Modulation of neurogenesis and selected neuropeptides expression in the hypothalamus of rats exposed to neuroleptic

2016 ◽  
Vol 4 ◽  
pp. 23-35
Author(s):  
Ewa Rojczyk ◽  
Artur Pałasz

Patients treated with neuroleptics suffer from significant weight gain. Hypothalamus consists of neuronal circuits responsible for food intake regulation. Moreover, last finding suggest that adult neurogenesis occurs in the hypothalamus, which could play a role in the energy expenditure control. Considering that neuroleptics affect neural formation in the canonical neurogenic sites, we made a hypothesis that they could modulate hypothalamic neurogenesis and change expression of orexigenic/anorexigenic neuropeptides and their receptors. Experiments were carried out on adult male rats injected intraperitoneally for 1 or 28 days by the neuroleptics: olanzapine, chlorpromazine and haloperidol. Hypothalami were isolated in order to perform RT-PCR reaction and also whole brains were sliced for immunohistochemical assay. We observed that antipsychotics administered chronically supported the origin of newborn cells (Ki67 +) in the hypothalamic regions and affect the number of DCX-positive immature neurons. Furthermore, they have a distinct ability to upregulate preproorexin and orexin A expression and to increase the level of some anorexigenic factors (POMC, α-MSH), at the same time strongly decreasing nesfatin-1 signalling. Our results highlight the role of neuroleptics as potential modulators of the hypothalamic neurogenesis and contribute to better understanding the mechanisms of their side effects. They also underline the complexity of interplay between monoamine receptors, hypothalamic peptidergic pathways and adult neurogenesis which has putative but possible pharmacological applications.

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.


2018 ◽  
Vol 818 ◽  
pp. 43-49 ◽  
Author(s):  
Zahra. Mirmohammadsadeghi ◽  
Masoud. Shareghi Brojeni ◽  
Abbas. Haghparast ◽  
Afsaneh. Eliassi

1999 ◽  
Vol 24 ◽  
pp. 37-54 ◽  
Author(s):  
K. L. Ingvartsen ◽  
N. C. Friggens ◽  
P. Faverdin

AbstractThe dip in food intake, which starts in late pregnancy and continues into early lactation, has traditionally been interpreted as a depression in intake due to physical constraints. However, the rôle of physical constraints on intake has been overemphasized, particularly in early lactation. There is mounting evidence that the presence and mobilization of body reserves in early lactation play an important rôle in regulating intake at this time.Conceptually, the dip in intake in early lactation observed when cows have access to non-limiting foods can be accounted for by assuming that the cow has a desired level of body reserves. When the cow is not compromised, the changes with time in body reserves and the dip in intake represent the normal case and provide the basis against which to assess true depressions in intake which may occur when the cow is compromised by limiting nutrition or environment.The regulation of body reserves and intake in the periparturient cow is orchestrated through nervous and hormonal signals. Likely factors that are involved in intake regulation are reproductive hormones, neuropeptides, adrenergic signals, insulin and insulin resistance and leptin. Furthermore, oxidation of NEFA in the liver may result in feedback signals that reduce intake. The relative importance of these is discussed. A better understanding of the physiological signals involved in intake regulation and their interrelations with body weight regulation may provide important indicators of the degree of compromise that periparturient cows may experience.


2015 ◽  
pp. 63-68
Author(s):  
Ádám Simon ◽  
András Jávor ◽  
Levente Czeglédi

Energy balance is the net result of the energy intake (nutrition) and expenditure (basic metabolic rate). The purpose of the daily feed intake is to provide energy and nutrients for maintenance, production and fill and maintain energy storages in form of glycogen and fat. Animals can adjust their feed intake to ensure their energy demand. Food intake regulation in animals and human is a very complex process, in which the digestive system, the central nervous system, the joining hormonal and non-hormonal factors, and the integrating hypothalamus take part. This review primarily focuses on the action mechanism of some important appetite regulating neuropeptides, and their impacts on the performance traits of the economically significant animal species.


Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2835
Author(s):  
Parisa Vidafar ◽  
Sean W. Cain ◽  
Ari Shechter

Short and/or poor sleep are established behavioral factors which can contribute to excess food intake, and emerging evidence suggests that disturbed circadian rhythms may also impact food intake regulation. Together, disturbed sleep and circadian rhythms may help explain the excess risk for obesity seen in shift workers. To date, however, the details of how shift work may impact food intake regulation are still not fully defined. Here we examined the relationship between sleep characteristics and hedonic control of appetite in shift workers. A total of 63 shift workers (mean (M) age: 36.7 years, standard deviation (SD): 12.0; 59% women) completed an online survey comprising self-reported measures of body weight regulation, sleep (Pittsburgh Sleep Quality Index, Sleep Hygiene Index), and hedonic control of appetite (Food Craving Inventory, Power of Food Scale). Seventy-one percent reported some weight change since starting shift work, and 84% of those reported weight gain (M = +11.3 kg, SD = 9.1). Worse sleep quality and shorter sleep duration were associated with more food cravings, and worse sleep quality and hygiene were associated with higher appetitive drive to consume palatable food (greater hedonic drive). This preliminary study suggests hedonic pathways are potentially contributing to weight gain in shift workers with disturbed sleep.


Gut ◽  
2020 ◽  
Vol 69 (9) ◽  
pp. 1620-1628 ◽  
Author(s):  
Sei Higuchi ◽  
Tiara R Ahmad ◽  
Donovan A Argueta ◽  
Pedro A Perez ◽  
Chen Zhao ◽  
...  

ObjectivesLipid mediators in the GI tract regulate satiation and satiety. Bile acids (BAs) regulate the absorption and metabolism of dietary lipid in the intestine, but their effects on lipid-regulated satiation and satiety are completely unknown. Investigating this is challenging because introducing excessive BAs or eliminating BAs strongly impacts GI functions. We used a mouse model (Cyp8b1–/– mice) with normal total BA levels, but alterations in the composition of the BA pool that impact multiple aspects of intestinal lipid metabolism. We tested two hypotheses: BAs affect food intake by (1) regulating production of the bioactive lipid oleoylethanolamide (OEA), which enhances satiety; or (2) regulating the quantity and localisation of hydrolysed fat in small intestine, which controls gastric emptying and satiation.DesignWe evaluated OEA levels, gastric emptying and food intake in wild-type and Cyp8b1–/– mice. We assessed the role of the fat receptor GPR119 in these effects using Gpr119–/– mice.ResultsCyp8b1–/– mice on a chow diet showed mild hypophagia. Jejunal OEA production was blunted in Cyp8b1–/– mice, thus these data do not support a role for this pathway in the hypophagia of Cyp8b1–/– mice. On the other hand, Cyp8b1 deficiency decreased gastric emptying, and this was dependent on dietary fat. GPR119 deficiency normalised the gastric emptying, gut hormone levels, food intake and body weight of Cyp8b1–/– mice.ConclusionBAs regulate gastric emptying and satiation by determining fat-dependent GPR119 activity in distal intestine.


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