scholarly journals Hypothalamic arcuate nucleus tyrosine hydroxylase neurons play orexigenic role in energy homeostasis

2016 ◽  
Vol 19 (10) ◽  
pp. 1341-1347 ◽  
Author(s):  
Xiaobing Zhang ◽  
Anthony N van den Pol
Keyword(s):  
Tyrosine Hydroxylase ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Hypothalamic Arcuate Nucleus

scholarly journals Arcuate NPY neurons and energy homeostasis in diet-induced obese and resistant rats

1999 ◽  
Vol 276 (2) ◽  
pp. R382-R387 ◽  
Author(s):  
Barry E. Levin
Keyword(s):  
Metabolic Regulation ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Inbred Strains ◽  
Energy Restriction ◽  
Short Term ◽  
Diet Induced Obesity ◽  
Body Weights ◽  
Hypothalamic Arcuate Nucleus

The neuropeptide Y (NPY) neurons in the hypothalamic arcuate nucleus regulate and are regulated by short-term changes in energy homeostasis. Both outbred and inbred strains of rats that develop diet-induced obesity (DIO) or are diet resistant (DR) when fed a diet relatively high in energy, fat, and sucrose content (HE diet) were used to study arcuate NPY mRNA expression during long-term changes in energy balance. Outbred, chow-fed obesity-prone rats had 59% higher NPY levels than obesity-resistant rats. After 14 wk on HE diet, DIO rats had 17% lower NPY levels than DR rats made comparably obese on a highly palatable diet. When switched to chow, obese DR rats spontaneously reduced their intake and their body weights fell to control levels in association with a 10% decrease in NPY levels. DIO rats lost weight only with energy restriction associated with a 21% increase in their NPY levels. When again fed ad libitum, the weight and NPY levels in the rats returned to those of unrestricted DIO rats. Chow-fed, inbred DIO rats weigh more and are fatter than age-matched inbred DR rats. As with outbred DIO rats fed the HE diet, inbred DIO rats had 20% lower NPY levels than DR rats. Thus preobese, outbred DIO rats have high levels of NPY message that are not susceptible to metabolic regulation. When obesity develops in both inbred and outbred rats, the levels of NPY mRNA fall but become responsive to alterations in energy availability.

scholarly journals Astaxanthin Exerts Anabolic Effects via Pleiotropic Modulation of the Excitable Tissue

2022 ◽  
Vol 23 (2) ◽  
pp. 917
Author(s):  
Mónika Gönczi ◽  
Andrea Csemer ◽  
László Szabó ◽  
Mónika Sztretye ◽  
János Fodor ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Fatty Acid Biosynthesis ◽  
Synaptic Activity ◽  
Systematic Analysis ◽  
Protein Levels ◽  
General Metabolism ◽  
Hypothalamic Arcuate Nucleus

Astaxanthin is a lipid-soluble carotenoid influencing lipid metabolism, body weight, and insulin sensitivity. We provide a systematic analysis of acute and chronic effects of astaxanthin on different organs. Changes by chronic astaxanthin feeding were analyzed on general metabolism, expression of regulatory proteins in the skeletal muscle, as well as changes of excitation and synaptic activity in the hypothalamic arcuate nucleus of mice. Acute responses were also tested on canine cardiac muscle and different neuronal populations of the hypothalamic arcuate nucleus in mice. Dietary astaxanthin significantly increased food intake. It also increased protein levels affecting glucose metabolism and fatty acid biosynthesis in skeletal muscle. Inhibitory inputs innervating neurons of the arcuate nucleus regulating metabolism and food intake were strengthened by both acute and chronic astaxanthin treatment. Astaxanthin moderately shortened cardiac action potentials, depressed their plateau potential, and reduced the maximal rate of depolarization. Based on its complex actions on metabolism and food intake, our data support the previous findings that astaxanthin is suitable for supplementing the diet of patients with disturbances in energy homeostasis.

scholarly journals Insulin potentiates the synchronous firing of arcuate nucleus Kiss1 neurons that protects against diet-induced obesity

2020 ◽  
Author(s):  
Jian Qiu ◽  
Todd L. Stincic ◽  
Martha A. Bosch ◽  
Ashley M. Connors ◽  
Stefanie Kaech Petrie ◽  
...  
Keyword(s):  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Pubertal Development ◽  
Excitatory Postsynaptic Potential ◽  
Endoplasmic Reticulum Calcium ◽  
Calcium Sensing ◽  
Diet Induced Obesity ◽  
Synchronous Firing ◽  
Hypothalamic Arcuate Nucleus ◽  
Excitatory Drive

AbstractKisspeptin neurons in the hypothalamic arcuate nucleus (Kiss1ARH) co-express kisspeptin, neurokinin B, dynorphin and provide an episodic, excitatory drive to gonadotropin-releasing hormone (GnRH) neurons, which is critical for pubertal development and fertility. Previously, we showed that high frequency firing of Kiss1ARH neurons co-releases NKB and dynorphin onto neighboring Kiss1ARH neurons to generate a slow excitatory postsynaptic potential (EPSP) that entrains intermittent, synchronous firing of Kiss1ARH neurons (Qiu et al., 2016). Presently, we discovered that insulin significantly increased the amplitude of the slow EPSP, which we documented is mediated by TRPC5 channels, and augmented synchronous GCaMP6s ([Ca]i) oscillations in Kiss1ARH neurons. Deletion of the endoplasmic reticulum calcium-sensing protein stromal interaction molecule 1 in Kiss1ARH neurons amplified insulin’s actions and protected ovariectomized female mice from developing obesity and glucose intolerance with high-fat dieting. Therefore, insulin appears to be critical for facilitating synchronous firing of Kiss1ARH neurons and coordinating energy homeostasis with fertility.

scholarly journals Growth hormone receptor (GHR)-expressing neurons in the hypothalamic arcuate nucleus regulate glucose metabolism and energy homeostasis

2020 ◽  
Author(s):  
Juliana Bezerra Medeiros de Lima ◽  
Lucas Kniess Debarba ◽  
Manal Khan ◽  
Chidera Ubah ◽  
Olesya Didyuk ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Glucose Metabolism ◽  
Energy Homeostasis ◽  
Arcuate Nucleus ◽  
Brain Regions ◽  
Designer Drugs ◽  
Whole Body ◽  
Mouse Line ◽  
Hypothalamic Arcuate Nucleus

AbstractGrowth hormone (GH) receptor (GHR), expressed in different brain regions, is known to participate in the regulation of whole-body energy homeostasis and glucose metabolism. However, GH activation of these GHR-expressing neurons is less studied. We have generated a novel GHR-driven Cre recombinase transgenic mouse line (GHRcre) in combination with the floxed tdTomato reporter mouse line we tracked and activated GHR-expressing neurons in different regions of the brain. We focused on neurons of the hypothalamic arcuate nucleus (ARC) where GHR was shown to elicit a negative feedback loop that regulates GH production. We found that ARCGHR+ neurons are co-localized with AgRP, GHRH, and somatostatin neurons, which were activated by GH stimulation. Using designer receptors exclusively activated by designer drugs (DREADDs) to control GHRARC neuronal activity, we revealed that activation of GHRARC neurons was sufficient in regulating distinct aspects of energy balance and glucose metabolism. Overall, our study provides a novel mouse model to study in vivo regulation and physiological function of GHR-expressing neurons in various brain regions. Furthermore, we identified for the first time specific neuronal population that responds to GH and directly linked it to metabolic responses in vivo.

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