The Regulation of Energy Balance by the Central Nervous System

2005 ◽  
Vol 28 (1) ◽  
pp. 25-38 ◽  
Author(s):  
Karine Proulx ◽  
Randy J. Seeley
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
The Central Nervous System

scholarly journals Tachykinin-1 in the Central Nervous System Regulates Adiposity in Rodents

Endocrinology ◽  
2015 ◽  
Vol 156 (5) ◽  
pp. 1714-1723 ◽  
Author(s):  
Chitrang Trivedi ◽  
Xiaoye Shan ◽  
Yi-Chun Loraine Tung ◽  
Dhiraj Kabra ◽  
Jenna Holland ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
Mass Gain ◽  
Neural System ◽  
Negative Energy ◽  
Microarray Gene Expression ◽  
Ghrelin Receptor ◽  
Ovariectomized Mice ◽  
The Central Nervous System

Ghrelin is a circulating hormone that targets the central nervous system to regulate feeding and adiposity. The best-characterized neural system that mediates the effects of ghrelin on energy balance involves the activation of neuropeptide Y/agouti-related peptide neurons, expressed exclusively in the arcuate nucleus of the hypothalamus. However, ghrelin receptors are expressed in other neuronal populations involved in the control of energy balance. We combined laser capture microdissection of several nuclei of the central nervous system expressing the ghrelin receptor (GH secretagoge receptor) with microarray gene expression analysis to identify additional neuronal systems involved in the control of central nervous system-ghrelin action. We identified tachykinin-1 (Tac1) as a gene negatively regulated by ghrelin in the hypothalamus. Furthermore, we identified neuropeptide k as the TAC1-derived peptide with more prominent activity, inducing negative energy balance when delivered directly into the brain. Conversely, loss of Tac1 expression enhances the effectiveness of ghrelin promoting fat mass gain both in male and in female mice and increases the susceptibility to diet-induced obesity in ovariectomized mice. Taken together, our data demonstrate a role TAC1 in the control energy balance by regulating the levels of adiposity in response to ghrelin administration and to changes in the status of the gonadal function.

scholarly journals Gastrointestinal hormones regulating appetite

2006 ◽  
Vol 361 (1471) ◽  
pp. 1187-1209 ◽  
Author(s):  
Owais Chaudhri ◽  
Caroline Small ◽  
Steve Bloom
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
Food Intake ◽  
Gastrointestinal Hormones ◽  
Gut Hormones ◽  
Gut Peptides ◽  
Appetite Control ◽  
Local Effects ◽  
The Central Nervous System

The role of gastrointestinal hormones in the regulation of appetite is reviewed. The gastrointestinal tract is the largest endocrine organ in the body. Gut hormones function to optimize the process of digestion and absorption of nutrients by the gut. In this capacity, their local effects on gastrointestinal motility and secretion have been well characterized. By altering the rate at which nutrients are delivered to compartments of the alimentary canal, the control of food intake arguably constitutes another point at which intervention may promote efficient digestion and nutrient uptake. In recent decades, gut hormones have come to occupy a central place in the complex neuroendocrine interactions that underlie the regulation of energy balance. Many gut peptides have been shown to influence energy intake. The most well studied in this regard are cholecystokinin (CCK), pancreatic polypeptide, peptide YY, glucagon-like peptide-1 (GLP-1), oxyntomodulin and ghrelin. With the exception of ghrelin, these hormones act to increase satiety and decrease food intake. The mechanisms by which gut hormones modify feeding are the subject of ongoing investigation. Local effects such as the inhibition of gastric emptying might contribute to the decrease in energy intake. Activation of mechanoreceptors as a result of gastric distension may inhibit further food intake via neural reflex arcs. Circulating gut hormones have also been shown to act directly on neurons in hypothalamic and brainstem centres of appetite control. The median eminence and area postrema are characterized by a deficiency of the blood–brain barrier. Some investigators argue that this renders neighbouring structures, such as the arcuate nucleus of the hypothalamus and the nucleus of the tractus solitarius in the brainstem, susceptible to influence by circulating factors. Extensive reciprocal connections exist between these areas and the hypothalamic paraventricular nucleus and other energy-regulating centres of the central nervous system. In this way, hormonal signals from the gut may be translated into the subjective sensation of satiety. Moreover, the importance of the brain–gut axis in the control of food intake is reflected in the dual role exhibited by many gut peptides as both hormones and neurotransmitters. Peptides such as CCK and GLP-1 are expressed in neurons projecting both into and out of areas of the central nervous system critical to energy balance. The global increase in the incidence of obesity and the associated burden of morbidity has imparted greater urgency to understanding the processes of appetite control. Appetite regulation offers an integrated model of a brain–gut axis comprising both endocrine and neurological systems. As physiological mediators of satiety, gut hormones offer an attractive therapeutic target in the treatment of obesity.

NPY ablation in C57BL/6 mice leads to mild obesity and to an impaired refeeding response to fasting

2003 ◽  
Vol 284 (6) ◽  
pp. E1131-E1139 ◽  
Author(s):  
Gabriella Segal-Lieberman ◽  
Daniel J. Trombly ◽  
Viral Juthani ◽  
Xiaomei Wang ◽  
Eleftheria Maratos-Flier
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Genetic Background ◽  
Mixed Genetic Background ◽  
The Central Nervous System ◽  
Mild Obesity

Neuropeptide Y (NPY) is an orexigenic (appetite-stimulating) peptide that plays an important role in regulating energy balance. When administered directly into the central nervous system, animals exhibit an immediate increase in feeding behavior, and repetitive injections or chronic infusions lead to obesity. Surprisingly, initial studies of Npy−/− mice on a mixed genetic background did not reveal deficits in energy balance, with the exception of an attenuation in obesity seen in ob/ob mice in which the NPY gene was also deleted. Here, we show that, on a C57BL/6 background, NPY ablation is associated with an increase in body weight and adiposity and a significant defect in refeeding after a fast. This impaired refeeding response in Npy−/− mice resulted in a deficit in weight gain in these animals after 24 h of refeeding. These data indicate that genetic background must be taken into account when the biological role of NPY is evaluated. When examined on a C57BL/6 background, NPY is important for the normal refeeding response after starvation, and its absence promotes mild obesity.

scholarly journals Model for the regulation of energy balance and adiposity by the central nervous system

1999 ◽  
Vol 69 (4) ◽  
pp. 584-596 ◽  
Author(s):  
Michael W Schwartz ◽  
Denis G Baskin ◽  
Karl J Kaiyala ◽  
Stephen C Woods
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
The Central Nervous System

A review of the neurobiology of obesity and the available pharmacotherapies

CNS Spectrums ◽  
2017 ◽  
Vol 22 (S1) ◽  
pp. 29-38 ◽  
Author(s):  
Mehala Subramaniapillai ◽  
Roger S. McIntyre
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Balance ◽  
Physical Health ◽  
Food Consumption ◽  
Eating Behavior ◽  
Reward System ◽  
The Central Nervous System ◽  
Treatment Mechanisms ◽  
The Brain

Obesity is becoming an increasing problem worldwide. In addition to causing many physical health consequences, there is increasing evidence demonstrating that obesity is toxic to the brain and, as such, can be considered a disease of the central nervous system. Peripheral level regulators of appetite, such as leptin, insulin, ghrelin, and cholecystokinin, feed into the appetite center of the brain, which is controlled by the hypothalamus, to maintain homeostasis and energy balance. However, food consumption is not solely mediated by energy balance, but is also regulated by the mesolimbic reward system, where motivation, reward, and reinforcement factors influence obesity. The purpose of this review is to highlight the neurobiology of eating behavior and obesity and to describe various neurobiological treatment mechanisms to treat obesity.

Sign in / Sign up

Export Citation Format

Share Document