scholarly journals Cold-induced hyperphagia requires AgRP-neuron activation in mice

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jennifer Deem ◽  
Chelsea L Faber ◽  
Christian Pedersen ◽  
Bao Anh Phan ◽  
Sarah A Larsen ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Cold Environment ◽  
Energy Demands ◽  
Acute Cold Exposure ◽  
Neuron Activation ◽  
Increase Food Intake

To maintain energy homeostasis during cold exposure, the increased energy demands of thermogenesis must be counterbalanced by increased energy intake. To investigate the neurobiological mechanisms underlying this cold-induced hyperphagia, we asked whether agouti-related peptide (AgRP) neurons are activated when animals are placed in a cold environment and, if so, whether this response is required for the associated hyperphagia. We report that AgRP-neuron activation occurs rapidly upon acute cold exposure, as do increases of both energy expenditure and energy intake, suggesting the mere perception of cold is sufficient to engage each of these responses. We further report that silencing of AgRP neurons selectively blocks the effect of cold exposure to increase food intake but has no effect on energy expenditure. Together, these findings establish a physiologically important role for AgRP neurons in the hyperphagic response to cold exposure.

scholarly journals Cold-induced hyperphagia requires AgRP neuron activation in mice

2020 ◽  
Author(s):  
Jennifer D. Deem ◽  
Chelsea L. Faber ◽  
Christian Pedersen ◽  
Bao Anh Phan ◽  
Sarah A. Larsen ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Cold Environment ◽  
Energy Demands ◽  
Acute Cold Exposure ◽  
Neuron Activation ◽  
Increase Food Intake

ABSTRACTTo maintain energy homeostasis during cold exposure, the increased energy demands of thermogenesis must be counterbalanced by increased energy intake. To investigate the neurobiological mechanisms underlying this cold-induced hyperphagia, we asked whether agouti-related peptide (AgRP) neurons are activated when animals are placed in a cold environment and, if so, whether this response is required for the associated hyperphagia. We report that AgRP-neuron activation occurs rapidly upon acute cold exposure, as do increases of both energy expenditure and energy intake, suggesting the mere perception of cold is sufficient to engage each of these responses. We further report that silencing of AgRP neurons selectively blocks the effect of cold exposure to increase food intake. Together, these findings establish a physiologically important role for AgRP neurons in the hyperphagic response to cold exposure.

scholarly journals Mild cold effects on hunger, food intake, satiety and skin temperature in humans

2016 ◽  
Vol 5 (2) ◽  
pp. 65-73 ◽  
Author(s):  
M Langeveld ◽  
C Y Tan ◽  
M R Soeters ◽  
S Virtue ◽  
G K Ambler ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Skin Temperature ◽  
Energy Intake ◽  
Cold Exposure ◽  
Vital Signs ◽  
Free Food ◽  
Cold Response ◽  
Hunger Sensation

Background Mild cold exposure increases energy expenditure and can influence energy balance, but at the same time it does not increase appetite and energy intake. Objective To quantify dermal insulative cold response, we assessed thermal comfort and skin temperatures changes by infrared thermography. Methods We exposed healthy volunteers to either a single episode of environmental mild cold or thermoneutrality. We measured hunger sensation and actual free food intake. After a thermoneutral overnight stay, five males and five females were exposed to either 18°C (mild cold) or 24°C (thermoneutrality) for 2.5 h. Metabolic rate, vital signs, skin temperature, blood biochemistry, cold and hunger scores were measured at baseline and for every 30 min during the temperature intervention. This was followed by an ad libitum meal to obtain the actual desired energy intake after cold exposure. Results We could replicate the cold-induced increase in REE. But no differences were detected in hunger, food intake, or satiety after mild cold exposure compared with thermoneutrality. After long-term cold exposure, high cold sensation scores were reported, which were negatively correlated with thermogenesis. Skin temperature in the sternal area was tightly correlated with the increase in energy expenditure. Conclusions It is concluded that short-term mild cold exposure increases energy expenditure without changes in food intake. Mild cold exposure resulted in significant thermal discomfort, which was negatively correlated with the increase in energy expenditure. Moreover, there is a great between-subject variability in cold response. These data provide further insights on cold exposure as an anti-obesity measure.

scholarly journals Arcuate nucleus and lateral hypothalamic CART neurons in the mouse brain exert opposing effects on energy expenditure

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Aitak Farzi ◽  
Jackie Lau ◽  
Chi Kin Ip ◽  
Yue Qi ◽  
Yan-Chuan Shi ◽  
...  
Keyword(s):  
Physical Activity ◽  
Food Intake ◽  
Energy Expenditure ◽  
Lateral Hypothalamus ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Neuronal Populations ◽  
Neuron Activation ◽  
Important Regulator ◽  
Opposing Effects

Cocaine- and amphetamine-regulated transcript (CART) is widely expressed in the hypothalamus and an important regulator of energy homeostasis; however, the specific contributions of different CART neuronal populations to this process are not known. Here, we show that depolarization of mouse arcuate nucleus (Arc) CART neurons via DREADD technology decreases energy expenditure and physical activity, while it exerts the opposite effects in CART neurons in the lateral hypothalamus (LHA). Importantly, when stimulating these neuronal populations in the absence of CART, the effects were attenuated. In contrast, while activation of CART neurons in the LHA stimulated feeding in the presence of CART, endogenous CART inhibited food intake in response to Arc CART neuron activation. Taken together, these results demonstrate anorexigenic but anabolic effects of CART upon Arc neuron activation, and orexigenic but catabolic effects upon LHA-neuron activation, highlighting the complex and nuclei-specific functions of CART in controlling feeding and energy homeostasis.

scholarly journals Severe protein deficiency induces hepatic expression and systemic level of FGF21 but inhibits its hypothalamic expression in growing rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joanna Moro ◽  
Catherine Chaumontet ◽  
Patrick C. Even ◽  
Anne Blais ◽  
Julien Piedcoq ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Dietary Protein ◽  
Protein Deficiency ◽  
Protein Diet ◽  
Growing Rats ◽  
Low Protein ◽  
Protein Diets

AbstractTo study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and to assess the role of FGF21 in the adaptation to a low protein diet. Thirty-six weanling rats were fed diets containing 3%, 5%, 8%, 12%, 15% and 20% protein for three weeks. Body weight, food intake, energy expenditure and metabolic parameters were followed throughout this period. The very low-protein diets (3% and 5%) induced a large decrease in body weight gain and an increase in energy intake relative to body mass. No gain in fat mass was observed because energy expenditure increased in proportion to energy intake. As expected, Fgf21 expression in the liver and plasma FGF21 increased with low-protein diets, but Fgf21 expression in the hypothalamus decreased. Under low protein diets (3% and 5%), the increase in liver Fgf21 and the decrease of Fgf21 in the hypothalamus induced an increase in energy expenditure and the decrease in the satiety signal responsible for hyperphagia. Our results highlight that when dietary protein decreases below 8%, the liver detects the low protein diet and responds by activating synthesis and secretion of FGF21 in order to activate an endocrine signal that induces metabolic adaptation. The hypothalamus, in comparison, responds to protein deficiency when dietary protein decreases below 5%.

Limits to sustained energy intake

2001 ◽  
Vol 204 (11) ◽  
pp. 1947-1956 ◽  
Author(s):  
M. S. Johnson ◽  
S. C. Thomson ◽  
J. R. Speakman
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Litter Size ◽  
Resting Metabolic Rate ◽  
Control Group ◽  
Lower Mass ◽  
Daily Food Intake ◽  
Energy Demands ◽  
Daily Food ◽  
Pregnancy And Lactation

SUMMARYTo determine whether mice were limited in their capacity to absorb energy during late lactation, we attempted to increase the energy burden experienced by a group of female mice during late lactation by mating them at the postpartum oestrus, hence combining the energy demands of pregnancy and lactation. These experimental mice were therefore concurrently pregnant and lactating in their first lactation, and were followed through a normal second lactation. In a control group, females also underwent two lactations but sequentially, with the second mating after the first litter had been weaned. Maternal mass and food intake were measured throughout the first lactation, second pregnancy and second lactation. Maternal resting metabolic rate (RMR) was measured prior to the first mating and then at the peak of both the first and second lactations. Litter size and litter mass were also measured throughout both lactations. In the first lactation, experimental mice had a lower mass-independent RMR (F1,88=5.15, P=0.026) and raised significantly heavier pups (t=2.77, d.f.=32, P=0.0093) than the control mice. Experimental mice delayed implantation at the start of the second pregnancy. The extent of the delay was positively related to litter size during the first lactation (F1,19=4.58, P=0.046) and negatively related to mean pup mass (F1,19=5.78, P=0.027) in the first lactation. In the second lactation, the experimental mice gave birth to more (t=2.75, d.f.=38, P=0.0092) and lighter (t=−5.01, d.f.=38, P<0.0001) pups than did the controls in their second lactation. Maternal asymptotic daily food intake of control mice in the second lactation was significantly higher (t=−4.39, d.f.=37, P=0.0001) than that of the experimental mice and higher than that of controls during their first lactation. Despite the added burden on the experimental females during their first lactation, there was no increase in their food intake, which suggested that they might be limited by their capacity to absorb energy. However, control females appeared to be capable of increasing their asymptotic food intake beyond the supposed limits estimated previously, suggesting that the previously established limit was not a fixed central limitation on food intake. As RMR increased in parallel with the increase in food intake during the second lactation of control mice, the sustained energy intake remained at around 7.0×RMR.

Nutrition: Macronutrient metabolism

2020 ◽  
pp. 1839-1854
Author(s):  
Keith N. Frayn ◽  
Rhys D. Evans
Keyword(s):  
Amino Acids ◽  
Food Intake ◽  
Energy Expenditure ◽  
Complex Systems ◽  
Metabolic Control ◽  
Energy Intake ◽  
Energy Supply ◽  
The Body ◽  
Daily Lives ◽  
Storage Pools

Food intake is sporadic and, in many cultures, occurs in three daily boluses. At the same time, energy expenditure is continuous and can vary to a large extent independently of the pattern of energy intake, although fixed or predictable demands (e.g. through occupation) means that in most persons food intake and energy expenditure are soon balanced. The body has developed complex systems that direct excess nutrients into storage pools; as they are needed, they also regulate the mobilization of nutrients from these pools. Carbohydrate, lipid, and protein (the latter a source of amino acids) are the three types of energy supply that are stored variably and assimilated from food each day. That we can carry on our daily lives without thinking about whether to store or mobilize fuels, and which to use, attests to the remarkable efficiency and refinement of these systems of metabolic control.

scholarly journals Gqα/G11α deficiency in dorsomedial hypothalamus leads to obesity resulting from decreased energy expenditure and impaired sympathetic nerve activity

2020 ◽  
Author(s):  
Eric A. Wilson ◽  
Hui Sun ◽  
Zhenzhong Cui ◽  
Marshal T. Jahnke ◽  
Mritunjay Pandey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
Energy Homeostasis ◽  
Dorsomedial Hypothalamus ◽  
Ambient Temperatures ◽  
Brown Adipose ◽  
Inhibit Food Intake ◽  
Specific Deletion

The G protein subunits Gqα and G11α (Gq/11α) couple receptors to phospholipase C, leading to increased intracellular calcium. In this study we investigated the consequences of Gq/11α deficiency in the dorsomedial hypothalamus (DMH), a critical site for the control of energy homeostasis. Mice with DMH-specific deletion of Gq/11α (DMHGq/11KO) were generated by stereotaxic injection of AAV-Cre-GFP into the DMH of Gqαflox/flox:G11α-/- mice. Compared to control mice that received DMH injection of AAV-GFP, DMHGq/11KO mice developed obesity associated with reduced energy expenditure without significant changes in food intake or physical activity. DMHGq/11KO mice showed no defects in the ability of the melanocortin agonist melanotan II to acutely stimulate energy expenditure or to inhibit food intake. At room temperature (22oC) DMHGq/11KO mice showed reduced sympathetic nervous system activity in brown adipose tissue (BAT) and heart, accompanied with decreased basal BAT Ucp1 gene expression and lower heart rates. These mice were cold intolerant when acutely exposed to cold (6oC for 5 hours) and had decreased cold-stimulated BAT Ucp1 gene expression. DMHGq/11KO mice also failed to adapt to gradually declining ambient temperatures and to develop adipocyte browning in inguinal white adipose tissue although their BAT Ucp1 was proportionally stimulated. Consistent with impaired cold-induced thermogenesis, the onset of obesity in DMHGq/11KO mice was significantly delayed when housed under thermoneutral conditions (30ºC). Thus, our results show that Gqα and G11α in the DMH are required for the control of energy homeostasis by stimulating energy expenditure and thermoregulation.

Analysis of energy expenditure at different ambient temperatures in mice lacking DGAT1

2003 ◽  
Vol 284 (1) ◽  
pp. E213-E218 ◽  
Author(s):  
Hubert C. Chen ◽  
Zuleika Ladha ◽  
Steven J. Smith ◽  
Robert V. Farese
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Ambient Temperature ◽  
Cold Environment ◽  
Normal Surface ◽  
Ambient Temperatures ◽  
Active Mechanism ◽  
Key Enzyme ◽  
Secondary Mechanism ◽  
Obesity Resistance

Mice lacking acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), a key enzyme in triglyceride synthesis, have increased energy expenditure and therefore are resistant to obesity. Because ambient temperature can significantly affect energy expenditure in mice, we undertook these studies to determine the effects of different ambient temperatures on energy expenditure, food intake, and thermoregulation in DGAT1-deficient [ Dgat1(−/−)] mice. Dgat1(−/−) mice had increased energy expenditure irrespective of changes in the ambient temperature. Although core temperature was normal, surface temperature was increased in Dgat1(−/−) mice, most likely reflecting an active mechanism to dissipate heat from increased thermogenesis. Dgat1(−/−) mice had increased food intake at baseline, and this hyperphagia became more pronounced upon exposure to cold. When fasted in a cold environment, Dgat1(−/−) mice developed hypothermia, which was associated with hypoglycemia. These results suggest that the hyperphagia in Dgat1(−/−) mice is a secondary mechanism that compensates for the increased utilization of fuel substrates. Our findings offer insights into the mechanisms of hyperphagia and increased energy expenditure in a murine model of obesity resistance.

scholarly journals What processes are involved in the appetite response to moderate increases in exercise-induced energy expenditure?

1999 ◽  
Vol 58 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Neil A. King
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Weak Coupling ◽  
Eating Behaviour ◽  
Tight Coupling ◽  
Living Situation ◽  
Energy Value ◽  
Exercise Induced ◽  
Response To Exercise

It is intuitive that an energy deficit induced by exercise induces an automatic increased drive for food (hunger and energy intake). However, the absence of a compensatory increase in energy intake (EI) in response to an exercise-induced increase in energy expenditure (EE) is now well documented. Thus, there is a weak coupling between exercise-induced increases in EE and EI. One paradox related to the phenomenon of a weak coupling between the exercise-induced EE and EI is the observation of a positive relationship between physical activity and food intake in the long-term free-living situation (i.e. tight coupling between EE and EI). It is possible, therefore, that a period of transition (uncoupling) occurs in the short-term, before a steady-state (coupling) condition is achieved. It is likely that a combination of physiological and behavioural adaptations occur in order to achieve a tight coupling between EE and EI. The precise physiological and behavioural changes that take place to obtain a new equilibrium (i.e. coupling between EE and EI) are still undetermined. The expectation that exercise-induced increases in EE should drive up hunger and food intake tends to be based on the concept of a strong coupling between physiology and behaviour. However, because of the individual's strong volitional control over eating behaviour, the psychological influences on the appetite response to exercise should not be undervalued. The psychological position of the individual (e.g. dietary restraint, food-related cognitions, reasons for exercising) could have a very strong influence on the food intake response to exercise. Misjudgements concerning the energy value of the food (EI) relative to the energy value of the exercise (EE) could be one possibility why exercise fails to be a successful method of weight loss for some individuals.

scholarly journals Endocrine factors in the hypothalamic regulation of food intake in females: a review of the physiological roles and interactions of ghrelin, leptin, thyroid hormones, oestrogen and insulin

2011 ◽  
Vol 24 (1) ◽  
pp. 132-154 ◽  
Author(s):  
V. Somogyi ◽  
A. Gyorffy ◽  
T. J. Scalise ◽  
D. S. Kiss ◽  
G. Goszleth ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Thyroid Hormones ◽  
Energy Homeostasis ◽  
The Body ◽  
Feedback Information ◽  
Hypothalamic Regulation ◽  
The Individual ◽  
Desire To Eat ◽  
The Brain

Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.

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