Plasma nesfatin-1 concentrations in restricting-type anorexia nervosa

Ogiso, Kazuma; Asakawa, Akihiro; Amitani, Haruka; Nakahara, Toshihiro; Ushikai, Miharu; Haruta, Izumi; Koyama, Ken; Amitani, Marie; Harada, Toshiro; Yasuhara, Daisuke; Inui, Akio

doi:10.1016/j.peptides.2010.10.004

Cited by 77 publications

(50 citation statements)

References 25 publications

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“…Administration of nesfatin-1 reduced blood glucose levels in hyperglycemic db/db mice, and this effect was insulin dependent (Su et al 2010). In humans, healthy subjects given an oral glucose drink had higher levels of nesfatin-1 in circulation relative to saline-treated controls (Li et al 2010), whereas nesfatin-1 levels in restricting-type anorexia nervosa were lower in the anorexic group compared to those in the control group (Ogiso et al 2010). These reports suggest that nesfatin-1 in the circulation is regulated by nutritional status and response to starvation.…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 Exerts a Direct, Glucose-Dependent Insulinotropic Action on Mouse Islet Beta and MIN6 Cells

G¹,

Reingold²,

Gao³

et al. 2011

Journal of Endocrinology

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Nesfatin-1 is a recently discovered multifunctional metabolic hormone abundantly expressed in the pancreatic islets. The main objective of this study is to characterize the direct effects of nesfatin-1 on insulin secretion in vitro using MIN6 cells and islets isolated from C57BL/6 mice. We also examined the expression of the nesfatin-1 precursor protein, nucleobindin 2 (NUCB2) mRNA, and nesfatin-1 immunoreactivity (ir) in the islets of normal mice and in the islets from mice with streptozotocininduced type 1 diabetes and diet-induced obese (DIO) mice with type 2 diabetes. Nesfatin-1 stimulated glucose-induced insulin release in vitro from mouse islets and MIN6 cells in a dose-dependent manner. No such stimulation in insulin secretion was found when MIN6 cells/islets were incubated with nesfatin-1 in low glucose. In addition, a fourfold increase in nesfatin-1 release from MIN6 cells was observed following incubation in high glucose (16 . 7 mM) compared to low glucose (2 mM). Furthermore, we observed a significant reduction in both NUCB2 mRNA expression and nesfatin-1-ir in the pancreatic islets of mice with type 1 diabetes, while a significant increase was observed in the islets of DIO mice. Together, our findings indicate that nesfatin-1 is a novel insulinotropic peptide and that the endogenous pancreatic islet NUCB2/nesfatin is altered in diabetes and diet-induced obesity.

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Section: Discussionmentioning

confidence: 99%

Nesfatin-1 Exerts a Direct, Glucose-Dependent Insulinotropic Action on Mouse Islet Beta and MIN6 Cells

G¹,

Reingold²,

Gao³

et al. 2011

Journal of Endocrinology

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“…Nesfatin-1 is an 82-amino acid residue derived from the nucleobindin-2 (NUCB2) peptide, possibly through proteolysis by prohormone convertases (7). Nesfatin-1̸NUCB2 immunoreactive cells were found to be expressed in the pancreas, stomach, duodenum, adipose tissue, central amygdaloid nucleus, hypothalamus, nucleus accumbens, cerebellum and Effects of aging on the plasma levels of nesfatin-1 and adiponectin JIANG-BO LI 1,2 , MIYUKI NISHIDA 1 , KAORI KAIMOTO 1 , AKIHIRO ASAKAWA 1 , HUHE CHAOLU 1 , KAI-CHUN CHENG 1 , YING-XIAO LI 1 , MUTSUMI TERASHI 1 , KEN ICHIRO KOYAMA 1 , microdissected lumbar spinal cord in rodents, suggesting that nesfatin-1̸NUCB2 may be crucial in the physiological regulation of carbohydrate metabolism, gastrointestinal function and nutrient absorption (8)(9)(10)(11)(12)(13)(14). Furthermore, the nesfatin-1-induced inhibition of food intake may be mediated through the inhibition of orexigenic NPY neurons (15) and the activation of POMC and CART (16).…”

Section: Introductionmentioning

confidence: 99%

Effects of aging on the plasma levels of nesfatin-1 and adiponectin

Nishida

Kaimoto

et al. 2013

Biomedical Reports

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Abstract. Gastric and adipose tissue secrete a number of hormones that are involved in energy metabolism. The biological functions of these hormones, including their effects on aging, are currently under investigation. Adiponectin was shown to be directly involved in appetite and the control of body weight. However, the effects of aging of nesfatin-1, an appetite-suppressing peptide that was recently identified, have not yet been fully elucidated. The aim of this study was to determine the effects of aging on the plasma levels of nesfatin-1 and adiponectin. Our results demonstrated no significant differences in the nesfatin-1 plasma levels among three age groups (2, 6 and 24 months) of female BALB̸c mice. The plasma nesfatin-1 levels̸visceral fat (VF) ratio in the 24-month-old mice was significantly lower compared to that in the 2-and 6-month-old mice. In addition, there were no significant differences in the plasma adiponectin levels among the three age groups. The plasma adiponectin levels̸VF ratio in the 24-month-old mice was significantly lower compared to that in the 2-and 6-month-old mice. In conclusion, there were no age-related changes in the plasma levels of nesfatin-1 and adiponectin, although the ratio of plasma levels of nesfatin-1 and adiponectin per VF was decreased with advancing age. Our results indicated that nesfatin-1 and adiponectin may be involved in controlling energy balance during aging.

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“…The interplay between obestatin and acyl ghrelin, des-acyl ghrelin, as well as nesfatin-1 is interesting, but is not yet well recognized. In patients with restricting-type anorexia nervosa, obestatin, as well as acyl ghrelin, des-acyl ghrelin and nesfatin-1, are important regulators responsive to starvation and re-nutrition (38). Following a PubMed search, the current study is the first to explore the impact of ICV obestatin on these above-mentioned peptides.…”

Section: Discussionmentioning

confidence: 99%

Impact of intracerebroventricular obestatin on plasma acyl ghrelin, des-acyl ghrelin and nesfatin-1 levels, and on gastric emptying in rats

et al. 2012

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Abstract. Obestatin, which is a putative 23-amino-acid peptide, is derived from the C-terminal part of the mammalian preproghrelin gene. Nesfatin-1 mRNA is co-expressed with ghrelin in gastric endocrine X/A-like cells; therefore, nesfatin-1 may also interact with preproghrelin gene products in the stomach. In this study, we investigated the impact of obestatin on the plasma levels of acyl ghrelin, des-acyl ghrelin and nesfatin-1, and on the gastric emptying of a solid nutrient meal 2 h after an intracerebroventricular (ICV) injection in conscious, fasted rats. The rats were implanted with ICV catheters. Plasma levels of acyl ghrelin, des-acyl ghrelin and nesfatin-1, expected to be co-expressed with obestatin, were measured, whereas the human/rat corticotropin-releasing factor (h/rCRF) was applied as an inhibitor of gastric emptying. The ICV administration of obestatin (0.1, 0.3 and 1.0 nmol/rat) did not modify the plasma acyl ghrelin and des-acyl ghrelin levels, the acyl ghrelin/ des-acyl ghrelin ratio and nesfatin-1 concentrations. The ICV acute administration of obestatin had no influence on the 2-h rate of gastric emptying of a solid nutrient meal, but the ICV h/rCRF injection delayed it. The weight of food ingested 1 h before ICV injection significantly, but negatively correlated with the gastric emptying of a solid nutrient meal. Our study indicates that the ICV injection of obestatin does not change the 2-h rate of gastric emptying of a solid nutrient meal and the relatively weak interrelationships between ghrelin gene products and nesfatin-1. However, the weight of the ingested food negatively affects the gastric emptying of a solid nutrient meal in conscious, fasted rats.

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Plasma nesfatin-1 concentrations in restricting-type anorexia nervosa

Cited by 77 publications

References 25 publications

Nesfatin-1 Exerts a Direct, Glucose-Dependent Insulinotropic Action on Mouse Islet Beta and MIN6 Cells

Nesfatin-1 Exerts a Direct, Glucose-Dependent Insulinotropic Action on Mouse Islet Beta and MIN6 Cells

Effects of aging on the plasma levels of nesfatin-1 and adiponectin

Impact of intracerebroventricular obestatin on plasma acyl ghrelin, des-acyl ghrelin and nesfatin-1 levels, and on gastric emptying in rats

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