scholarly journals Silencing of OB-RGRP in mouse hypothalamic arcuate nucleus increases leptin receptor signaling and prevents diet-induced obesity

2007 ◽  
Vol 104 (49) ◽  
pp. 19476-19481 ◽  
Author(s):  
C. Couturier ◽  
C. Sarkis ◽  
K. Seron ◽  
S. Belouzard ◽  
P. Chen ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Receptor Signaling ◽  
Diet Induced Obesity ◽  
Hypothalamic Arcuate Nucleus

scholarly journals Identification of Sox2 and NeuN Double-Positive Cells in the Mouse Hypothalamic Arcuate Nucleus and Their Reduction in Number With Aging

2021 ◽  
Vol 12 ◽  
Author(s):  
Ayumu Sugiura ◽  
Tatsuhiro Shimizu ◽  
Takeshi Kameyama ◽  
Tomohiko Maruo ◽  
Shin Kedashiro ◽  
...  
Keyword(s):  
Stem Cells ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
High Fat ◽  
Double Positive ◽  
Diet Induced Obesity ◽  
Hypothalamic Arcuate Nucleus ◽  
Hypothalamic Cells ◽  
Induced Changes ◽  
Insight Into

The hypothalamus plays a central role in homeostasis and aging. The hypothalamic arcuate nucleus (ARC) controls homeostasis of food intake and energy expenditure and retains adult neural stem cells (NSCs)/progenitor cells. Aging induces the loss of NSCs and the enhancement of inflammation, including the activation of glial cells in the ARC, but aging-associated alterations of the hypothalamic cells remain obscure. Here, we identified Sox2 and NeuN double-positive cells in a subpopulation of cells in the mouse ARC. These cells were reduced in number with aging, although NeuN-positive neuronal cells were unaltered in the total number. Diet-induced obesity mice fed with high-fat diet presented a similar hypothalamic alteration to aged mice. This study provides a new insight into aging-induced changes in the hypothalamus.

scholarly journals Three weeks of postweaning exercise in DIO rats produces prolonged increases in central leptin sensitivity and signaling

2009 ◽  
Vol 296 (3) ◽  
pp. R537-R548 ◽  
Author(s):  
Christa M. Patterson ◽  
Sebastien G. Bouret ◽  
Ambrose A. Dunn-Meynell ◽  
Barry E. Levin
Keyword(s):  
Food Intake ◽  
Receptor Binding ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
High Energy ◽  
Decrease Food Intake ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity

In rats selectively bred to develop diet-induced obesity (DIO) 3 wk of postweaning exercise reduces weight and adipose regain for 10 wk after exercise cessation, despite intake of 31% fat high-energy (HE) diet. To test the hypothesis that this effect is due to increased central leptin sensitivity, 4-wk-old DIO rats were fed the HE diet and left sedentary (Sed), exercised for 3 wk, and then remained sedentary for 10 additional weeks (Ex/Sed) or continued exercise for a full 13 wk (Ex). After 3 wk, leptin (5 mg/kg ip) induced a 36% decrease in 24-h food intake in Ex rats, while Sed rats had no change in 24-h intake. Ex rats also had 23% more leptin-induced phospho-STAT3 (pSTAT3)-expressing neurons in the arcuate nucleus (ARC) and 95% and 68% higher 125I-labeled leptin receptor binding in the ventromedial and dorsomedial nuclei than did Sed rats, respectively. At 7 wk after onset, leptin decreased 24-h intake by 20% in Ex and 24% in Ex/Sed rats without altering Sed intake. After a total of 13 wk, compared with Sed rats, Ex and Ex/Sed rats had 58% and 38% less fat, respectively, but leptin failed to decrease food intake in any group. Nevertheless, Ex, but not Ex/Sed rats, still had 32% more ARC leptin-induced pSTAT3-expressing neurons than Sed rats. These data suggest that brief postweaning exercise in DIO rats that are inherently leptin resistant causes a sustained resistance to obesity on HE diet, which is, in part, due to increased central leptin sensitivity.

scholarly journals Hypothyroidism Compromises Hypothalamic Leptin Signaling in Mice

2013 ◽  
Vol 27 (4) ◽  
pp. 586-597 ◽  
Author(s):  
Claudia Groba ◽  
Steffen Mayerl ◽  
Alies A. van Mullem ◽  
Theo J. Visser ◽  
Veerle M. Darras ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Double Knockout ◽  
Hypothalamic Arcuate Nucleus ◽  
The Central Nervous System ◽  
Leptin Expression ◽  
The Impact

Abstract The impact of thyroid hormone (TH) on metabolism and energy expenditure is well established, but the role of TH in regulating nutritional sensing, particularly in the central nervous system, is only poorly defined. Here, we studied the consequences of hypothyroidism on leptin production as well as leptin sensing in congenital hypothyroid TRH receptor 1 knockout (Trhr1 ko) mice and euthyroid control animals. Hypothyroid mice exhibited decreased circulating leptin levels due to a decrease in fat mass and reduced leptin expression in white adipose tissue. In neurons of the hypothalamic arcuate nucleus, hypothyroid mice showed increased leptin receptor Ob-R expression and decreased suppressor of cytokine signaling 3 transcript levels. In order to monitor putative changes in central leptin sensing, we generated hypothyroid and leptin-deficient animals by crossing hypothyroid Trhr1 ko mice with the leptin-deficient ob/ob mice. Hypothyroid Trhr1/ob double knockout mice showed a blunted response to leptin treatment with respect to body weight and food intake and exhibited a decreased activation of phospho-signal transducer and activator of transcription 3 as well as a up-regulation of suppressor of cytokine signaling 3 upon leptin treatment, particularly in the arcuate nucleus. These data indicate alterations in the intracellular processing of the leptin signal under hypothyroid conditions and thereby unravel a novel mode of action by which TH affects energy metabolism.

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.

Expression of leptin receptor mRNA in the hypothalamic arcuate nucleus - relationship with NPY neurones

Neuroreport ◽  
1996 ◽  
Vol 7 (18) ◽  
pp. 3087-3092 ◽  
Author(s):  
Marie-Louise Håkansson ◽  
Anna-Lena Hulting ◽  
Björn Meister
Keyword(s):  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Receptor Mrna ◽  
Hypothalamic Arcuate Nucleus

scholarly journals Appropriate Inhibition of Orexigenic Hypothalamic Arcuate Nucleus Neurons Independently of Leptin Receptor/STAT3 Signaling

2007 ◽  
Vol 27 (1) ◽  
pp. 69-74 ◽  
Author(s):  
H. Munzberg ◽  
E. E. Jobst ◽  
S. H. Bates ◽  
J. Jones ◽  
E. Villanueva ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Stat3 Signaling ◽  
Hypothalamic Arcuate Nucleus

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.

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