Nesfatin-1, a potent anorexic agent, decreases exploration and induces anxiety-like behavior in rats without altering learning or memory

Ge, Jin‐Fang; Xu, Yayun; Qin, Gan; Pan, Xue‐Yin; Cheng, Jiang-Qun; Chen, Feihu

doi:10.1016/j.brainres.2015.10.027

Cited by 44 publications

(29 citation statements)

References 55 publications

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“…Considering the increased plasma nesfatin‐1 levels in patients with impaired glucose tolerance and newly diagnosed T2DM, hyperglycaemia and hyperlipidaemia in NAFLD might also contribute to the increased nesfatin‐1 abundance. Moreover, the results of our previous studies have suggested an association between nesfatin‐1 and the hypothalamic‐pituitary‐adrenal axis . In NAFLD rats, the plasma corticosterone concentration was increased (66.25±2.51 nmol/L vs 51.13±4.25 nmol/L; unpublished data), which might be another contributor to the change in plasma nesfatin‐1 levels in NAFLD rats.…”

Section: Discussionmentioning

confidence: 73%

“…Increased plasma nesfatin‐1 levels have been reported in MDD patients, as associated with elevated scores of anxiety and depression . The results of our previous studies have also demonstrated that chronic administration of nesfatin‐1 could decrease exploration and induce anxiety‐like and depression‐like behaviours in rats . However, little is known about the role of nesfatin‐1 in NAFLD, which presents not only glucose and lipid metabolism disorders, but also neuropsychiatric injuries.…”

Section: Introductionmentioning

confidence: 85%

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Impaired learning and memory in rats induced by a high‐fat diet: Involvement with the imbalance of nesfatin‐1 abundance and copine 6 expression

Chen

et al. 2017

J Neuroendocrinology

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Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease, resulting not only in liver dysfunction, glucose and lipid metabolism disorder, but also in neuropsychiatric damage. In the present study, a NAFLD rat model was established via feeding of a high-fat diet, and behaviour was observed via the open field test (OFT), the sucrose preference test (SPT), the elevated plus maze (EPM), the forced swimming test (FST) and the Morris water maze (MWM). The plasma concentrations of alanine aminotransferase (ALT), glucose, free fatty acid (FFA), total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were detected using chemiluminescence technique. The plasma levels of nesfatin-1, leptin and insulin were measured via enzyme-linked immunosorbent assay, and the protein expressions of p-glycogen synthase kinase-3β (GSK-3β), GSK-3β, p-β-catenin, β-catenin, cyclinD and copine 6 in the hippocampus and prefrontal cortex (PFC) were detected using western blotting. After 4 consecutive weeks of feeding with a high-fat diet, the rats showed obesity; increased plasma concentrations of ALT, glucose, FFA, TC, TG, HDL-C and LDL-C; decreased plasma levels of leptin and insulin; and inflammation and mild hepatocyte steatosis in the liver. Although there was no significant difference between groups with regard to performance in the OFT, EPM or FST, the NAFLD rats showed a decreased sucrose preference index in the SPT and impaired learning and memory in the MWM task. Moreover, the present study provides the first evidence of an increased plasma nesfatin-1 concentration in NAFLD rats, which was significantly correlated with plasma lipid concentrations and behavioural performance. Furthermore, copine 6 and p-β-catenin protein expression decreased and p-GSK-3β increased in the hippocampus and PFC of NAFLD rats. These results suggest that consuming of a high-fat diet for 4 consecutive weeks could successfully induce a NAFLD rat model. More importantly, these results provide the first evidence that impaired learning and memory in NAFLD rats was, at least partly, associated with increased plasma nesfatin-1 concentration and decreased copine 6 expression in the hippocampus and PFC.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 85%

Impaired learning and memory in rats induced by a high‐fat diet: Involvement with the imbalance of nesfatin‐1 abundance and copine 6 expression

Chen

et al. 2017

J Neuroendocrinology

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“…In addition, when animals were exposed to a novel environment, nesfatin-1 not only increased the latency to eat palatable food but also decreased the amount consumed (Merali et al 2008). In an open field test, both an acute central nervous ) and a peripheral chronic administration of nesfatin-1 (Ge et al 2015) increased anxiety-like behavior. The latter was accompanied by reduced brain-derived neurotrophic factor (BDNF) and ERK 1 and 2 phosphorylation in the prefrontal cortex and hippocampus (Ge et al 2015).…”

Section: :1mentioning

confidence: 92%

“…In an open field test, both an acute central nervous ) and a peripheral chronic administration of nesfatin-1 (Ge et al 2015) increased anxiety-like behavior. The latter was accompanied by reduced brain-derived neurotrophic factor (BDNF) and ERK 1 and 2 phosphorylation in the prefrontal cortex and hippocampus (Ge et al 2015). Moreover, nesfatin-1-induced anxiety was blocked by the co-administration of SHU9119 ), indicating that nesfatin-1 participates in stress response mechanisms by recruiting the central melanocortin system.…”

Section: :1mentioning

confidence: 96%

Nesfatin-1: functions and physiology of a novel regulatory peptide

Dore

Levata

Lehnert

et al. 2017

Journal of Endocrinology

114

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Nesfatin-1 was identified in 2006 as a potent anorexigenic peptide involved in the regulation of homeostatic feeding. It is processed from the precursor-peptide NEFA/ nucleobindin 2 (NUCB2), which is expressed both in the central nervous system as well as in the periphery, from where it can access the brain via non-saturable transmembrane diffusion. In hypothalamus and brainstem, nesfatin-1 recruits the oxytocin, the melancortin and other systems to relay its anorexigenic properties. NUCB2/nesfatin-1 peptide expression in reward-related areas suggests that nesfatin-1 might also be involved in hedonic feeding. Besides its initially discovered anorexigenic properties, over the last years, other important functions of nesfatin-1 have been discovered, many of them related to energy homeostasis, e.g. energy expenditure and glucose homeostasis. Nesfatin-1 is not only affecting these physiological processes but also the alterations of the metabolic state (e.g. fat mass, glycemic state) have an impact on the synthesis and release of NUCB2 and/or nesfatin-1. Furthermore, nesfatin-1 exerts pleiotropic actions at the level of cardiovascular and digestive systems, as well as plays a role in stress response, behavior, sleep and reproduction. Despite the recent advances in nesfatin-1 research, a putative receptor has not been identified and furthermore potentially distinct functions of nesfatin-1 and its precursor NUCB2 have not been dissected yet. To tackle these open questions will be the major objectives of future research to broaden our knowledge on NUCB2/nesfatin-1.

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“…Nesfatin-1, another new anorexigenic peptide hormone, plays an important role in the integration of food intake, energy expenditure, and glucose homeostasis (9). In the past decade, nesfatin-1 has been found to be involved in a variety of affective disorders, including anxiety disorder (10), depression (11), and psychosis (12). However, no studies on the relationship between nesfatin-1 in AD and craving have been conducted.…”

Section: Introductionmentioning

confidence: 99%

Nesfatin-1, a potent anorexic agent, decreases exploration and induces anxiety-like behavior in rats without altering learning or memory

Cited by 44 publications

References 55 publications

Impaired learning and memory in rats induced by a high‐fat diet: Involvement with the imbalance of nesfatin‐1 abundance and copine 6 expression

Impaired learning and memory in rats induced by a high‐fat diet: Involvement with the imbalance of nesfatin‐1 abundance and copine 6 expression

Nesfatin-1: functions and physiology of a novel regulatory peptide

Evidence of a Relationship Between Plasma Leptin, Not Nesfatin-1, and Craving in Male Alcohol-Dependent Patients After Abstinence

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