Similar metabolic responses to calorie restriction in lean and obese Zucker rats

Chiba, Takuya; Komatsu, Toshimitsu; Nakayama, Masahiko; Adachi, Toshiyuki; Tamashiro, Yukari; Hayashi, Hiroko; Yamaza, Haruyoshi; Higami, Yoshikazu; Shimokawa, Isao

doi:10.1016/j.mce.2009.05.001

Cited by 31 publications

(44 citation statements)

References 48 publications

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“…The levels of serum insulin and inflammatory cell infiltration in Zucker fatty rats were significantly higher than those of lean rats (data not shown), which were similar to other studies. 39,40 We have already reported that periodontitis induces the initial stage of atherosclerosis in normal rats. 19 Therefore, we focused on the combined effects of periodontitis and obesity on aorta in this study.…”

Section: Discussionmentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n ¼ 24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factora (TNF-a), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic b-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-a were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

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Section: Discussionmentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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“…For instance, suppression of growth and reproduction, and activation of stress response, could be induced by the activities of NPY neurons [12][13][14] . This neuroendocrine adaptation hypothesis of the anti-aging effects of CR was supported, in part, by the findings of NPY neuron activation upon CR in animal models [20][21][22] . Considering that NPY activity is crucial for the beneficial effects of CR, NPY-knockout mice should not demonstrate an extended lifespan from CR.…”

Section: Regulatory Center For Metabolic Shift On Crmentioning

confidence: 84%

“…On the other hand, ghrelin, which is secreted from the gastro-intestinal tract, is a positive regulator of NPY 18,19) . These hormonal changes favor up-regulation of NPY under CR conditions; namely, CR decreases leptin and insulin levels, but increase ghrelin levels 20) . Signal transduction pathways of these ligands and receptors may play important roles in CR-mediated anti-aging effects, because these mechanisms explain the effects of CR from an evolutionary point of view.…”

Section: Regulatory Center For Metabolic Shift On Crmentioning

confidence: 99%

Mechanisms of lifespan extension and preventive effects of calorie restriction on tumor development: Possible link between central neuroendocrine system and peripheral metabolic adaptation

Chiba

Dong

Nishizono

et al. 2013

JPFSM

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Restriction of food intake (calorie restriction [CR]) in laboratory animals extends their lifespan and delays the onset of various age-associated diseases, including cancer development. Recent studies revealed that the molecular mechanisms underlying CR-mediated antiaging effects may be regulated by a confined number of signal transduction pathways that are triggered by neuropeptide Y (NPY) neurons in the neuroendocrine system. On the other hand, possible peripheral regulators of the beneficial effects of CR involve a transcriptional regulator complex, the hepatocyte nuclear factor 4α/peroxisome proliferator-activated receptor gamma coactivator 1-α (HNF-4α/PGC-1α) complex. This complex could regulate not only glucose and lipid metabolism, but also DNA damage responses in the liver. Therefore, maintenance of optimal glucose and lipid levels to prevent metabolic syndrome, and activation of the DNA damage response for suppression of tumor development, may depend on the HNF-4α/PGC-1α complex. Hence, small molecules modulating the activity of this complex could be an important target for development of CR mimetics (CRM), which mimic the beneficial effects of CR without actual food restriction.

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“…Recently Chiba et al suggested a model where NPY and ghrelin play a crucial role during food deprivation in rats (Chiba et al 2009). They proposed that caloric restriction decreased plasma insulin and leptin levels, whereas it increased ghrelin levels and that these hormonal changes result in an increased NPY expression in the arcuate nucleus.…”

mentioning

confidence: 99%

“…NPY/AgRP neurons project their axons to downstream neurons such as GHRH neurons suppressing them. They also suggested that NPY up-regulation could also enhance oxidative stress resistance and hepatic glucose production (Chiba et al 2009). In addition, intraventricular injection of NPY inhibited GH secretion, and a NPY antiserum led to elevated plasma GH levels and partially restored GH secretory pulses in food-deprived rats (Muller et al 1999).…”

mentioning

confidence: 99%

Ghrelin neutralization during fasting-refeeding cycle impairs the recuperation of body weight and alters hepatic energy metabolism

Sangiao‐Alvarellos

Helmling

Vázquez

et al. 2011

Molecular and Cellular Endocrinology

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Ghrelin neutralization during fasting-refeeding cycle impairs the recuperation of body weight and alters hepatic energy metabolism.. Molecular and Cellular Endocrinology, Elsevier, 2011, 335 (2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 37A c c e p t e d M a n u s c r i p t A c c e p t e d M a n u s c r i p t 2 ABSTRACT Ghrelin, a hormone whose levels increase during food deprivation, plays a pivotal role in the regulation of food intake, energy metabolism and storage, as well as in insulin sensitivity. Here, we investigated the effects of acyl-ghrelin neutralization with the acyl-ghrelin-binding compound NOX-B11(2) during the fasting-refeeding cycle. Our data demonstrate that ghrelin neutralization with NOX-B11(2) impairs recuperation of lost body weight after food deprivation. Analysis of enzymes involved in glucose and lipid metabolism in liver of fed, fasted and refed rats revealed that neutralization of acyl-ghrelin resulted in minor decreases in the enzymes of glycolytic and lipogenic pathways during fasting. However, during refeeding these enzymes as well as glycogen levels recovered more slowly when acyl-ghrelin was blocked. The high levels of ghrelin in response to food deprivation may contribute to an adequate decrease in hepatic glycolytic and lipogenic enzymes and aid in the recovery of body weight and energetic reserves once food becomes available after the fasting period.

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Similar metabolic responses to calorie restriction in lean and obese Zucker rats

Cited by 31 publications

References 48 publications

Effects of periodontitis on aortic insulin resistance in an obese rat model

Effects of periodontitis on aortic insulin resistance in an obese rat model

Mechanisms of lifespan extension and preventive effects of calorie restriction on tumor development: Possible link between central neuroendocrine system and peripheral metabolic adaptation

Ghrelin neutralization during fasting-refeeding cycle impairs the recuperation of body weight and alters hepatic energy metabolism

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