Cafeteria diet-induced obesity reduces leptin-stimulated NADPH-diaphorase reactivity in the hypothalamic arcuate nucleus of rats

2020 ◽  
Vol 122 (7) ◽  
pp. 151616 ◽  
Author(s):  
Milen Hristov ◽  
Boycho Landzhov ◽  
Krassimira Yakimova
Keyword(s):  
Arcuate Nucleus ◽  
Nadph Diaphorase ◽  
Cafeteria Diet ◽  
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 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 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.

Dysregulation of arcuate nucleus preproneuropeptide Y mRNA in diet-induced obese rats

1997 ◽  
Vol 272 (5) ◽  
pp. R1365-R1370 ◽  
Author(s):  
B. E. Levin ◽  
A. A. Dunn-Meynell
Keyword(s):  
Arcuate Nucleus ◽  
High Energy ◽  
Energy Restriction ◽  
Dopamine Turnover ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Hypothalamic Arcuate Nucleus

Neuropeptide Y (NPY) neurons in the hypothalamic arcuate nucleus (ARC) produce metabolic and physiological effects that promote the development and maintenance of obesity. In turn, NPY metabolism in these neurons is inhibited by dopamine release. In this study, ARC prepro-NPY mRNA and ARC/median eminence (ME) dopamine turnover were assessed in chow-fed male Sprague-Dawley rats prone to develop diet-induced obesity (DIO) or to be diet resistant (DR) when fed a high-energy (HE) diet. By in situ hybridization, DIO-prone rats had 39% more ARC NPY mRNA expression than DR-prone rats under chow-fed conditions. DIO-prone rat ARC/ME dopamine levels were 14% higher, but dopamine half-life was 176% longer and turnover was 59% less than DR-prone rats. Neither a 48-h fast nor 50% energy intake restriction for 5 days affected the already increased ARC NPY mRNA levels in DIO-prone rats. Both manipulations increased NPY expression to the level of DIO-prone rats in DR-prone rats by 23 and 35%, respectively. Finally, when fed HE diet for 2 wk, neither DIO- nor DR-prone rats altered their ARC NPY expression despite the development of obesity and hyperinsulinemia in DIO rats. Thus DIO-prone rats overexpress and fail to regulate ARC NPY mRNA to energy restriction or hyperinsulinemia. This dysregulation is possibly secondary to reduced inhibition because of defective ARC/ME dopamine turnover. Both may be important predisposing factors in the development of DIO.

scholarly journals Effect of Argyreia speciosa root extract on cafeteria diet-induced obesity in rats

2011 ◽  
Vol 43 (2) ◽  
pp. 163 ◽  
Author(s):  
Shiv Kumar ◽  
KR Alagawadi ◽  
MRaghavendra Rao
Keyword(s):  
Cafeteria Diet ◽  
Root Extract ◽  
Diet Induced Obesity

Diet-derived nutrients mediate the inhibition of hypothalamic NPY neurons in the arcuate nucleus of mice during refeeding

2009 ◽  
Vol 297 (1) ◽  
pp. R100-R110 ◽  
Author(s):  
Csilla Becskei ◽  
Thomas A. Lutz ◽  
Thomas Riediger
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Small Reduction ◽  
Hypothalamic Arcuate Nucleus ◽  
Ad Libitum ◽  
Fos Expression

Fasting activates orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus (ARC) of mice, which is reversed by 2 h refeeding with standard chow. Here, we investigated the contribution of diet-derived macronutrients and anorectic hormones to the reversal of the fasting-induced ARC activation during 2 h refeeding. Refeeding of 12-h-fasted mice with a cellulose-based, noncaloric mash induced only a small reduction in c-Fos expression. Refeeding with diets, containing carbohydrates, protein, or fat alone reversed it similar to chow; however, this effect depended on the amount of intake. The fasting-induced ARC activation was unchanged by subcutaneously injected amylin, CCK (both 20 μg/kg), insulin (0.2 U/kg and 0.05 U/kg) or leptin (2.6 mg/kg). Insulin and leptin had no effect on c-Fos expression in neuropeptide Y or proopiomelanocortin-containing ARC neurons. Interestingly, CCK but not amylin reduced the ghrelin-induced c-Fos expression in the ARC in ad libitum-fed mice, suggesting that CCK may inhibit orexigenic ARC neurons when acting together with other feeding-related signals. We conclude that all three macronutrients and also non-nutritive, ingestion-dependent signals contribute to an inhibition of orexigenic ARC neurons after refeeding. Similar to the previously demonstrated inhibitory in vivo action of peptide YY, CCK may be a postprandial mediator of ARC inhibition.

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