scholarly journals What Makes Mice Fat? How the Brain Controls Energy Balance

PLoS Biology ◽  
2005 ◽  
Vol 3 (12) ◽  
pp. e438
Keyword(s):  
Energy Balance ◽  
The Brain

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

Insulin in the Brain: A Hormonal Regulator of Energy Balance*

1992 ◽  
Vol 13 (3) ◽  
pp. 387-414 ◽  
Author(s):  
MICHAEL W. SCHWARTZ ◽  
DIANNE P. FIGLEWICZ ◽  
DENIS G. BASKIN ◽  
STEPHEN C. WOODS ◽  
DANIEL PORTE
Keyword(s):  
Energy Balance ◽  
The Brain

Insulin in the brain: a hormonal regulator of energy balance

1992 ◽  
Vol 13 (3) ◽  
pp. 387-414 ◽  
Author(s):  
M. W. Schwartz
Keyword(s):  
Energy Balance ◽  
The Brain

scholarly journals AMPK in the brain: its roles in energy balance and neuroprotection

2009 ◽  
Vol 109 ◽  
pp. 17-23 ◽  
Author(s):  
Gabriele V. Ronnett ◽  
Santosh Ramamurthy ◽  
Amy M. Kleman ◽  
Leslie E. Landree ◽  
Susan Aja
Keyword(s):  
Energy Balance ◽  
The Brain

Differential effects of fasting and leptin on proopiomelanocortin peptides in the arcuate nucleus and in the nucleus of the solitary tract

2007 ◽  
Vol 292 (5) ◽  
pp. E1348-E1357 ◽  
Author(s):  
Mario Perello ◽  
Ronald C. Stuart ◽  
Eduardo A. Nillni
Keyword(s):  
Energy Balance ◽  
Arcuate Nucleus ◽  
Transcriptional Level ◽  
Solitary Tract ◽  
Energy Status ◽  
Melanocyte Stimulating Hormone ◽  
Pomc Mrna ◽  
Induced Changes ◽  
The Brain ◽  
Processing Mechanism

The α-melanocyte-stimulating hormone (α-MSH), derived from proopiomelanocortin (POMC), is generated by a posttranslational processing mechanism involving the prohormone convertases (PCs) PC1/3 and PC2. In the brain, α-MSH is produced in the arcuate nucleus (ARC) of the hypothalamus and in the nucleus of the solitary tract (NTS) of the medulla. This peptide is key in controlling energy balance, as judged by changes observed at transcriptional level. However, little information is available regarding the biosynthesis of the precursor POMC and the production of its processed peptides during feeding, fasting, and fasting plus leptin in the ARC compared with the NTS in conjunction with the PC activity. In this study we found that, in the ARC, pomc mRNA, POMC-derived peptides, and PC1/3 all decreased during fasting, and administration of leptin reversed these effects. In contrast, in the NTS, where there is a large amount of a 28.1-kDa peptide similar in size to POMC, the 28.1-kDa peptide and other POMC-derived peptides, including α-MSH, were further accumulated in fasting conditions, whereas pomc mRNA decreased. These changes were not reversed by leptin. We also observed that, during fasting, PC2 levels decreased in the NTS. These data suggest that, in the NTS, fasting induced changes in POMC biosynthesis, and processing is independent of leptin. These observations indicate that changes in energy status affect POMC in the brain in a tissue-specific manner. This represents a novel aspect in the regulation of energy balance and may have implications in the pathophysiology of obesity.

Effects of intracerebroventricular and intra-accumbens melanin-concentrating hormone agonism on food intake and energy expenditure

2009 ◽  
Vol 296 (3) ◽  
pp. R469-R475 ◽  
Author(s):  
Benjamin Guesdon ◽  
Éric Paradis ◽  
Pierre Samson ◽  
Denis Richard
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Third Ventricle ◽  
Substrate Oxidation ◽  
Nucleus Accumbens Shell ◽  
Experimental Conditions ◽  
Male Wistar Rats ◽  
Melanin Concentrating Hormone ◽  
The Brain

The brain melanin-concentrating hormone (MCH) system represents an anabolic system involved in energy balance regulation through influences exerted on the homeostatic and nonhomeostatic controls of food intake and energy expenditure. The present study was designed to further delineate the effect of the MCH system on energy balance regulation by assessing the actions of the MCH receptor 1 (MCHR1) agonism on both food intake and energy expenditure after intracerebroventricular (third ventricle) and intra-nucleus-accumbens-shell (intraNAcSH) injections of a MCHR1 agonist. Total energy expenditure and substrate oxidation were assessed following injections in male Wistar rats using indirect calorimetry. Food intake was also measured. Pair-fed groups were added to evaluate changes in thermogenesis that would occur regardless of the meal size and its thermogenic response. Using such experimental conditions, we were able to demonstrate that acute MCH agonism in the brain, besides its orexigenic effect, induced a noticeable change in the utilization of the main metabolic fuels. In pair-fed animals, MCH significantly reduced lipid oxidation when it was injected in the third ventricle. Such an effect was not observed following the injection of MCH in the NAcSH, where MCH nonetheless strongly stimulated appetite. The present results further delineate the influence of MCH on energy expenditure and substrate oxidation while confirming the key role of the NAcSH in the effects of the MCH system on food intake.

scholarly journals Deletion of the Brain-Specific α and δ Isoforms of Adapter Protein SH2B1 Protects Mice From Obesity

2020 ◽  
Author(s):  
Jessica L. Cote ◽  
Lawrence S. Argetsinger ◽  
Anabel Flores ◽  
Alan C. Rupp ◽  
Joel M. Cline ◽  
...  
Keyword(s):  
Energy Balance ◽  
Adapter Protein ◽  
Wild Type ◽  
Leptin Sensitivity ◽  
High Fat Diets ◽  
Independent Mechanism ◽  
Alternatively Spliced ◽  
Fat Diets ◽  
The Brain ◽  
Inactivating Mutations

Mice lacking SH2B1 and humans with inactivating mutations of SH2B1 display severe obesity and insulin resistance. SH2B1 is an adapter protein that is recruited to the receptors of multiple hormones and neurotrophic factors. Of the four known alternatively-spliced SH2B1<i> </i>isoforms<i>,</i> SH2B1b and SH2B1g exhibit ubiquitous expression, whereas SH2B1a and SH2B1d are essentially restricted to the brain. To understand the roles for SH2B1a and SH2B1d in energy balance and glucose metabolism, we generated mice lacking these brain-specific isoforms (adKO mice). adKO mice exhibit decreased food intake, protection from weight gain on standard and high fat diets, and an adiposity-dependent improvement in glucose homeostasis. SH2B1 has been suggested to impact energy balance via the modulation of leptin action. However, adKO mice exhibit leptin sensitivity that is similar to that of wild-type mice by multiple measures. Thus, decreasing the abundance of SH2B1a and/or SH2B1d relative to the other SH2B1 isoforms likely shifts energy balance towards a lean phenotype via a primarily leptin-independent mechanism. Our findings suggest that the different alternatively-spliced isoforms of SH2B1 perform different functions <i>in</i> <i>vivo</i>. <br>

Glucagon Regulates Energy Balance via FGF-21 Signaling in the Brain

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1806-P
Author(s):  
SHELLY NASON ◽  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
JODI PAUL ◽  
BRIAN FINAN ◽  
...  
Keyword(s):  
Energy Balance ◽  
The Brain
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