here, a humanized AD model, the 5xFAD mouse model, was used to further explore food intake, energy expenditure, neuroinflammation, and neuroendocrine signaling in the hypothalamus. Experiments were performed on 6-month-old male and female full transgenic (Tg5xFAD/5xFAD), heterozygous (Tg5xFAD/-), and non-transgenic (Non-Tg) littermates. Although histological analysis showed absence of Aβ plaques in the hypothalamus of 5xFAD mice, this brain region displayed increased protein levels of GFAP and IBA1 in both Tg5xFAD/- and Tg5xFAD/5xFAD mice and increased expression of IL-1β in Tg5xFAD/5xFAD mice, suggesting neuroinflammation. This condition was accompanied by decreased body weight, food intake, and energy expenditure in both Tg5xFAD/- and Tg5xFAD/5xFAD mice. Negative energy balance was associated with altered circulating levels of insulin, GLP-1, GIP, ghrelin, and resistin; decreased insulin and leptin hypothalamic signaling; dysregulation in main metabolic sensors (phosphorylated IRS1, STAT5, AMPK, mTOR, ERK2); and neuropeptides controlling energy balance (NPY, AgRP, orexin, MCH). These results suggest that glial activation and metabolic dysfunctions in the hypothalamus of a mouse model of AD likely result in negative energy balance, which may contribute to AD pathogenesis development.

Are the proposed limits of energy intake:basal metabolic rate and dietary nitrogen:urinary nitrogen ratios suitable for validation of food intake?

2001 ◽  
Vol 85 (6) ◽  
pp. 725-731 ◽  
Author(s):  
Claudia P. Sánchez-Castillo ◽  
Michael Franklin ◽  
Geraldine McNeill ◽  
María de Lourdes Solano ◽  
Shelagh Bonner ◽  
...  
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Mexico City ◽  
Activity Level ◽  
Mexican Women ◽  
Urine Collection ◽  
Aminobenzoic Acid ◽  
Approximate Relationship ◽  
Activity Diary

The validity of 7 d weighed records of diet obtained for pre-menopausal Mexican women was assessed by two independent methods: the energy intake:BMR (EI:BMR) and the dietary N:urinary N (DN:UN). For the latter, complete urine collections are required and completeness was assessed from measurements of para-aminobenzoic acid (PABA) excretion. There were forty-six adult female subjects in the study, thirty-four were from Mexico City and twelve were from a rural population in the Central Highlands, Mexico. However, data were rejected from five urban women for whom the PABA excretion data suggested incomplete urine collection on four or more days. BMR was measured with Oxylog portable O2 consumption meters, and physical activity level was assessed from a self-completed activity diary. An approximate relationship between the EI:BMR ratio and the DN:UN ratio suggested that the rejection limits on the EI:BMR ratio recommended by are wider than the limits on the DN:UN ratio recommended by . Using the recommended cut-off points for EI:BMR but wider limits for DN:UN, twenty-one and twenty-five women respectively had acceptable intake records by the two methods, and sixteen of them by both methods. In conclusion the modification of the DN:UN limits to 0.92 and 1.70 to set acceptable intake values makes the use of measurements of N and energy balance comparable. Urine values with PABA recoveries greater than 100±15 % should be rejected, as should UN values validated by less than 3 d.

scholarly journals Cross talk between physical activity and appetite control: does physical activity stimulate appetite?

2003 ◽  
Vol 62 (3) ◽  
pp. 651-661 ◽  
Author(s):  
J. E. Blundell ◽  
R. J. Stubbs ◽  
D. A. Hughes ◽  
S. Whybrow ◽  
N. A. King
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Negative Energy ◽  
Positive Energy ◽  
Exact Nature ◽  
Appetite Control ◽  
Men And Women ◽  
The Impact

Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control. There is, however, no evidence for such an immediate or automatic effect. Short (1–2 d)-term and medium (7–16 d)-term studies demonstrate that men and women can tolerate substantial negative energy balances of ≤4MJ energy cost/d when performing physical activity programmes. Consequently, the immediate effect of taking up exercise is weight loss (although this outcome is sometimes difficult to assess due to changes in body composition or fluid compartmentalization). However, subsequently food intake begins to increase in order to provide compensation for about 30% of the energy expended in activity. This compensation (up to 16 d) is partial and incomplete. Moreover, subjects separate into compensators and non-compensators. The exact nature of these differences in compensation and whether it is actually reflective of non-compliance with protocols is yet to be determined. Some subjects (men and women) performing activity with a cost of ≤4 MJ/d for 14 d, show no change in daily energy intake. Conversely, it can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure. Consequently, this situation creates a substantial positive energy balance accompanied by weight gain. The next stage is to further characterize the compensators and non-compensators, and to identify the mechanisms (physiological or behavioural) that are responsible for the rate of compensation and its limits.

scholarly journals Central Administration of Ghrelin and Agouti-Related Protein (83–132) Increases Food Intake and Decreases Spontaneous Locomotor Activity in Rats

Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4645-4652 ◽  
Author(s):  
Mads Tang-Christensen ◽  
Niels Vrang ◽  
Sylvia Ortmann ◽  
Martin Bidlingmaier ◽  
Tamas L. Horvath ◽  
...  
Keyword(s):  
Physical Activity ◽  
Locomotor Activity ◽  
Food Intake ◽  
Current Model ◽  
Peptide Hormone ◽  
Dependent Manner ◽  
Central Administration ◽  
Related Protein ◽  
Agouti Related Protein

Abstract Ghrelin was recently identified as an endogenous ligand of the GH secretagogue receptor. The novel peptide hormone is produced by gastric A-like cells, and circulating levels rise before feeding, suggestive of ghrelin as an endogenous hunger factor. ghrelin stimulates food intake and promotes adiposity after peripheral or central administration, likely by activating hypothalamic neurons expressing the orexigenic neuropeptides neuropeptide Y (NPY) and agouti-related protein (AGRP). To examine whether ghrelin-induced feeding resembles NPY and AGRP [AGRP fragment (83–132)] induced orexia, we compared the short- and long-term orexigenic capacity of the three peptides. A single intracerebroventricular injection of ghrelin (0.2, 1.0, and 5.0 μg) increased food intake in a dose-dependent manner. A prolonged and uncompensated increase in feeding was seen after the highest dose of ghrelin. The prolonged effects on feeding (+72 h) closely resembled those of AGRP (83–132) but not NPY. Surprisingly, ghrelin injections reduced overall locomotor activity by 20% during the first 24-h observation period. AGRP (83–132) had similar effects on locomotor behavior, whereas NPY had no effect. In summary, ghrelin causes long-term increases of food intake and, like AGRP, plays a previously unknown role as a suppressor of spontaneous physical activity. Expanding the current model of food intake control to include mechanisms regulating physical activity may promote our understanding of two major etiological factors causing obesity.

scholarly journals Endocannabinoids and the Gut-Brain Control of Food Intake and Obesity

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1214
Author(s):  
Nicholas V. DiPatrizio
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Cannabinoid Receptors ◽  
Afferent Neurons ◽  
Palatable Food ◽  
Diet Induced Obesity ◽  
Gut Epithelium ◽  
Vagal Afferent ◽  
The Impact ◽  
Upper Gastrointestinal

Gut-brain signaling controls food intake and energy homeostasis, and its activity is thought to be dysregulated in obesity. We will explore new studies that suggest the endocannabinoid (eCB) system in the upper gastrointestinal tract plays an important role in controlling gut-brain neurotransmission carried by the vagus nerve and the intake of palatable food and other reinforcers. A focus will be on studies that reveal both indirect and direct interactions between eCB signaling and vagal afferent neurons. These investigations identify (i) an indirect mechanism that controls nutrient-induced release of peptides from the gut epithelium that directly interact with corresponding receptors on vagal afferent neurons, and (ii) a direct mechanism via interactions between eCBs and cannabinoid receptors expressed on vagal afferent neurons. Moreover, the impact of diet-induced obesity on these pathways will be considered.

scholarly journals The Effects of Erythropoietin Dose Titration during High-Fat Diet-Induced Obesity

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Amanda Foskett ◽  
Mawadda Alnaeeli ◽  
Li Wang ◽  
Ruifeng Teng ◽  
Constance T. Noguchi
Keyword(s):  
Physical Activity ◽  
Body Weight ◽  
Food Intake ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
High Fat Diet ◽  
Metabolic Effects ◽  
High Fat ◽  
Diet Induced Obesity

Erythropoietin (Epo) is a pleotropic cytokine with several nonhematopoietic tissue effects. High-dose Epo treatment-mediated effects on body weight, fat mass and glucose tolerance have recently been reported, thus extending its pleotropic effects to fat and glucose metabolism. However, the exact dose range of Epo treatment required for such effects remains unidentified to date. We investigated Epo dosage effect (up to 1000 U/kg) on hematocrit, body weight, body composition, glucose metabolism, food intake, and physical activity, during high-fat diet-induced obesity. We report that Epo doses (1000, 600, 300, and 150 U/kg) significantly reduced body weight gain and fat mass, while, only Epo doses of 300 U/kg and higher significantly affected glucose tolerance. None of the tested Epo doses showed any detectable effects on food intake, and only 1000 U/kg dose significantly increased physical activity, suggesting that these parameters may only be partially responsible for the metabolic effects of Epo treatment.

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