scholarly journals The Obesity Gene, FTO, Is of Ancient Origin, Up-Regulated during Food Deprivation and Expressed in Neurons of Feeding-Related Nuclei of the Brain

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2062-2071 ◽  
Author(s):  
Robert Fredriksson ◽  
Maria Hägglund ◽  
Pawel K. Olszewski ◽  
Olga Stephansson ◽  
Josefin A. Jacobsson ◽  
...  
2007 ◽  
Vol 152 (2-3) ◽  
pp. 225-230 ◽  
Author(s):  
P. Kiss ◽  
D. Reglődi ◽  
A. Tamás ◽  
A. Lubics ◽  
I. Lengvári ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 219 ◽  
Author(s):  
Beatriz Cuevas-Fernández ◽  
Carlos Fuentes-Almagro ◽  
Juan Peragón

Long-term starvation provokes a metabolic response in the brain to adapt to the lack of nutrient intake and to maintain the physiology of this organ. Here, we study the changes in the global proteomic profile of the rat brain after a seven-day period of food deprivation, to further our understanding of the biochemical and cellular mechanisms underlying the situations without food. We have used two-dimensional electrophoresis followed by mass spectrometry (2D-MS) in order to identify proteins differentially expressed during prolonged food deprivation. After the comparison of the protein profiles, 22 brain proteins were found with altered expression. Analysis by peptide mass fingerprinting and MS/MS (matrix-assisted laser desorption-ionization-time of flight mass spectrometer, MALDI-TOF/TOF) enabled the identification of 14 proteins differentially expressed that were divided into 3 categories: (1) energy catabolism and mitochondrial proteins; (2) chaperone proteins; and (3) cytoskeleton, exocytosis, and calcium. Changes in the expression of six proteins, identified by the 2D-MS proteomics procedure, were corroborated by a nanoliquid chromatography-mass spectrometry proteomics procedure (nLC-MS). Our results show that long-term starvation compromises essential functions of the brain related with energetic metabolism, synapsis, and the transmission of nervous impulse.


1986 ◽  
Vol 399 (1) ◽  
pp. 200-203 ◽  
Author(s):  
Satoru Tsujii ◽  
Yoshikatsu Nakai ◽  
Toshikiyo Koh ◽  
Hideo Takahashi ◽  
Takeshi Usui ◽  
...  

1971 ◽  
Vol 29 (2) ◽  
pp. 655-665 ◽  
Author(s):  
Irmingard I. Lenzer

The effects of two concurrently changing drive variables, food deprivation and estrogen level, on the self-stimulation rate in the hypothalamus, septum, caudate nucleus, or dorsal hippocampus of 15 female albino rats were studied. When the effects of hunger were calculated using only scores on days of diestrus and the effects of estrogen were calculated using only scores on days of 0-hr. food deprivation, the correlation of these hunger and estrogen effects amounted to 0.67. When the hunger effects were calculated using only scores on days of estrus and these hunger effects correlated with the previously calculated estrogen effects, the correlation amounted to −0.49. These results are consistent with the concept of diffuse overlapping motivational systems in the brain. Controls indicated that the changes in self-stimulation rate were not artifacts of changes in nonspecific activity.


2017 ◽  
Vol 313 (5) ◽  
pp. R572-R582 ◽  
Author(s):  
Elizabeth A. Flatow ◽  
Evilin N. Komegae ◽  
Monique T. Fonseca ◽  
Camila F. Brito ◽  
Florin M. Musteata ◽  
...  

To elucidate the role of leptin in acute systemic inflammation, we investigated how its infusion at low, physiologically relevant doses affects the responses to bacterial lipopolysaccharide (LPS) in rats subjected to 24 h of food deprivation. Leptin was infused subcutaneously (0–20 μg·kg−1·h−1) or intracerebroventricularly (0–1 μg·kg−1·h−1). Using hypothermia and hypotension as biomarkers of systemic inflammation, we identified the phase extending from 90 to 240 min post-LPS as the most susceptible to modulation by leptin. In this phase, leptin suppressed the rise in plasma TNF-α and accelerated the recoveries from hypothermia and hypotension. Suppression of TNF-α was not accompanied by changes in other cytokines or prostaglandins. Leptin suppressed TNF-α when infused peripherally but not when infused into the brain. Importantly, the leptin dose that suppressed TNF-α corresponded to the lowest dose that limited food consumption; this dose elevated plasma leptin within the physiological range (to 5.9 ng/ml). We then conducted in vitro experiments to investigate whether an action of leptin on macrophages could parallel our in vivo observations. The results revealed that, when sensitized by food deprivation, LPS-stimulated peritoneal macrophages can be inhibited by leptin at concentrations that are lower than those reported to promote cytokine release. It is concluded that physiological levels of leptin do not exert a proinflammatory effect but rather an anti-inflammatory effect involving selective suppression of TNF-α via an action outside the brain. The mechanism of this effect might involve a previously unrecognized, suppressive action of leptin on macrophage subpopulations sensitized by food deprivation, but future studies are warranted.


1999 ◽  
Vol 276 (3) ◽  
pp. E479-E482 ◽  
Author(s):  
Abba J. Kastin ◽  
Victoria Akerstrom

Neuropeptide Y (NPY) is found and is active both in the periphery and brain, but its crossing of the blood-brain barrier (BBB) in either direction has not been measured. We used multiple time-regression analysis to determine that radioactively labeled NPY injected intravenously entered the brain much faster than albumin, with an influx constant of 2.0 × 10−4ml ⋅ g ⋅ −1 ⋅ min−1. However, this rate of entry was not significantly changed by injection of 10 μg/mouse of excess NPY, by leptin, or by food deprivation. HPLC showed that most of the NPY entering the brain was intact, and capillary depletion with and without washout showed that the NPY did not remain bound to endothelial cells or associated with vascular elements. Perfusion in a blood-free solution eliminated binding to serum proteins as an explanation for the lack of saturation. Efflux of labeled NPY from the brain occurred at the same rate as albumin, reflecting the normal rate of reabsorption of cerebrospinal fluid. Thus NPY can readily enter the brain from blood by diffusion across the BBB.


2021 ◽  
Author(s):  
Juan C Jimenez ◽  
Jorge Miranda-Barrientos ◽  
Mireya Becerra-Diaz ◽  
Florencio Miranda

INTRODUCTION: AMPH and METH are known to increase DAergic signaling in the brain reward system by stimulating the release of DA through the reversal of DAT function. However, there is evidence that insulin signaling pathways have the ability to modulate DAT functions. Some studies have reported that hypoinsulinemia attenuates DAT functions, and as a consequence, psychostimulant-induced behaviors are reduced. In the present study, we examined the effects of acute food deprivation, which also reduces insulin levels, on METH-induced locomotor sensitization. METHODS: Separate groups of rats were treated with METH (1 mg/kg i.p.) or saline for 5 days (development phase). On the test day (expression phase), the groups were treated with METH or saline after food deprivation for 24 h. Furthermore, in separate groups of rats, levels of glucose, insulin, and phosphorylation of Akt at Ser473 were also examined after food deprivation for 24 h. RESULTS: The results showed that repeated administration of METH induced a progressive increase in locomotor activity in rats during the development phase. However, METH administration in the expression phase produced a decrease in locomotor activity after 24 h of food deprivation. In addition, the results showed that a reduction in glucose, insulin, and Akt levels occurred as a result of food deprivation. CONCLUSION: These results are in line with previous studies and suggest that food deprivation reduces some behavioral effects of psychostimulants such as AMPH and METH.


2001 ◽  
Vol 74 (6) ◽  
pp. 423-432 ◽  
Author(s):  
Abba J. Kastin ◽  
Victoria Akerstrom ◽  
Laszlo Hackler
Keyword(s):  

2008 ◽  
Vol 295 (6) ◽  
pp. R1737-R1746 ◽  
Author(s):  
Erin Keen-Rhinehart ◽  
Timothy J. Bartness

Food deprivation stimulates foraging and hoarding and to a much lesser extent, food intake in Siberian hamsters. Leptin, the anorexigenic hormone secreted primarily from adipocytes, may act in the periphery, the brain, or both to inhibit these ingestive behaviors. Therefore, we tested whether leptin given either intracerebroventricularly or intraperitoneally, would block food deprivation-induced increases in food hoarding, foraging, and intake in animals with differing foraging requirements. Hamsters were trained in a running wheel-based food delivery foraging system coupled with simulated burrow housing. We determined the effects of food deprivation and several peripheral doses of leptin on plasma leptin concentrations. Hamsters were then food deprived for 48 h and given leptin (0, 10, 40, or 80 μg ip), and additional hamsters were food deprived for 48 h and given leptin (0, 1.25, 2.5, or 5.0 μg icv). Foraging, food intake, and hoarding were measured postinjection. Food deprivation stimulated food hoarding to a greater degree and duration than food intake. In animals with a foraging requirement, intracerebroventricular leptin almost completely blocked food deprivation-induced increased food hoarding and intake, but increased foraging. Peripheral leptin treatment was most effective in a sedentary control group, completely inhibiting food deprivation-induced increased food hoarding and intake at the two highest doses, and did not affect foraging at any dose. Thus, the ability of leptin to inhibit food deprivation-induced increases in ingestive behaviors differs based on foraging effort (energy expenditure) and the route of administration of leptin administration.


Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1503
Author(s):  
Marcos Antonio López-Patiño ◽  
Arleta Krystyna Skrzynska ◽  
Fatemeh Naderi ◽  
Juan Miguel Mancera ◽  
Jesús Manuel Míguez ◽  
...  

In teleosts, brain monoamines (dopamine and serotonin) participate in the early response to different acute stressors. However, little is known regarding their role during chronic stress. In a 2 × 2 factorial design, the influence of a high stocking density (HSD) and/or food deprivation (FD) on the brain monoaminergic activity in gilthead sea bream (Sparus aurata) was evaluated. Following a 21-day experimental design, samples from the plasma and brain regions (telencephalon, hypothalamus, and optic tectum) were collected. The dopamine (DA), serotonin (5HT), and their main metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5 hydroxyindoleacetic acid (5HIAA), contents were HPLC-assessed in brain tissues, and the ratios DOPAC/DA and 5HIAA/5HT were calculated as indicators of enhanced monoaminergic activity. The plasma levels of cortisol and catecholamine were also evaluated. The cortisol levels increased in fish exposed to HSD and normally fed but, also, in all FD groups, whereas the NA levels decreased in LSD-FD animals. Within the brain, the dopaminergic and serotonergic activities in telencephalon and hypothalamus increased in fish subjected to HSD and in the telencephalon of LSD-FD fish. While DA (hypothalamus) and 5HT (telencephalon) increased in the animals submitted to a HSD, food-deprived fish did not show such an increase. Taken together, our results supported the hypothesis of brain monoaminergic activity participating in maintaining and orchestrating the endocrine response to chronic stress in fish.


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